Psychobiology Flashcards

1
Q

Levels of organisation

A

Organelle, Cell, Tissue, Organ, Organ System, Organism

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2
Q

Parts of the cell

A
  • Cell membrane - surrounds cell, proteins
  • Cytoplasm - includes watery cytosol (water, ions, small molecules, amino acids, soluble protiens)
  • Cytoskeleton - consists of filaments and tubules that crisscross the cytoplasm and help to maintain the cell’s shape
  • Nucleus - contains DNA and acts as control centre
  • Ribosomes - at the site of protein synthesis
    Endoplasmic Reticulum - helps make proteins and lipids and transports proteins in the cell
    Golgi Apparatus - modifies, sorts and packages proteins for secretion out of the cell, or for use within the cell
    Lysosomes - organelles that use enzymes to break down molecules so their components can be recycled
    Mitochondria - produce ATP from energy in glucose
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3
Q

Protein synthesis

A

In nucleus: transcription (DNA -> RNA) and splicing (alternative splicing = sticking together different exons to produce different proteins)
- exported to cytoplasm
In cytoplasm: translation and folding

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4
Q

ATP synthesis

A
  • Glycolysis - produces glucose, 2 ATP and phosphate
  • Citric acid cycle - produces 2 ATP and CO2
  • Electron Transport Chain and Oxidative Phosphorylation - produces 32 ATP and H2O
  • ADP + Pi -> ATP
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5
Q

Tinbergen’s 4 questions

A

(why we and other animals do stuff) - How behaviour increases fitness, modified by evolution, causes of behaviour, how behaviour developed over lifetime

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5
Q

Development of concepts of mind and brain

A

Aristotle - mind controls behaviour, heart is the seat of the mind in the body (brain = cooling system)

Hippocrates - brain is the seat of the mind, connected to sense organs and muscles

Galen - Experiments to link different nerves to function; link brain injury to loss of consciousness

Ibn Sina - first descriptions of neurological and psychiatric conditions, linking bodily changes with emotions

Descartes - brain and body as a machine (unconscious processing); soul directs the brain via pineal gland (conscious processing)

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6
Q

Are mind and brain separate?

A

Dualism - mind and body are different
Materialism - brain controls behaviour - mind is an epiphenomenon (not tangible)

  • evidence that brain underlies behaviour - evolutionarily preserved different behaviour - different brains produce the same responses
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7
Q

Peroxisomes

A

These are membranous sacs of oxidase enzymes. They detoxify harmful substances and break downfree radicals.

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8
Q

Centrosome

A

The centrosome is composed of two centrioles surrounded by an amorphous mass of protein. Centrosomes are associated with the nuclear membrane during prophase of the cell cycle. Inmitosisthe nuclear membrane breaks down and the centrosome can interact with the chromosomes to build the mitotic spindles.

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9
Q

Centrioles

A

These are self-replicating organelles made up of nine bundles of microtubules. They appear to help in organizing cell division, but aren’t essential to the process

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10
Q

a-Microfilaments and b-Microtubules

A

a-Microfilaments- Microfilaments are solid rods made of proteins called actin. These filaments are important supports of the cytoskeleton.

b-Microtubules-These straight, hollow cylinders are found throughout the cytoplasm of all human cells and carry out a variety of functions, ranging from transport to structural support.

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11
Q

The seven characteristics of life

A

1.Cells -All living organisms have cells; cells are the building blocks of life.
2.Metabolism -All living organisms eat, drink, breathe and excrete.
3.Growth -All living organisms take in material from the environment to enlarge and sustain.
4.Reproduction - All living organisms are able to produce a copy of themselves.
5.Irritability -All living organisms are able to react to a change in their environment.
6.Adaptation- All living organisms are able to compete with each other for food and space to survive.
7.Movement - All living organisms are able to move.

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12
Q

Macromolecule

A

A macromolecule is a large molecule (carbohydrates, lipids, proteins, nucleic acids).

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13
Q

Types of physiology

A

Cell physiology - This is the cornerstone of human physiology; it is the study of the functions of cells.

