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PSYC 301 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Neuropsychology

A

study of brain disfunction

Parkinson’s disease: lack of motor ability and tremors

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2
Q

Cognitive neuroscience

A

cognitive psychology with brain imaging

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3
Q

Phineas Gage

A

managed people working on the railway
Job to dig up hole and but blasting cap on -> must tamp (press down) to flatten down blasting cap
One day, there were explosives but no blasting cap so when he was tamping down, the tamping iron shoots through his head
He never rendered unconscious and explained that his brain ha shot through
Had brain bits coming out and pulsing from his skull
Then he vomited and half a teacup of brain bits fell out of his brain
Phineas’s family and friends noticed:
Before: capable, efficient, sharp, energetic and persistent at executing his plans
Afer: fitful, indulgent, impatient of restraint or advice when when it conflicts with desires, arranging plans then abandoning
change in personality
Ability to speak and count were all in tact
Materialist: you are your brain; when your brain is dysfunctional/damage = you are dysfunctional as well
Good evidence that gage recovered -> gage got a responsible job (horse carriage driver)
Died of seizures; epilepsy was generated from the traumatic brain injury

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4
Q

Golgi’s stain

A

mixes together silver nitrate stain

Stained 10% of neurons -> can see neurons in totality (shape + connections + dendrites)

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5
Q

Golgi: reticular theory

A

Golgi: reticular theory (neurons look like mesh) -> all cells are continuously connected together (how thoughts and signals are flown around in a big net)

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6
Q

Ramon y Cajal’s (spain) drawings

A

neurons are quite distinct (discontinuous)
Looked like they had specialized functions
There is a space between neurons through which they communicate = synapse
Drugs change how the nervous system functions -> can only do that if there is a place like the synapse
Ramon y Caja: neuron doctrine - principles upon which all of the neuroscience was performed
Ramon y Cajal correct with neurotransmitters

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7
Q

neurogenesis development

A

neurons you have from about a year old onward are not replaced - never gonna have any more than that
But not entirely true, there is adult neurogenesis in one part of the hippocampus to a certain extent

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8
Q

Adult Neurogenesis

A

In utero (in development), developing lots of neurons
Clearly shown in animal models that adult neurogenesis happens
In rats, adult neurogenesis only happens in a subregion of the hippocampus
Adult neurogenesis tapers off rapidly around puberty
Weak evidence of adult neurogenesis in some people who died in a car accident at 12
Only in part of hippocampus
Neurons lost to brain injury or damage -> serious, neurons are gone
Could add new neurons in theory (stem cell therapy) but they would not hold the memories or information stored within the neuron
But there is potential for new learning

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9
Q

Brain of insect- LOCUST

A

collection of ganglia
Sensory organs at front of body with lots of nervous tissues close together
Insects have ganglia throughout their body -> brain is spread out across the body
Sensory motor integration is much faster -> faster reflexes

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10
Q

Fish brain- vertebrates are similar

A

Spinal cord -> medulla -> cerebellum -> optic lobe -> cerebrum
Fish cerebrum is much smaller than humans
Most of the activity in the midbrain + cerebellum + brain stem is not accessible to consciousness
Cerebrum is most connected to consciousness
Large behavioural repertoire and nonconsious nervous system components

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11
Q

Rat: brain

A

Cerebrum so large that it is covering the midbrain and larger than the cerebellum
Olfactory bulb at the front -> smell
Not convuluted
Spinal cord coming out back - same plane

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12
Q

Dog brain

A 
spinal cord coming out of back
Convoluted brain
Front of brain is the olfactory bulb not frontal cortex
Front of brain is relatively undeveloped
Understand pointing - cognitive ability
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13
Q

Monkey brain

A

Spinal cord coming out of bottom
Bipedal
Convoluted but less than humans
differentiation of different lobes

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14
Q

Chimpanzee brain

A

Much more convolution - doesnt match human brain
Bigger cerebrum
Frontal lobe is larger in humans
Increasing cognitive sophistication

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15
Q

Dolphin brain

A

Very convoluted
Larger brain mass
Very smart -> but not as smart as humans
Exception to trends for brain size

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16
Q

Macaw brain (grey parrot)

A

Smartest nonhuman animal known
Not convoluted
Amazing sophisticated machinery
Can count to very high numbers, categorize items and subcategories

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17
Q

Trends for brain sophistication (does not tell us anything mechanistic) - these trends are not absolute

A

Bigger cerebrum -> more cognitive capabilities
Cerebellum and midbrain -> remains similar size
Brains get more convoluted the more sophisticated the animal
Frontal cortex grows more with sophistication
Disproportionately large brain -> indicates intelligence

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18
Q

Brain cell density

A

Brain with the greater number of neurons wins
Size and the number of neurons are different
Humans have the densist brain with the most amount of neurons in a cubic cm/ weight
Primates have disproportionately dense brain

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19
Q

Matter:

A

Grey matter: cell body of neurons, and whole unmyelinated neurons
White matter: represnets the long connections (axons) which are myelinated (fatty sheath)
Our brain regions -> usually referring to grey matter areas

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20
Q

Staining reveals “matter”
Nissl-stained (cresyl violet)
Fiber stain

A

Must take brain and slice up (post mortem)
E.g. Alzeimhers was never diagnosed until post mortem
Nissl-stained (cresyl violet) - reveals where the grey matter is located (purple area)
Fiber stain (many types) - stains white matter (darker area)
Distinction of location of white matter and grey matter is slightly arbitrary

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21
Q

Two basic cell types:

A

Neurons

Glia

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22
Q

Neurons

A

main communicating cell in the nervous system (all cells communicate and virtually all cells release chemicals that are received by other cells)
Neurons can send signals very quickly and be targeted to very large distances
Many types/shapes but similar design
Dendrite -> soma -> axon -> terminal
Input layer integrate and come together and goes to output where chemicals are released
Cell determines whether it will fire an Action potential at the axon from the integrated signals from the dendrite
AP travels down axon and chemicals (NT) are released at the terminal
Apical dendrites at the end; basal dendrites near the cell body
Every time there is a synapse -> opportunity to modify the signal

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23
Q

Neurons:

  • Pyramidal
  • Stellate
  • Purkinje
A

Pyramidal- major feature of cerebral cortex, pyramid shape
Stellate- cell found in deeper brain areas (cortical areas), star shape
Purkinje (cerebellem) - many many branches that branch off the collateral

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24
Q

2 basic types of neurons:

A

Projection neurons

Interneurons

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25
Q

Projection neurons

A

long axons that project to other distant brain areas (pyramidal cells)
Projection neurons send their long projections to other brain area connecting to another projection neuron (like wires with stops at synapses where interneurons can alter signal)

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26
Q

Interneurons

A

neurons that have short axons that project locally (stellate cell), nonmyelinated axons
Function: modify or modulate travelling signals between projection neurons
To adjust timing (movement, perception- shift attention), to stop it (ignore senses during sleep)

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27
Q

Glia:

A

Important for structure and support
Influence way neurons fire (communication)
Microglia

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28
Q

Microglia

A

immune system in brain which is separated from external environment (blood brain barrier)
Brian is walled off from their immune system so they need a protector
Detects of foreign bodies or agents -> when detected, microglia enter a prime state (larger and more active) -> engulfs foreign body, and digests it
Oligodendrocyte + Schwann cell -> both are myelinating glia and produces myelin which wraps around axon and speeds up neuronal communication but they do it in different ways and places

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29
Q

Schwann cells

A

wrap themselves around one axon found in the peripheral nervous system (not in brain and spinal cord)

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30
Q

Oligodendrocytes

A

myelinate several axons in the CNS (brain + spinal cord)

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31
Q

Glial networks (astrocytes)

A

Keep nervous system healthy and function
Part of blood-brain barrier
They wrap around the capillary/blood vessel to make sure blood does not enter the brain
Blood is toxic to the brain, meaning neurons do not have access to oxygen, glucose
Astrocytes mediate all the nutritional transfer
scaffolding neuronal migration in development

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32
Q

Astrocytes are wrapping themselves around the neuron + especially around synapses

  • can control
  • can influence
A

Can control the environment (chemical composition of area) around neuron + synapse
Can influence how the neurons talk to each other: they have gliotransmitters and receptors that receive signals from the neurons

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33
Q

gliosis

A

If there is damage or scarring to the brain

- the astrocytes form those glial scars

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34
Q

Gap junctions

A

protein on astrocyte fits in with another protein on another astrocyte, creating a continuous hole between astrocytes
The reticular theory is kind of true for astrocytes
This is how they quickly buffer out an ion to control the concentration of ions depending on the environment
Signals can travel very fast through astrocytes due to continuous connection
Fast adaptation from states