Special physiology - This is the study of the functions of specific organs. For example, renal physiology is the study of kidney function.

Systemic physiology - It includes all aspects of the function of the body systems, such as cardiovascular physiology, respiratory physiology, reproductive physiology etc..

Pathophysiology - It is the study of the effects of diseases on organ or system functions (pathos is the Greek word for disease).

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14
Q

PET Imaging

A
  • Positron emission tomography
  • Inject radioactive tracer and detect radiation
  • Binding of tracer molecules - quantify number of endogenous proteins and their activity
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15
Q

MRI

A
  • Magnetic resonance imaging
  • Structural
  • Functional
  • Can measure diffusion properties of the tissues
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16
Q

Experiments using animals because …

A
  • Mammalian brain structures similar to humans
  • Experiments - ethology (natural environment), behaviourism, physiology, neuroanatomy, neurophysiology
  • Anatomy (structure, cells there and how connected)
  • Physiology - recording brain activity
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17
Q

Peripheral NS

A
  • Made up of the autonomic NS and Somatic NS
  • via motor and sensory neurons sned signals to and from the CNS
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18
Q

Somatic NS

A
  • external environment
  • Motor ways and sensory pathways in spinal cord
  • Dermatomes – strip of skin innervated by one nerve from one dorsal root ganglion
  • Myotomes – group of muscles innervated by same motor nerve
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19
Q

Automatic NS

A
  • internal environment
  • Sympathetic NS (fight or flight), Parasympathetic NS (rest and restore), Enteric NS (gut)
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20
Q

Where things are in the body

A

Anterior (front) vs posterior (back)
Superior (up) vs inferior (down)
Dorsal (back) vs Ventral (stomach)
Rostral (towards beak) – caudal (towards tail) –
lateral (sides of brain) and medial (middle)

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21
Q

Hind Brain

A

Brainstem and Cerebellum called the hind brain)

- Overall: Inputs from senses – outputs to muscles or organs.
- In each region: Inputs from upstream and downstream regions.
- What a brain region does depends on the nature of the inputs, and outputs and how the information is integrated in that brain area.
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22
Q

Brain stem

A
  • information from body to spinal cord but information from head to brain stem
  • medulla at bottom, then pons and midbrain at the top
  • information crosses hemispheres at the brain stem - decussation
  • (Superior colliculus - quick reactions)
  • Sensory and motor nuclei (deal with ingoing and outgoing information) and neuromodulatory nuclei (neuromodulation - spread over wide area of brain - widely change state of brain - arousal and motivation)
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23
Q

Cerebellum

A
  • means little brain
  • layered organised structure - – 5 main types of neurons
  • different connections can cause behaviour
  • Cerebellum-cerebral cortex loop involved in refining sequences of movements
  • Neural circuitry helps to underlie this function – lots of information from different modalities carried in parallel fibres from granule cells and associated together at Purkinje cells.
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24
Q

Forebrain

A

Diencephalon (thalamus and the hypothalamus)
Cerebrum
Basal ganglia
Amygdala
Hippocampus
Cerebral Cortex

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25
Q

Diencephalon

A

Thalamus
- ‘Information hub’ - relays ascending and descending information from widespread brain areas
- Links to cortical areas - thalamic relay - Relay and gatekeeping – filter and modify information.

Hypothalamus
- Underneath thalamus
- Regulates several homeostatic processes
- Links brain to endocrine system (hormones)
- Many different kinds of nuclei with different functions e.g. appetite regulation, memory

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26
Q

Cerebrum

A
  • Cerebral cortex
  • Sub-cortical structures - hippocampus, basal ganglia, amygdala
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27
Q

Basal ganglia

A
  • Information loops from cortex (and hippocampus), through basal ganglia, thalamus and back to cortex
  • Modulated by dopamine from VTA/substantia nigra
  • Computations: Co-ordinating movement (via dorsal striatum), and motivated behaviour (via ventral striatum)
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28
Q