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35
Q

The tripartite synapse

Conversion of three (presynaptic neuron, postsynaptic neuron, astrocyte

A

astrocyte is receiving signal from the presynaptic axon as well
sending own signals that can influence how the axon or dendrites respond
Can send signals that decrease how many neurotransmitters are released from the presynaptic axon
Can also affect the efficacy of the presynaptic axon signal on the dendrites - influence how neurons talk to each other

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36
Q

Glia play a key role in brain function

A

Glia not neurons most affected by the brain aging
Glial cells play a key role in regulating motivation for drug in heroin addiction
Glial cells are critical players in brain response to social stress
Glial cells shape nerve endings through previously unknown molecular pathway
Memory - change in structure and/or function of your nervous system not just synapse

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37
Q

Myelination is related to learning how

A

the thicker the myelin around the axon, the more effectively it will insulate the axon
Learning can be affected by myelination -> neurons must be sending signals to the oligodendrocytes

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38
Q

The central dogma of molecular biology:

A

DNA ->(transcribed)-> mRNA->(translated)-> protein
Our DNA interacts with environmental factors
If learning and memory is just a change in structure and/or function of the neurons
One way to change is by transcription or translation

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39
Q

Cell membrane

A

phospholipid bilayer

Barrier to things except - Steroids hormones can enter the cell

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40
Q

Cytoskeleton

  • 3 types
  • expand on Microtubules
A

neurofilaments
Microfilaments
Microtubules- primary (biggest) part of cytoskeleton
Travel down axon
Have proteins that transport vesicles down to axon terminal to carry essential things
Kinesins: anterograde transport
Dyneins: retrograde transport

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41
Q

Alzheimer’s disease, and chronic traumatic encephalopathy (repeated head injuries) related to

A

Remodeling and shaping cytoskeleton

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42
Q

Synapse

A 
Every time there is a synapse -> opportunity to modify the signal
site of neural communication
Presynaptic: NT release
Postsynaptic: receptors
Axodendritic synapse
Axoscretory
Axoaxonic
Axoextracellular
Axosomatic
Axosynaptic
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43
Q

Axodendritic synapse

A

presynaptic axon to postsynaptic dendrite

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44
Q

Synapse

Axoscretory

A

Axons that release their NT/hormones into the bloodstream

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45
Q

Synapse

Axoaxonic

A

Axon synapsing with axon

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46
Q

Synapse

Axoextracellular

A

Axon not synapsing to environment

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47
Q

Synapse

Axosomatic

A

Axon that is on cell body

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48
Q

Synapse

Axosynaptic

A

Axon synapse on another synapse

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49
Q

Dendrites

A

Receiving signals, input layer
Spiny or non spiny
Blobs that compartmentalize the synapse - dedicated area to modify instead of modifying all
Glutamatergic neurons are often spiny neurons
Many neurons are non spiny (e.g. gabaergic)
We are a product of our dendritic spines (quantitatively and qualitatively) = We are the synapses

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50
Q

Higher than average dendritic spine number is associated with

A

autism spectrum disorder

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51
Q

Decrease in dendritic spine number associated with

  • early life
  • late life
A

schizophrenia in teen years, whereas later on in life may be related to Alzheimer’s disease

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52
Q 
The Vertebrate Nervous system
Peripheral NS
Somatic Nervous system (SNS)
- Afferent fibers
- Efferent fibers
A

Somatic Nervous system (SNS): connects to the external environment
external environment, (mostly) conscious excess to
Afferent fibers: from the body to the brain
Sensory signals; touch, sensation, stretch
Efferent fibers: out of brain to body
Motor control: controlling body
Muscles that the somatic NS controls- muscles attached to to skeleton (striated muscles)
Conscious control

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53
Q 
The Vertebrate Nervous system
Peripheral NS
Autonomic NS (ANS)
Afferent: 
efferents:
A

Autonomic NS (ANS): Internal environment, (mostly) non-conscious
Afferent: sensation signals from inside of body
efferents:
Digest faster or slower
Not always mutually exclusive to one another
No voluntary control of viscera
Sympathetic
Parasympathetic

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54
Q

Sympathetic:

A 
mobilize energy (fight or flight)
Getting ready to deal with unexpected and stressful event
Heart rate speeds up, lungs dilate (more O2), digestion slows down
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55
Q

Parasympathetic:

A

conserve energy
Innervates all the same targets (efferent)
Complementary or opposite of SNS
Focused on conserving energy: slows down heart rate, constricts lungs, increase digestion
Rest and digest

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56
Q

Cell clusters

A

grey matter -> cortex + underneath cortex and white matter
nucleus/nuclei (CNS) vs. ganglion/ganglia (PNS)
Dorsal root ganglia - where cell bodies for somatosensory system
Touch receptor going up spinal cord
Basal ganglia are nuclei!

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57
Q

Bundle of axons

A

white matter- many myelinated axons
tract (CNS) vs. nerve (PNS) vs. fibres (all)
Emerging from eye -> optic nerve
When entering the brain (optic chiasm) when in brain (optic tract)

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58
Q

Anatomical dimensions

A 
Top: superior/dorsal
Bottom: inferior/ventral
Down midline: medial
Lateral: sides
Left and right are from the perspective of the person who owns the brain
Anterior: toward top of spinal cord
Posterior: toward bottom of spinal cord
Dorsal: back side of spine
Ventral: front (Stomach) side of spine
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59
Q

Spinal Cord

  • order
  • dorsal side
  • ventral side
  • middle of spinal cord
A

Cervical -> thoracic -> lumbar -> sacral -> coccygeal
Dorsal side: white matter for sensory information (Afferent)
Ventral side: white matter for motor signals (efferent)
Middle of spinal cord: grey matter

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60
Q

why does the Spinal Cord narrows/tapers when from cervical to coccygeal

A

Ends in cauda equina (tapering frays)
All of afferent have not yet entered the CNS near the top; all of the efferent signals have not yet left the spinal cord -> thickest near the top where the most about of signals are traveling
limited amount of points where nerves can leave or enter the spinal cord -> Intermittent projections from the spinal cord

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61
Q

how does Information leaves or enters the spinal cord?

A

in nerves (bundles of white matter) -> spinal cord is inside bone

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62
Q

Spinal cord damage: loss of function related to segment damage

A

Damage at cervical region is most severe (most nerves affected) compared to lower down the spinal cord

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63
Q

3 Major divisions of the brain and when does it appear

A

Appears early in development around 18-21 day old embryo

  1. Forebrain: we have a disproportionately large forebrain
  2. Midbrain (Mesencephalon)
  3. Hindbrain
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64
Q

Forebrain:

A
  • we have a disproportionately large forebrain
    1. Telencephalon
    2. Diencephalon
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65
Q

Telencephalon

A 
Cerebral cortex
Major fissures
Major gyri
Four lobes
Limbic system
Basal ganglia
Cerebral commissures (corpus callosum)
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66
Q

Cerebral cortex

A
  • Neocortex

- Hippocampus

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67
Q

Major fissures

A
  • Central fissure
  • Lateral fissure
  • Longitudinal fissure
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68
Q

Major gyri

A
  • Precentral gyrus
  • Postcentral gyrus
  • Superior temporal gyrus
  • Cingulate gyrus
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69
Q

Four lobes

A
  • Frontal lobe
  • Temporal lobe
  • Parietal lobe
  • Occipital lobe
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70
Q

Limbic system

A
  • Amygdala
  • Hippocampus
  • Fornix
  • Cingulate cortex
  • Septum
  • Mammillary bodies
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71
Q

Basal ganglia

A
  • Amygdala
  • Striatum
  • Caudate
  • Putamen
  • Globus pallidus
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72
Q

Diencephalon

A 
Thalamus
Hypothalamus - Mammillary bodies
Optic chiasm
Pituitary gland
Immediately adjacent to midbrain
small
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73
Q

Thalamus structures

A

Massa intermedia
Lateral geniculate nuclei
Medial geniculate nuclei
Ventral posterior nuclei

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74
Q

Midbrain (Mesencephalon)

A 
Tectum
- Superior colliculi
- Inferior colliculi
Tegmentum
- Reticular formation
- Cerebral aqueduct
- Periaqueductal gray
- Substantia nigra
- Red nucleus
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75
Q

Hindbrain

A 
Metencephalon
- Reticular formation
- Pons
- cerebellum
Myelencephalon
- Reticular formation
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76
Q

Myelencephalon (aka the medulla oblongata)

A

Junction between the spinal cord and brain
Lots of tracts
Oldest part of brain
Involuntary control of life sustaining functions (maintains heart beating, and diaphragm moving)
Doctors reluctant to perform surgery here - slight damage could be fatal

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77
Q

Opioid overdose -> respiratory depression -> affects which brain region that could be fatal

A

medulla - could be fatal fatal (posterior)

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78
Q

The reticular formation

A

Aka the reticular activating system (not true system but a collection of nuclei)
~100 nuclei
Runs from myelencephalon to mesencephalon -> travels through hindbrain and midbrain
Critical for arousal, wakefulness, attention sleep -> maintaining consciousness

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79
Q

Damage to the reticular formation

A

Aka the reticular activating system (not true system but a collection of nuclei)
~100 nuclei
Runs from myelencephalon to mesencephalon -> travels through hindbrain and midbrain
Critical for arousal, wakefulness, attention sleep -> maintaining consciousness
Damage to this region causes major disruptions to life, and/or can be (posterior) fatal -> difficulty maintaining consciousness

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80
Q

Metencephalon

A

(more anterior hindbrain)
Lots of tracts
Comprised of multiple regions
Houses the reticular formation -> damage can cause disorders of consciousness and/or difficulty with sensation and movement

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81
Q

pons

+ damage

A

Metencephalon
The pons: (ventral) large white-matter bulge, continuing from spinal cord/medulla
Both afferent and efferent
Damage: affect sensation and ability to feel things
Loss of sensation
Interfere with ability to control muscles (paralysis, plegia)

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82
Q

cerebellum

+ damage

A

The cerebellum: (dorsal)
10% of brain volume (small)
>50% of neurons
Critical for motor coordination, corrects movement
Integration of sensory and motor information
Damage: problems with motor coordination, and movement

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83
Q

Mesencephalon

Tectum

A

Tectum: dorsal
Comprised of two pairs of bumps (collliculi)
Aka the boston pizza part of your brain - integrating sensory information to control movement outside of your conscious control
Superior colliculi
Inferior colliculi
Outside of conscious access and often automatic

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84
Q

Mesencephalon

Tegmentum

A

more ventral/floor
Contains the top of reticular formation- nuclei involved in life-sustaining features
More fibres- lots of efferent and afferent
Periaqueductal grey
Dopamine-producing regions - movement related to motivation
Substantia nigra
Ventral tegmental area (VTA)
Red nucleus

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85
Q

Superior colliculi

in Mesencephalon Tectum

A

vision with respect to eye movement out of conscious control

Draws attention towards attention-grabbing things

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86
Q

Inferior colliculi

in Mesencephalon Tectum

A

audition with respect to head/body orientation
Draws attention toward loud sounds
Automatic and outside conscious

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87
Q

Tectum Damage (damage to superior colliculi)

A

Parinaud syndrome- inability to move eyes especially upwards and orienting towards sight or sound

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88
Q

Mesencephalon
Tegmentum
Red nucleus + damage

A

plays key role in movement and motor control in animals with smaller forebrain but our motor cortex does most of the movement related tasks
Species specific behaviour
Side effects of using anti-psychotic medication from this region
Damage from using anti-psychotic medication: strange motor quirks

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89
Q

Mesencephalon
Tegmentum
Periaqueductal grey

A

main target of amygdala
Fear or emotional emotions are generated here
Internal analgesia (suppresses pain)

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90
Q

Substantia nigra

Damage

A

Dopamine-producing regions - movement related to motivation
Substantia nigra
Damage: parkinson’s disease

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91
Q

Diencephalon (forebrain)

Thalamus

A

Many nuclei: inputs from sensory systems, cerebellum, basal ganglia
relay center for sensory information
Many different nuclei receives almost as much from cortex (many which are from sensory systems) as it sends to cortex
Every sense except olfactory system goes through the thalamus
Everytime an axon stops and creates a synapse -> opportunity to modify or influence the signal
Receives almost as much information from the cortex as it sends out to the cortex -> creating a loop
Corticothalamic loops
Has many different functions related to sensation and movement and consciousness

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92
Q

Corticothalamic loops

A

suggested that the generation of consciousness is from these loops from thalamus and the cortex that resonate is the substrate for conscious awareness

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93
Q

Thalamus damage

A

Damage to this region: problems with attention, difficulty sustaining consciousness, sensation, and motor

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94
Q

Diencephalon (forebrain)

Hypothalamus

A

Collection of Many nuclei
Master control center for endocrine system (hormone release)
Sending lots of outputs to pituitary gland
Key intersection with endocrine system via the pituitary gland
Diverse functions: sex, aggression, feeding, sleep/wake, gender

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95
Q

Hypothalamus damage

A

Damage: narcolepsy (falling asleep randomly), sex, aggression, eating

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96
Q

Telencephalon

A

The largest division of the human brian
Not just the cortex, but also underlying structures (e.g. hippocampus + amygdala)
Damage here is wide-ranging in its symptoms
Cerebral cortex: aka cortex, neocortex (outer layer)

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97
Q

Cerebral cortex

A

aka cortex, neocortex (outer layer)
Largest and most prominent feature of the human brain
The cortex is convoluted: (maximize surface area)
gyrus/gyri - bump (outer fold)
Sulci (sometimes fissures esp when important or particularly deep) - folds inward
Not much functional difference between gyrus and sulci
Damage may show up in only one specifically for sulci
Hippocampus - another cortex that is older

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98
Q

Hemisphere

A

The cerebrum is divided into two hemispheres
Separating the hemispheres: the longitudinal fissure (big vertical division - sagittal)
Left and right hemispheres are only connected by a few tracts (commissures)
Corpus callosum: the largest commissure, prominent white matter area

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99
Q

Disconnecting the hemispheres

A

Split brain patients: 2 indepently working hemispheres
They may guess and try to explain why they responded in such a way instead of saying they just didn’t know
Callosotomy, a rare treatment for severe epilepsy
Contralateral organization: left half of world governed by right side of brain, vice versa

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100
Q

Left hemisphere damage

A

Left hemisphere dominance for language - damage causes profound damage to language
Will be able to report words in their right visual field
Put something in right hand, able to verbally identify the thing

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101
Q

Right hemisphere damage

A

less damage to language
Won’t be able to report words in their left visual field
Put something in left hand, unable to verbally identify the thing

102
Q

Central fissures separates the

A

Central fissures separate frontal and parietal lobes

103
Q

Lateral fissures separates

A

Lateral fissures separates temporal lobe from frontal/parietal

104
Q

insula

A

Deep in the lateral fissure: the insula (cortex- plays a role in taste and emotions such as disgust or anger)

105
Q

The limbic system (not a system)

A

part of telencephalon
Aka The papez circuit (not circuit - distinct region that do different things)
Amygdala, HTh, mammillary body, hippocampus, fornix, cingulate cortex, septum, olfactory bulb
Hippocampus is important for formation of long term memory
Amygdala is important for emotional learning and behavioural outputs
Symptoms from damage can vary from region to region

106
Q

Basal ganglia circuitry

A

Deeper grey matter structures in telencephalon not considered part of the limbic system
Circuit that works together
Includes striatum (caudate + putamen) and globus pallidus, sometimes others (e.g. subthalamic nucleus)
Nucleus accumbens (motivation, movement, seeking award) is a subregion of striatum/caudate, sometimes called ventral striatum
Critical in movement, skills, habits, decision making, addiction

107
Q

Anatomy of cortical layers

A

Neocortex has 6 different layers
Different neurons at different layers
Input layers, output layers
Different parts of the cortex look different - differences in layer thickness but all have 6 layers
Layer 4 is a major input layer where sensory inputs come in
The somatosensory cortex or visual cortex would need lots of sensory inputs -> thicker layer 4
Output layer thicker in motor cortex
The differences between parts of the cortex can be used to make maps

108
Q

controlling voluntary movement - eating

uses which brain regions

A 
Prefrontal cortex- plan for food
Premotor areas - reach out for food
Motor cortex - lift food appropriately
Basal ganglia - correct movement appropriately
Pons- motor info travels down
Cerebellum - all the info integrated
Medulla - eating and swallowing
More
109
Q

Cerebral blood flow

A

All the blood that our brain receives
Right internal carotid arteries - along front
Vertebral arteries- along back
Left internal carotid arteries - along front
Limited supply- only 3 arteries
No reserves- a lot of energy used in brain
No redundancies- only a bit of overlap but mostly no overlap
Only 1 artery supplying blood for each brain region
Disruptions to cerebral -> brain will quickly die

110
Q

The blood brain barrier (BBB)

A

Capillary walls are tightly packed - no pores (tight junctions)
Series of astrocytes wrapped around capillaries to block off blood supply to the rest of the brain
Astrocytes are responsible for getting nutrients to the brain
Protein transporters to get larger molecules to brian
blood can have gross stuff
Blood has toxic effect on neurons if leaks onto brain (hemorrhage)
Protects brain
Active transport for large molecules

111
Q

Meninges

A

Primary protection for the brain from outside infection
Three layers of meninges:
Outermost, thickest layer: dura mater
Midde: arachnoid mater - hard to see
Inner layer: pia mater- think transparent layer (wrap)