Amygdala

A
  • Key connections with cortex, hippocampus, thalamus, hypothalamus, basal ganglia and brainstem
  • Computations: emotional learning, especially fear conditioning – associate environment with emotive state – respond appropriately
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29
Q

Hippocampus

A
  • 3 main subfields of the hippocampus – dentate gyrus, CA3 and CA1
  • Connection with neocortex - continuous - most inputs and outputs with the cortex - entorhinal cortex and subiculum
  • Hippocampus is allocortex and has 3 distinct cell layers
  • Cellular organisation makes it ideal for forming associative memories - learning relations between features and damage impairs memory
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30
Q

Cerebral Cortex

A
  • Made up of 4 main lobes and 2 hemispheres.
  • Neocortex – has 6 layers.
  • It’s very folded –allows a large surface area to fit in a small space.
  • Different regions have different roles:
    • Layers 1-3 integrate information from local and distance cortical areas, receiving inputs and sending outputs to other cortical areas.
      Layer 4 receives sensory information.
      Layers 5&6 send information to subcortical structures, thalamus and spinal cord.
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31
Q

Cerebrospinal fluid

A
  • Circulates around the brain and along large blood vessels as well as through the ventricles (fluid-filled spaces in the brain)
    (fills the small extracellular space around neurons)
  • CSF is produced from ependymal cells that line the ventricles
  • Meninges are membranes surrounding the brain – dura (tough outer membrane), arachnoid and pia (next to brain surface)
  • CSF cushions the brain from impacts to the head, but also clears the brain of unwanted products such as broken down proteins
  • Sets environment for brain cells (concentrations of molecules such as glucose and ions)
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32
Q

Blood supply

A
  • Brain has a specialised blood supply as needs lots (stroke from blocked blood supply
  • Highly vascularised
  • 4 main arteries - circle of Willis so others can compensate
  • brain can finely regulate its blood supply
  • means increase in regional brain activity increases blood supply to that region.
  • this increase in the blood supply is the basis of the signal detected using functional MRI.
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33
Q

Brain cell types

A
  • Neurons
  • Gila
    • Astrocytes - wrap processes around synapses and neurons, also contact blood vessels. Lots of supportive roles
    • Oligodendrocytes – wrap myelin sheath around axon to insulate the axon and allow impulses to travel faster
    • Microglia – the brain’s resident immune cell – surveys brain for infection or damage and gobbles up damaged tissue or infection.
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34
Q

Neuron parts

A

Dendrites – collect inputs from other neurons
Soma – cell body – contains nucleus (genetic material – DNA)
Axon – axon hillock, - where nerve impulse/action potential triggered (integrates all inputs)
myelin sheath - increases speed of transmission
and axon terminal – where neurotransmitter is released to signal to the next cell

  • Different shapes with different functions
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35
Q

Ohm’s law

A

Current = potential x conductance

Current = potential/resistance

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36
Q

Electrical signalling

A
  • Lucia and Luigi Galvani 1781 - electricity makes frogs’ leg muscles move
  • The Newgate Calendar describes what happened when the galvanic process (stimulating with electricity) was used on the body
  • Hermann von Helmholtz - measured speed of nerve conductions by stimulating frog sciatic nerve and measuring time to constrict muscle
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37
Q

Cell membrane electrochemical gradient

A
    • Outside the cell: lots of sodium (Na+; positively charged), lots of chloride (negatively charged; Cl-), some calcium (Ca2+)
  • Inside the cell: lots of proteins (negatively charged), lots of potassium (K+)
  • Potassium leak channels let potassium ions through (potassium positively charged)
  • Sodium potassium pump - 3 sodium out and 2 potassium in
  • resting potential of -70MV
  • Equilibrium potential (E) dictated by concentration difference and ion charge
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38
Q

Action potential

A
  1. Threshold potential reached
  2. Depolarisation due to opening of sodium channels
  3. Repolarisation due to inactivation of sodium channels and opening of voltage-gated potassium channels
  4. Hyperpolarisation as voltage-gated potassium channels are still open.
  5. Sodium channels released from inactivation (can fire AP again)
    (all or nothing)
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38
Q