112
Q

Cerebrospinal fluid (CSF between arachnoid and pia mater) and ventricles

A

CSF is produced in the brain (lateral ventricle)
Fluid moves from the lateral ventricle to the 3rd ventricle to the 4th ventricle through aqueducts and then out the central canal of the spine or around the brain
Support, protection from impact, nutrition, clear waste; ventricles are thought to play a similar role
some people’s central canal are discontinuous with stops

113
Q

Hydrocephalus

A

When CSF flow is blocked from getting out of the brain, the ventricles expand and damage the surrounding brain
Treated by a shunt - artificially remove fluid from skull and relieve that pressure

114
Q

Measuring Potential Energy (membrane potential/voltage)

A

A healthy neuron has a resting membrane potential (voltage) of between -60 and -80 mV
Often -65mV or -70mV
But can vary depending on protein density and concentration
Extracellular electrode
Intracellular electrode (very fine tip)- slightly negative compared to the outside
Potential: comparing inside and outside the cell

115
Q

Neuronal communication is chemical

A
  1. Primarily the result of two ions (chemicals), sodium (Na+) and potassium (K+)
    Movement of the ions
  2. Ions move into or out of the cell, but not freely
    Cross the membrane
    The PM is designed to keep everything out
    Need channels
116
Q

Neuronal communication is electrical

A
  1. Ions are positively and negatively charged (Na+ and K+ are both positive, as per “+”)
    The charge sums to voltage
    1 fewer electron (+ charge)
  2. As they move into or out of cell, they change the potential (voltage) at the membrane
    Note: absence of pos. is neg.!
    i.e. remove a pos., leave a neg
    Few positive charge ion leave the cell -> membrane potential is negative
117
Q

Channels and pumps

A

(made of proteins)
the plasma membrane keeps things out - esp water and lipids out
Some things diffuse the PM -> not fast or effective
Only certain molecules/ions are permitted to cross membrane, via channels and pumps
Some are nonspecific and allow many things through
But most are selective

118
Q

Channels

A

allow passive diffusion (i.e. along chemical gradient)
No control in the direction of movement
Moves from area of high concentration to the area of low concentration

119
Q

Pumps

A

actively push ions against their chemical gradient (low to high concentration)
Requires energy (ATP)
They are a double door system:
One door opens up -> ions comes into the middle -> door closes -> the other side door opens -> ions can leave
Can control the direction of ion movement
Active: require energy

120
Q

Sodium-potassium pumps

A

Use 2/3rds of all brain energy (ATP) to run Na+/K+ pumps
Anything that disrupts our energy affects these pumps
With ever mechanistic process, they are constantly:
3 Na+ out; 2 K+ in
Creates concentration gradient (net negative in cell)
essential to neuronal communication

121
Q

Potassium “leak” channels

A

Require no energy
Constantly open allowing K+ to move whatever way they want (concentration the gradient)
Typically, K+ leaves the cell as there is a higher concentration of K+ inside the cell due to the sodium potassium pump -> inside becomes net more negative
The most common method of lethal injection of capital punishment (high concentration of K+) leads to fatal results

122
Q

Cells are polarized

The ___ is an equilibrium between chemical forces and electrical forces; how does the cell maintain membrane potential

A

RMP; Na+/K+ pump (always working) -> inside negative (attracts positive things)
K+ channel (always open) -> can move freely
- Both are embedded in membrane
- Both are constantly working
Na+ channel (closed under resting conditions)

123
Q

____ _____ is fluctuations in our membrane potential

A

Neuronal communication

124
Q

When a neurotransmitter binds to a receptor, it can have one of two localized effects:

A
  1. Depolarize the membrane (e.g. from -70 to -67mV -> closer to 0mV) -> excitatory postsynaptic potential (EPSP) -> increase likelihood of an action potential (AP)
  2. Hyperpolarize the membrane (e.g. from -70 to -72mV -> away from 0mV) -> inhibitory postsynaptic potential (IPSP) -> decrease likelihood of AP
125
Q

The transmission of postsynaptic potentials (PSPs)

A

graded, rapid, and decremental: PSPs travel like an electrical signal along an uninsulated wire

126
Q

is one EPSP enough to cause an action potential

A

One EPSP is not enough to cause an action potential -> EPSPs and IPSPs sum spatially and temporally
The more neurotransmitters bind to more receptors, the larger the postsynaptic potential

127
Q

Spatial summation

A

two or more postsynaptic potentials arrive from different neurons at the same time, they can sum to fire an AP
Multiple IPSP all arrive at the same time -> make it unlikely for AP to fire
Unlikely: one EPSP and IPSP arrive at the same time -> two cancels each other out

128
Q

Temporal summation:

A

Bunch of EPSPs occurring in rapid succession (short amount of time), they add up together to result in a greater EPSP
Same with IPSP

129
Q

AP Generation

A

If the sum of the EPSPs and IPSPs that reaches the axon initial segment is sufficient to depolarize the membrane there above its threshold of excitation, then an action potential (AP) is generated
The AP is a massive, brief reversal of the membrane potential
(e.g. from -70 to +55 mV)
The AP is an all-or-none phenomenon
i.e. Not graded
Always same size/shape
The threshold of excitation is simply where voltage-gated Na+ channels open
With enough EPSP to reach the threshold, an AP is guaranteed to occur
All or none
AP: Flips from negative to positive
Threshold: the sodium channels (voltage gated) open up and rushes Na+ to rush in
The action potential is just ions moving across the membrane

130
Q

Proteins of the action potential

Voltage-gated sodium channels (Nav)

A

Open up at the threshold of excitation when cell is depolarized enough
Lots of Na+ rushes in vigorously and makes the inside of the cell positive (+40, +50) and outside the cell negative
Have an “auto-shutoff” (inactivation gate/aa ball and chain) after about 1ms
Ball flips up and closes the gate (inactivation state - refractory periods) -> reason why there is a peak of the AP
Stays inactivated until back down to the resting membrane potential
In this state, cannot send anymore AP

131
Q

stages of AP

A

Stage 1: Responsible for rising phase of AP (depolarization phase)
Stage 2: Leak channels- K+ flowing out of the cell to bring membrane potential back down (repolarization + slight hyperpolarization)

132
Q 
Proteins of the action potential 
Potassium channels (two types)
A

Leak channels- K+ flowing out of the cell to bring membrane potential back down (repolarization)
voltage-gated channels (Kv) that start to open during the rising phase of the AP
Provide opportunity for K+ to leave the cell
They are slow in opening and closing
Hyperpolarization (does not close fast enough when membrane potential is back to resting and causes cell to become more negative)
Start to opens up slowly (repolarization when cell becomes too positive during rising phase)
Responsible for repolarization & brief hyperpolarization

133
Q

does the sodium-potassium pump play a role in AP

A

the sodium-potassium pump is too slow to play a role in the AP
After each AP there’s a little more Na+ left inside the cell and a bit of K+ left outside the cell
NA+/K+ over time maintains the balance by sending Na+ out of cell and K+ into the cell

134
Q

how does AP looks the same all down axon

A

it does not decay/non decremental (it is constantly regenerated)

135
Q

Conduction in an Unmyelinated Axon

A

Na+ channels (Nav) are present all along axon -> brings in Na+ -> depolarize the membrane -> causes neighboring VG Na+ channels to open up -> and causes their neighbor’s Na+ channels open up -> AP spread
Domino effect: from initial part of axon to the axon terminal
Slows down the travel of AP due to the time of regeneration of many many Na+ channels
Unmyelinated axons: Nav everywhere
Conduction speed is limited by number of Nav (like doors in a hallway) -> the time of opening and closing the VG Na+ channels adds up and slows down the conduction speed
But if you have too few VG Na+ channel, the AP decays and not be regenerated at the next VG Na+ channel
Solution: bigger axon (for more AP to travel)

136
Q

Axon myelination

A

Myelin is produced by oligodendrocytes in the CNS and schwann cells in the PNS
Myelin wraps around axons as insolation
Myelin causes the AP to decay less quickly as it spreads
Allows for longer distance between VG Na+ channels

137
Q

Conduction in a Myelinated Axon

A

Nav are present all along the axon
Unmyelinated axons: Nav everywhere
Myelinated axons: Nav only at the Nodes of Ranvier
Fewer ”doors”, faster conduction down the “hall”
More spaced apart
Myelin in the vertebrate
Conduction speed of invertebrates is slower than vertebrates even though they have bigger axons

138
Q

Related to myelin: Multiple Sclerosis (MS)

A

A disorder that progressively damages myelin and other parts
chronic, inflammatory
Disruption to sensation and movement
AP decays faster due to damage to myelin and leads to numbness and loss of sensation, and vision impairments
55-75K in Canada (3 new/day)
Canadians have one of the highest rates of multiple sclerosis in the world
More common in females
Likely some connection to EpsteinBarr virus (a type of herpes virus) -> causes mono
And increases chance of MS
Part of the trigger
Shortens life expectancy
Higher risk of depression

139
Q 
PSPs (postsynaptic potentials)
Graded (more neurotransmitter binds, bigger the potential)
Strength
Rapid
Decremental
A 
Yes
AM (amplitude modulated)
Higher amplitude, larger the potential
Yes (passive spread of potential)
Yes (decay as they spread out)
140
Q 
APs
Graded (more neurotransmitter binds, bigger the potential)
Strength
Rapid
Decremental
A

No (all or nothing)
FM (frequency modulated)
Stronger signal when more frequent AP firing
Less so (do to constantly opening VG Na+ channels)
No (constantly regenerated)

141
Q

what happens where Axon ends in terminal boutons (include Ca2+)

A

Bouton has many vesicles filled with neurotransmitters
Action potential travels to bouton and depolarizes it
Causes voltage-gated Ca++ channels to open
VG Ca2+ normally closed
There is 10,000x more Ca2+ outside the cell
Ca2+ intense signaling molecules
Ca++ causes vesicles to fuse with membrane
Neurotransmitters released into synapse
NT bind to the receptors on the postsynaptic cell

142
Q

the synapse + receptors

A

Dendrite membrane has special receptors that fit, like lock and key, with the neurotransmitters
Receptors are often just (closed) channels that open when they bind with neurotransmitters!
i.e. ligand-gated ion channels (ligand = NT in this case)
i.e. EPSPs/IPSPs are just ions crossing the membrane
AMPA receptors common receptors for glutamate
Channel opens (little nonspecific) -> ions flow
Na+ enters cell
Cl- (chloride)-> more Cl- outside
When channel opens-> Cl- rushes in
Inhibitory effect (IPSP)

143
Q

Receptor types

A

Ionotropic (channels)

Metabotropic (signaling proteins)

144
Q

Ionotropic (channels)

A

AKA ligand-gated ion channels
Channels flow with the concentration gradient
Excitatory (depolarize) effects
Inhibitory (hyperpolarize) effects
Fast, transient effect (soon as NT no longer binds to receptor -> ionotropic receptor closes)
ON: channel open
OFF: channel closed
E.g. controlling Muscle movement (fast and transient)

145
Q

Metabotropic (signaling proteins)

A

AKA G-protein-coupled receptors (GPCRs)
Do not have a pore (no passage way for ions)
Inside the cell has proteins (G proteins) attached to these GPCR
When NT binds to the GPCRs, the G protein breaks off from the receptor and floats away and signals
These G proteins can turn things on or off
Can activate or block channels
Can indirectly cause EPSP or IPSP
Modulate cell function, inputs, and outputs
Can change shape, the presence of proteins
Modulate signals
Slow, longer lasting effect: there is a long chain of effects
hours, minutes, seconds (longer than ionotropic channels)
Cause signal cascades

146
Q

Receptor locations

A

Postsynaptic
Presynaptic
- Autoreceptors
- Heteroreceptors

147
Q

Autoreceptors

A

They are binding to the same molecules that the axon is releasing
E.g. axon releases dopamine but also has dopamine receptors on it
Sending signal to itself -> negative feedback (making sure signal was sent to ensure not to release too many NT)

148
Q

Heteroreceptors

A

Receptors for some other NT that is not part of the synapse (third neuron)
Axoaxonic synapse or axoextracellular synapse
Heteroreceptor turns up or down a signal that is present
NT binds to heteroreceptor can cause more NT release or less NT release
Modulate the circuit (volume of signal)
Usually metabotropic - often NTs like norepinephrine, adrenaline serotonin, dopamine

149
Q

Neurotransmitter clean-up reason and methods

A 
We do not want the NT to stay at the synapse and continue to activate the receptors
Need to turn off synapse
Diffusion
Enzymatic degradation
Re-uptake
150
Q

Diffusion

A

NT floats away
Rare as NT may effect elsewhere
Synapses are carefully guarded by our astrocytes - not as much opportunity for the NT to float away

151
Q

Enzymatic degradation

A

there is an enzyme that will take the NT and turn it into its metabolites
Comethylasterase: enzyme that turns dopamine into its component parts that cannot bind to the receptors
Not primary method of NT cleanup as it is not efficient to break down NT every time

152
Q

Re-uptake

A

(most common) Recycling
Transporters (all the things that end in T) brings NT back into the axon
PMAT: PM transporter
DAT: dopamine transporter but also work to some extent for similar NT (such as, norepinephrine, serotonin)
VMAT: vesicular monoamine transporter -> pushes NT back into the vesicle
They do not use ATP but work kind of like pumps (sometimes pumping against concentration gradients)
Pre-synaptic: bring NT back into the axon (common)

153
Q

Astrocytes

A

breaks down NT with enzymes within astrocytes and brings them back into the axon after repackaging

154
Q

Drug types -ways for drugs to affect the synapse

A

Changes how the neurons are communicating to each other
Agonist : increase the function of that NT system
Antagonist: block the function of that NT system
Not necessarily EPSP or IPSP, depends on the receptor function
Other (e.g. transporter blocker, reuptake inhibitor, enzyme inhibitor)

155
Q

Small-molecule Neurotransmitters

4+ subgroups

A 
1. Amino acids:
Glutamate
GABA
2. Monoamines  (smaller) - all metabotropic 
-  Catecholamines
Dopamine
Epinephrine (adrenaline)
Norepinephrine (noradrenaline)
- Indoleamine
histamines
Serotonin
3. Acetylcholine
4. Unconventional neurotransmitters
156
Q

Glutamate

A

Primary excitatory neurotransmitter (EPSP)
Used all throughout the brain
Ionotropic receptors
AMPAR - binds to AMPA
NMDAR - binds to NMDA
Kainate - functions similar to AMPA
Metabotropic receptors - not channel
mGluR - some have an inhibitory modulatory effect
NT does not determine the function - the receptor determines the function
Often not a great target for drugs as glutamate is all throughout the brain
Too distributed that we do not know what effects it may have

157
Q

glutamate drugs - all glutamate antagonists

A

(all glutamate antagonists - depressant effect of the brain) - reducing function of glutamate systems
Barbiturates - sedative and surgery (dangerous)
Nitrous oxide - laughing gas
Ketamine - horse tranquilizer
Ethanol - alcohol

158
Q

Glutamate agonist

A

Opposite of relaxed and sedated = anxiety (at lower levels) and seizure (higher levels)
May even kill neurons

159
Q

GABA

A 
aka gamma-Aminobutyric acid 
Primary inhibitory neurotransmitter 
Used throughout brain 
Ionotropic: GABAa
Allows Cl- to come in
IPSP to hyperpolarizing effect
Metabotropic: GABAb
Inhibitory modulatory effect
often not a great target for drugs: too distributed
160
Q

GABA drugs

A

(All agonist- sedative effect)
Benzodiazepines: relieve acute anxiety
Used recreationally
Ethanol
Chloroform: put on rag and then person goes unconscious
Ether: used for surgery, gas anesthetic
GABA antagonist would have a similar effect to glutamate agonists

161
Q

Dopamine projects from

A

Ventral Tegmental Area (VTA) to Nucleus Accumbens (NAcc; the ventral part of the striatum)

162
Q

Drugs: dopamine (agonist)

A

All addictive drugs directly or indirectly increase dopamine transmission
Directly increasing dopamine transmission: Amphetamine(adderall/speed) , cocaine, meth
indirectly increasing dopamine transmission: heroin, nicotine, oxycodone, ethanol, and so on

163
Q

Dopamine and Parkinson’s Disease and treatment

A

Caused by the loss of neurons in the Substantia nigra pars compacta (SNc)
Thin dark region of the brain
PD -> low levels of dopamine
One of two major dopamine-producing regions
Great difficulty initiating voluntary movement
L-DOPA (will cross BBB) as PD treatment
Enzymes transform L-DOPA into dopamine in the brain and relieves symptoms of parkinson’s disease - easier voluntary movement
But does not increase pleasure

164
Q

Drugs: dopamine (antagonists)

A

Schizophrenia medications
Drugs that bind strongly to the dopamine receptors and block them -> small dose
Drugs that bind weakly to the dopamine receptors and block them -> higher dose
In some aspects, schizophrenia is the opposite of PD
People with schizophrenia have hyperfunctioning dopamine systems
Positive symptoms: hallucinations, delusions, mania

165
Q

Separating Pleasure from Motivation (study with dopamine antagonist)
Taught a rat to make decisions in a T maze task
Low effort, low reward vs. high effort, high reward

A

In baseline: animals would put in a little more effort for a higher reward
Dopamine antagonists
Decrease motivation but not pleasure
Shift behavior: choose low effort and low reward option
Can be systemic or directly injected into VTA or NAcc
But without the barrier that makes it high effort for high reward, the animals take the higher reward
The animals are more than willing to obtain a larger reward, but they do not want to put in the extra effort

166
Q

Dopamine is more related to (3)

A

motivation, movement, and behaviour

167
Q

Norepinephrine (aka noradrenaline)

A

Originates in brain stem region called the locus coeruleus (reticular activating system, reticular formation) (latin for blue location)
Causes heterosynaptic facilitation (via heteroceptors)
Enhancement of memory by stress/emotion
Stress and arousal
Formation of flashbulb memories
Stronger signals
Evolutionarily useful
PTSD: unwanted and intrusive memories with awful effect

168
Q

Propranolol (norepinephrine receptor antagonist)

A

Propranolol (norepinephrine receptor antagonist, aka noradrenergic receptor antagonist)
Heart medication - reduce stress
Potential PTSD treatment via reconsolidation
Every time we remember something, opportunity to lay it down in a new way
Long term memory to working memory can alter memory
Recount traumatic memories and take propranolol to be less stressed when recalling memory
Less stressful to remember memory
People who went through bad breakups or relationships can also subside negative memories by recounting memory under the influence of propranolol
Thinking about an ex hurt less
Implications for therapy

169
Q

Serotonin

  • Primarily from the
  • Precursor
A

Primarily from the raphe nuclei (brain stem) (reticular activating system)(seam of nuclei)
Precursor: tryptophan (in anything with high aa content e.g. meat)
Cannot get tryptophan into brain easier without carbohydrates
People on diet are not in good mood

170
Q 
Serotonin depletion
Study with people living in the lab
One group eats normal food
Another group eats food completely depleted of tryptophan
results:
A

Over time serotonin levels go down in the bain
Leads to decreased cognitive flexibility -> Stroop task (identify colour of the font)
Congruent trials: red written in red - easy
Incongruent trials: red written in green - difficult to suppress the urge to read red
Increased aggression- measured how they punish other players in a game
Higher levels of impulsivity
Does not lead to changes in mood for healthy individuals with no family history of major depressive disorders

171
Q

when does serotonin depletion affect mood

A

Does affect the mood of healthy participants who have a family history of major depressive disorders

172
Q

Selective Serotonin Reuptake Inhibitors

A

aka SSRIs, e.g. Prozac (fluoxetine) - highly prescribed drugs
For depression
“Chemical imbalance” theory of depression
Idea that they had an imbalance of serotonin levels
Interfering with NT cleanup -> block the effect of serotonin reuptake transporters (SERT)
Block serotonin from being removed from the synapse - longer effect on synapse
Effects of SSRIs quick, improvements slow
Mechanistic effects happen quickly but improvements could be seen up to months
No concrete evidence for why there is slow improvement
Early evidence said that these drugs benefit us

173
Q

SSRI efficacy

A

There were many different results: not as effective we would want
Meta-analyses: SSRIs no better than placebo for mild to moderate depression
Or they found a very small effect size for SSRIs more than placebo
75% of studies on SSRIs were not published
May help with major depression (severe)
SSRIs do seem to have a more major effect
Regression to the mean: another explanation is that people that were severely depressed regressed to mean level of depression
Hard to say that the effect was due to the SSRIs

174
Q

Side effects of SSRIs:

A

Disruptions in your sleep
Sexual disfunction
weight

175
Q

Hallucinogens

A

Psychedelic drugs like LSD, DMT, psilocybin etc. are serotonin receptor agonists!
All activating serotonin receptors
Hallucinogens can cause radical changes to our conscious perception and our thoughts (subjective experience), but they have minimal effects on mood
Serotonin activity related to not seeing the world accurately as compared to normal conditions

176
Q

Large-molecule neurotransmitters

A

(pieces of protein)
Neuropeptides: Opioid peptides
Not much known about neuropeptides

177
Q

Acetylcholine

A

targeted to muscles
First NT found
The neuromuscular junction (between neuron and muscle cell)
Motor neurons that cause muscles to contract release acetylcholine
Cleaned up by enzymatic degradation
Also released from basal forebrain
Wakefulness, attention, vigilance etc.
Nicotine: acetylcholine receptor agonist - activating neurons in the basal forebrain

178
Q

Endocannabinoids

A

Travel from the postsynaptic dendrite dendrite to axon, i.e. retrograde transmission
Receptors for the endocannabinoids are on the presynaptic membrane
Weaken connection between two cells at a synapse
Endocannabinoid system: Cannabis mimics the effects of the system
Cannabis is a cannabinoid receptor agonist
THC are mimicking the NT we have

179
Q

Mechanistic function:

Endocannabinoid receptors

A

GCPR (metabotropic receptors)
Inhibitory effect - decrease of release of NT
System designed to weaken the connection between two cells
Memory is a change in the change in the structure of the synapse
Stronger connections between synapse, more NT release, more receptors = stronger memory
Molecular mechanism for forgetting -> impairments in memory
Some information is valuable to remember and some information that is not valuable to remember

180
Q

Adenosine

A

(produced by mitochondria)
Remember: ATP is cellular energy
ATP can be broken down to ADP and then to AMP and then to A (adensosine)
Adenosine is ATP by product
Build up of adenosine while we are awake
Adenosine can signal how sleepy you are
Found across entire brain and body
Inhibitory effect
Adenosine receptors - more active throughout the day
accumulation of daytime sleepiness driven by adenosine
not a NT system, only a byproduct of energy use throughout the day but sends signals to brain

181
Q

Caffeine/theophylline

A

adenosine receptor antagonist
Trying to block activity of adenosine receptors -> feel more awake
Over time tolerance will develop more caffeine
Body recognize that adenosine is not binding to receptors -> body adds more adenosine receptors so adenosine can bind

182
Q

Endogenous opioids

A

Name system after drug as they knew about drug before the NT system
aka Endorphins (endogenous morphine)
Same system that opioid drugs act on
Giant peptide neurotransmitters
The neurotransmitter system that exogenous opioids (e.g. heroin, morphine, fentanyl) mimic
The opioid drugs are opioid receptor agonist
These drugs have inhibitory effects and can block pain signals from reaching the brain
Gold standard for pain relief - part of analgesia pathway

183
Q

Fentanyl and naloxone (overdose kit)

A

Opioid receptor antagonist to counteract the effects of opioid drugs

184
Q

Opioid receptor

A

Receptors are all GPCRs (metabotropic)
Receptors found in places related to pain and euphoric effects: spinal cord (inhibit pain signals going up to brain), periaqueductal grey (PAG), nucleus accumbens, more

185
Q

X-Ray

A

X-ray tube, X-ray beam, film (or detectors)
Type of electromagnetic wave that passes through some solid objects
Different features that absorb more X-rays and passes through object onto image
Cannot show brain

186
Q

Cerebral Angiography

A

i.e. an angiogram (contrast X-ray technique)
Put dye (iodine) into bloodstream - see all of arteries in brain
Does not show real time blood flow
Structural imaging: See static features of brain (one instant)

187
Q

what can Cerebral Angiography allow you to see in brain?

A

Can look for ischemia (branch of blood vessel will stop)
Can see hemorrhagic stroke (bleeding inside brain) and flows in the brain and causes cloud
Can see Aneurysm - ballooning shape that can lead to hemorrhages

188
Q

Computed tomography (CT)

A

The tube and detector
Overcoming limitations of traditional X-ray “reconstruction”
Fire weak x-rays that fire at different angles, and reconstruct images to a 3D model (better image)
Compiling many images of brain at different angles - still static structural imaging
Only as good as its algorithm - computer programs have gotten better that increases the quality of image
Can see fluid and tissue - can identify stroke and fluid buildup
Cannot detect different types of tissue (gray matter, white matter, cancer)
Radioactive
Readily available, cheaper, quicker

189
Q

Magnetic Resonance Imaging (MRI)

3 steps

A

Step one: Align all the protons with the large magnetic field when enter magnetic field
Step two: Momentarily perturb that alignment with a second varying magnetic field that releases a tiny bit of energy (radio-frequency signal)
Step three: Measure radiofrequency (RF) signal produced during realignment with the large magnetic field (‘relaxation’)

190
Q

MRI and its magnetic mechanism

A

Reconstruction and structural imaging
Atoms will flip and align when in a strong magnetic field -> not aversive
The earth’s magnetic field is 1/1000 tesla
The magnetic field in MRI is 3 tesla
Giant magnets is continuously cold -> can turn off machine by warming it up (but very very expensive)
Conscious about metal near the machine
Does not image hair
Great resolution, voxel (3D pixel) -> can see fluid, and gray matter, white matter, tumors, ventricles

191
Q

Overlay plot

A

MRI shows damage for all individuals in study and shows common damage
Many patients with the same impairment type
The same area of impairment shows which impairment is related to which common damage among patients

192
Q

Diffusion Tensor Imaging (DTI)

A

Variant of MRI (structural imaging)
Relies on how water molecules (hydrogen) move in brain as they can move all around
Inside the extracellular space, water will move randomly
But intracellular hydrogen can only move along the axon
Gives image of white matter (myelinated axon) -> sometimes brain dysfunction is due to disconnection (white matter change) of brain regions
Broca’s area and Wernicke’s area disconnection can cause language impairments even if the brain structures are undamaged

193
Q

vegetative state

A

meaning that although she had sleep-wake cycles, she lacked conscious awareness

194
Q

Kate (vegetative state) into our positron-emission tomography (PET) scanner -> what did they see

A

showed her pictures of her friends and family by flashing them on a computer screen, and we looked for any signs of a response from her brain
Not only did her brain respond to the faces, but the pattern of brain activity was strikingly similar to what we and others had seen when showing the faces of loved ones to healthy, aware individuals.

195
Q

vegetative state patients brains respond to

A

we observed brain activity in putatively vegetative patients that looked like that of healthy participants—speech perception regions of the brain would often respond when we played them speech but did not respond when we played them the speechlike noises

196
Q

Brain death

A

All functions of the brain and brain stem have permanently ceased.

197
Q

Coma

A

Loss of consciousness is complete; cycles of waking and sleeping disappear, and the eyes remain closed. Coma, which rarely lasts more than two to four weeks, is usually temporary; afterward, patients emerge into consciousness or one of the states below

198
Q

Vegetative state

A

Sleep-wake cycles occur, and the eyes may open spontaneously or in response to stimulation, but the only behaviors displayed tend to be reflexive

199
Q

Minimally conscious state

A

Patients may seem vegetative but sometimes show signs of awareness, such as reaching for an object, following a command or responding to their environment.

200
Q

Locked-in syndrome

A

Technically, this state is not a disorder of consciousness, because patients are fully conscious; however, they cannot move and may mistakenly be deemed vegetative or minimally conscious. Many patients do retain the ability to blink and move their eyes

201
Q

in every healthy participant we scanned, the tennis task elicited strong fMRI activity in the

A

premotor cortex, a brain region that plays a role in planning movement.

202
Q

mentally touring one’s home activated the

A

parietal lobe and a deep-brain region called the parahippocampal gyrus, both of which are involved in representing and navigating spatial locations

203
Q

EEG activity difference in what

A

found that if he asked healthy participants to imagine clenching their right hand or their toes, he could detect the difference, based on the EEG pattern that was generated

204
Q

Electroencephalograph (EEG)

A

Only real way to measure brain activity is through electrodes (cannot place inside skull- too invasive)
EEG places electrodes on the scalp (not precise)
Can only tell what is going on in cortex

205
Q

EEG + sleep

A

Indicates individuals brain state (e.g. sleep state)
Awake - high frequency small waves (gamma waves)
Deep sleep - low frequency with high amplitude (delta waves)

206
Q

Positron Emission Tomography (PET)

A

PET using radiolabeled cocaine (look at regions where cocaine binds to -> DA regions)
Same principle as CT and MRI -> reconstruction of many images into 3D model
The stronger the binding, the hotter the colors are (heat map)
Structural and (functional) imaging
Indirect brain activity measure (as is fMRI) -> more glucose binding = more brain activity
All correlative

207
Q

How does PET work

A

Scanner is looking for the release of radiation
Put slightly radioactive molecule into bloodstream
commonly radioactive glucose as active areas in the brain will require more glucose
We can see which areas glucose are binding to -> indicates areas of activity in the brain

208
Q

Mean difference images PET

A

Subtraction method/mean difference images (similar for some fMRI)
Want to compare control condition and stimulation condition
Level 1: Subtract control condition from stimulation condition to leave only the activity that is related to the task (in theory)
Level 2: put all of the average activity of each individual into a big average of all of the individuals -> to get mean difference image
Potential problem: averages may sometimes not reflect what any of the individuals look like

209
Q

PET is less common now because:

A

Very expensive - due to radioactive molecules (they have decay - must generate radioactive molecules through cyclotron which is expensive)
Temporally slow - Poor temporal resolution - snapshot is 45mins long
Cannot study moment to moment studies
Poor spatial resolution: voxels are larger than MRI - not very good picture

210
Q

PET useful for

A

Can create a radioactive molecule to target a specific system
Useful for looking at specific systems (e.g. DA) or proteins (tau- cytoskeletal protein) in living healthy human
Useful for looking at lifespan/condition changes (e.g. stroke, maybe CTE)
As individuals get older, less and less of radioactive molecules are binding to DA receptor/transporters
Dopamine system gets weaker across the lifespan

211
Q

Using PET to image Diaschisis:

A

When the brain is damaged (dark fluid)
Functional damage is larger than anatomical damage (prefrontal)
Less binding in the temporal and occipital lobe
Other brain areas are losing their inputs - become hypoactive
As diaschisis goes away, the individual will recover those connections and gain back their brain activity
Can measure diaschisis fell with PET

212
Q

Functional MRI (fMRI): the BOLD response

A

Relies on magnetic properties of atoms
Information has to do with blood
Oxygenated and deoxygenated blood has different magnetic properties
Blood Oxygen Level Dependent
Time 0: present stimulus
The more activated areas of the brain will require more oxygenated blood
TIme 6 s: peak of O2 blood arrive
Hemodynamic response
When brain area is active -> see bigger BOLD response
Take scans of brain repeated to see changes in blood oxygen level

213
Q

What is the mechanism of BOLD

A

glutamate (or other NT) binding to glutamate receptors on astrocytes -> causes more Ca++ to enter the cell especially with stronger activity -> causes vasodilation on blood vessels as astrocytes (glia) are wrapped around blood vessels so astrocytes can control how much blood travels to a particular area -> more oxygenated blood will arrive
Our axon will release NT onto our dendrites and causes activity in neurons

214
Q

Paired image subtraction:

A

Use control and stimulation and subtract to know about specific task related brain activity
Stimulus - control = specific task/ desired brain activity

215
Q

Paired image subtraction: The quality of your results depends on the ….

A

The quality of your results depends on the quality of your controls
Must have similar task as control to match as much of the other variables
The more different the control from the task, the more activity in varying areas of the brain and it will not capture desired brain activity

216
Q

Event-related fMRI

A

Have the same event occur and average out the signals of the event
Our brain signals are noisy -> average out by repetition of tasks for a smoother signal
Mostly the norm in fMRI these days
Allows you to avoid paired image subtraction - valuable
Has many of its own challenges (e.g. many many trials - boredom)

217
Q

Event-related fMRI example: decision-making task: intertemporal choice - smaller value for sooner vs. larger value for later

A

Can track these variables -> track aspects of a trial
As reward size goes up -> track the BOLD response
Do not need control condition

218
Q

Problems with interpreting fMRI studies?

A
  1. Spatial averaging - happens at many levels (e.g. trials, participants)
  2. Spatial resolution - measured according to voxel (3)
  3. Temporal resolution
  4. Not necessarily necessity - brain activity that is left behind may not be necessarily necessary for a specific task
  5. Focus on increases in activity: some regions are more active at rest than during task
  6. Regional hemodynamics
  7. Confounds: anxiety, boredom
  8. Confounds: drugs
  9. Anticipatory hemodynamics
  10. Reliability
  11. Statistics
219
Q

Problems with interpreting fMRI studies: Spatial averaging

A

Mean difference may not truly represent any of the specific trials - Epiphenomena
Event related MRI reduces this

220
Q

Problems with interpreting fMRI studies: Spatial resolution

A

Each voxel can contain many many neurons - activity cannot be specific to a single neuron

221
Q

Problems with interpreting fMRI studies: Temporal resolution

A

Constantly taking scans for fMRI (e.g. 2 seconds) cannot capture activity between at which many AP can fire

222
Q

Problems with interpreting fMRI studies: Focus on increases in activity

A

Some brain regions do not have a BOLD response (e.g. hippocampus not showing up for memory tasks even though we know it is important for memory. Since Hippocampus is active all the time, it gets subtracted out during subtraction process)

223
Q

Default mode network: resting state functional connectivity MRI

A

Different type of analysis
Measure baseline (mind wandering) state and record BOLD activity
They chose activity in seed region (where they decide to focus on) and see is activity in relation to other regions to see correlations in brain activity
There are highly correlated functional network
Default mode network: Includes MPC (medial prefrontal cortex) and PCC (posterior cingulate cortex) and IPC (inferior parietal cortex) an sometimes MTL (medial temporal lobe)

224
Q

Problems with interpreting fMRI studies: Regional hemodynamics

A

All of analyses are under the assumption that the thermodynamic peak will occur at 6 seconds
If thermodynamic response looks different in different parts of the brain - analyses will be wrong and operating on wrong assumptions
Hemodynamic response looks different in different parts of the brain

225
Q

Problems with interpreting fMRI studies: Confounds: drugs

A

All of us use psychoactive drugs could impact the way our brain is active

226
Q

Problems with interpreting fMRI studies: Anticipatory hemodynamics

A

When you perform a task many many times -> the BOLD level response will anticipate before task time (anticipatory hemodynamic responses), making it look like activity is happening earlier than it actually is

227
Q

Problems with interpreting fMRI studies: Reliability

A

Meta-analyses revealed that overlap in voxels between day 1 and day 2 -> only 30% looks the same
Signal is noisy - need better statistical power
Test-retest is not as accurate

228
Q

Problems with interpreting fMRI studies: Statistics

A

Take structural MRI then lay fMRI image on top
p < 0.05 -> significant- likely that the findings are not by chance
Multiple comparisons must be corrected to be more stringent
Each one of the voxels in the brain is its own statistical test (comparison) which has a lot of voxels
Doing 60,000 to 1M statistical tests (comparisons) for each voxel in the brain
A p value of 0.05 with that many statistical tests is an unacceptable p-value
There may be more false positives -> must correct for the multiple comparisons and need a more stringent p-value for these studies
The uncorrected brain is more active but with correction (there is less and more precise activity of the brain)

229
Q

The heavy metal brain: altered resting-state functional connectivity of default-mode network and sensorimotor network in heavy metal music lovers crtitique

A

They compared heavy metal music lovers with classical musical lovers - not good comparison
Not meaningful or important
The disorders of behavioral and emotional cognition in HMML compared with CML and are consistent with predictions
They simile looked at resting state structural connectivity without studying behavior, cognition, or emotion but they made a conclusion about behavior, cognition, and emotion
They made assumptions based on differences in brain activity without studying all the components that were discussed in the conclusion.

230
Q

Neurological examination

A

A neurological examination is a series of tests conducted by a neurologist to evaluate the integrity of the nervous system for many reasons, including (but not limited to): infer problems from the function of nervous system
Following trauma or stroke
When there are suspected neurodegenerative changes (often age related)
Following exposure to a neurotoxic agent

231
Q

neurological examination

Localization:

A

Damage to the periphery -> unilateral - damage to 1 arm and not the other
Cerebral Hemisphere (Telencephalon)
Internal Capsule - white matter tract that goes to the cortex and down through brainstem and beyond)
Stroke or damage to this area can cause motor and other functional impairments even if there is no damage to the nuclei
Brainstem (Diencephalon, Mesencephalon, Metencephalon, or Myelencephalon?)
Spinal Cord
Cranial Nerves
Neuromuscular Junction - damage cause change in reflexes
Muscle

232
Q

Overview of common components of neurological exam

A 
Obtain Patient history 
Cranial nerve function 
Motor function (e.g., reflexes) 
Somatosensory function 
Coordination 
Mental status - assess sophisticated cognitive function
233
Q

Patient History

Age, education, and handedness

A

Education is an inverse correlate to a number of later life decline problems
Better education is less likely to lead to dementia and other age related neurological decline
Handedness - some lateralized function in the brain
Handedness to some degree will predict lateralization
Right handed people (90%) have left hemisphere dominant for language (95%)
Left handed people (10%) have left hemisphere dominant for language (75%)
Remaining 25% of left handed people
½ have bilateral dominance = equal dominance of language
½ have right hemisphere dominance for language
Ambidextrousness is very rare

234
Q

Patient History

Past medical history

A

previous illnesses may have complications that cause neurological impairment

235
Q

Patient History

Use of medication and/or recreational drugs

A

important as it changes our cognition

A number of drugs that are targeting other sites in the body can have psychoactive effects

236
Q

Patient History

Family medical history

A

When a person has symptoms that could lead one way or the other, it’s more likely that the person has the same disorders that their parents or family had based on probability

237
Q

Patient History

Disease Process:

A

temporal profile: sudden vs. gradual; acute vs. chronic
change over time: static, improvement, worsening
identify triggers/relievers of symptoms
gauge severity of symptoms

238
Q

Cranial nerves colour

A

Pale in comparison to the cortex

239
Q

Cranial Nerve: Only one ostrich tried to assassinate fake Van Gogh very abruptly hahah

A 
Olfactory
optic
oculomotor
trochlear
trigeminal
abducens
facial
vestibulocochlear
Glossopharyngeal
vagus
accessory
hypoglossal
240
Q

Axons: Some Say Money Matter, But My Brother Says Big Brains Matter More”

A 
Sensory axons (afferent)
sensory
Motor (efferenent)
motor
both
motor
both
sensory
both
both
motor
motor
241
Q

Cranial nerve I

A

Olfactory
Sensory axons (afferent)
smell
ethmoid ridge, cribriform plate and TBI
Ask patient if their smell something while closing one nostril
Dysfunction in cranial nerve I is very common from mild head injury
Ethmoid ridge where sensory axons are coming through up through the bone (cribriform) - impact can cut the nerve in the plate where axons are

242
Q

Cranial nerve II

A

optic
sensory
vision
standard visual acuity tests for eyes
Visual field confrontation
Papilledema and intracranial pressure
Snellen chart tests visual acuity while covering one eye at a time from usually 10 feet away
Fundoscopy - viewing the fundus (inside back of the eyeball) -> look for blurred disk around fovea
E.g. papilledema - optic disk is swelling

243
Q

Cranial nerve III

A

oculomotor
Motor (efferent)
Most eye movement, eyelid movement
4 of the eye muscles are controlled by the oculomotor nerve + muscle of eyelid
Check for ptosis: dropping of eyelid and covering pupil
Test eye movement

244
Q

Cranial nerve IV

A

trochlear
motor
Eye movement - only one muscle - smallest muscle
controls one muscle (trochlear muscle)

245
Q

Cranial nerve V

A

trigeminal
both
Most Facial sensation (sensory), movement of biting/chewing/swallowing jaw muscles
Biggest cranial nerve
Has three branches coming off of it
Must both sensory and motor aspects to test this nerve
largest cranial nerve
Trigeminal nerve branches into 3 nerve size branches
facial somatosensation- have face touched at different parts of the face
Different types of touch receptors -> use different items to touch face to test all touch receptors
Motor function- Biting and chewing and using jaw:
Hold someone’s chin and ask them to apply force against it
Touch the muscles of the jaw and feel for the quality of the muscles
Firm = good muscles; soft = atrophy/muscle wasting away
If someone has damage in one of their trigeminal nerves, notice asymmetry in muscle tone of side of body

246
Q

Cranial nerve VI

A

abducens
motor
Eye movement - controlling one small muscle
control abducens muscle
Follow an object/light without moving their head -> if eyes do not follow the stimuli eveningly -> blurry vision
Gaze restrictions
Our eyes and brainstem are really good at following movement
There may be a disconnect between automatic eye movements - mainly cranial nerves and brainstem nuclei
Voluntary moving something is much more the cortex

247
Q

Cranial nerve VII

A

facial
both
Taste from anterior tongue (sensory), a little facial sensation, all muscles of facial expression (control facial expression- motor)
Cranial nerve important for controlling the muscles of the face - for facial expression
Damage to CN VII - dramatic changes
Ask patient to make a number of facial expressions
Facial asymmetries (Bell’s Palsy)-
where one side of face has lost facial muscles control (drooping face)
Bell’s Palsy goes away with time

248
Q

Cranial nerve VIII

A

vestibulocochlear
sensory
Sound (cochlear information), sense of balance
Sensation from inner ear

Auditory perception
Test ability to hear - cover one ear and whisper at different distances
Test balance

249
Q

Cranial nerve IX

A

Glossopharyngeal
both
Taste and sensation from posterior tongue (back of tongue), muscles of pharynx (speech, swallowing)
Taste and sensation from posterior tongue
We do not test for taste normally
Test ability to speak and swallow- ask them to drink water

250
Q

Cranial nerve X

A

vagus
both
Outer ear canal sensation (sensory), motor control of heart, lungs, viscera, larynx control/motor (speech), more
Sends info far -> to heart, hungs, guts
Pain to study as we do not know if it is the tissue or the nerve’s problem
Swallowing and voice
Gag reflex
Inspect inside of mouth - palate should move up
Innervates function in hearts, lungs, guts

251
Q

Cranial nerve XI

A

accessory
motor
Movement of muscles of head rotation and shoulder shrug
Shrugging of shoulders
Apply force on shoulder and ask people to shrug their shoulders
Head resistance
Apply force on head and ask the patient to apply force against it

252
Q

Cranial nerve XII

A

hypoglossal
motor
Movement of tongue muscles (speech, swallowing)
Stick out the tongue, lateral movement
Looking for strength of tongue -> tongue push against hand on cheek
Look at symmetry of tongue muscle tone

PSYC 301 (3 decks)

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