Refractory periods

A

In absolute refractory period can’t fire another action potential, in the relative refractory period a very strong stimulus can re-open the sodium channels and generate an action potential - Therefore strong stimuli can generate high frequency action potentials by intruding into the relative refractory period

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39
Q

Action potential propagation

A
  • Action potentials propagate (transmit) along axons (They are the same size all along)
  • Affected by resistance of membrane (slower if more charge can leak out), capacitance of cell (how easy to change membrane voltage)
  • How far along axon - Affected by membrane resistance - more leaky membrane -> depolarisation spreads less far
    Affected by diameter (internal resistance to flow down the axon) – big diameters conduct faster
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40
Q

Saltatory conduction and the myelin sheath

A
  • Myelin insulates membrane - less charge lost (less leak), action potentials travelling from one node of Ranvier to the next = saltatory conduction, faster and more efficient (fewer ions flow, so less ATP needed to pump them back)
  • Unmyelinated axons – lots of channels – depolarisation dissipates before travelling far down axon. Need to have lots of sodium channels close together for action potential conduction – so that next bit of membrane can be depolarised.
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41
Q

Synaptic transmission

A
  1. Action potential travels down axon and arrives at the end of the axon - the axon terminal
  2. The depolarization of the axon terminal opens voltage-gated calcium channel. Activated when membrane potential reaches -10 mV (more depol than sodium channels). Calcium enters cell
  3. Calcium causes vesicles - little bags of membrane containing a neurotransmitter – to fuse with the axon terminal membrane and release their contents.
  4. Neurotransmitter diffuses through the synaptic cleft
  5. Neurotransmitter binds to ligand-gated Ion channel (a channel that opens when a molecule binds to it)
  6. Ions flow through the channel, depolarizing or hyperpolarizing the post-synaptic membrane.
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42
Q

Excitatory vs inhibitory

A
  • If the ion channels allow sodium in, the membrane potential becomes more depolarized – the post synaptic cell is nearer to the threshold for opening voltage gated sodium channels – the cell is more likely to fire an action potential. This is an excitatory synapse.
  • If the ion channel lets chloride in, the membrane potential will be held near the chloride resting membrane potential - below threshold for firing action potentials. This makes the cell less likely to fire an action potential - the synapse is inhibitory
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43
Q

Glutamate and AMPA receptor

A
  • Depolarisation of dendrites by ion flow through glutamate receptors generates an excitatory post-synaptic potential (EPSP) – drives membrane potential towards the threshold for action potential firing.
  • Glutamate is the major excitatory neurotransmitter in the brain, opens cation (positive ion) channels (AMPA is fast opening and causes EPSP)
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44
Q

Other neurotransmitter examples

A
  • NMDA lets in calcium too - cause changes in synapse to make it work better or worse - important for associative learning
  • Metabotropic glutamate receptors – bind glutamate and trigger lots of intracellular signalling pathways
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45
Q

Excitatory vs temporal vs spatial summation

A
  • single EPSP is sub-threshold
  • temporal - many EPSPs from 1 synapse add over time to reach threshold
  • spatial - 1 EPSP at the same time from many synapses add to reach threshold
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46
Q

GABA

A
  • GABA is the main inhibitory neurotransmitter in the brain.
  • It opens chloride channels (GABA receptors), allowing negative charge into the), generating an inhibitory post-synaptic potential (IPSP), and/or making it harder to depolarise the membrane.
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47
Q

Synaptic integration

A

Synaptic integration = summation of excitatory and inhibitory inputs

  • Neuronal computation – sum up inputs and produce an output
  • Input weight affected by:
    • Distance from axon hillock
      Shape of neuron
      Location relative to inhibitory inputs (gating).
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48
Q

Lateral inhibition

A
  • With lateral inhibition, there is a bigger change in perceived light at boundaries - high firing neurons inhibit their neighbours. At the boundary, the high firing rate light-activated neuron receives less inhibition than the high firing rate neurons far from the boundary, and the low firing rate neurons are more inhibited near the boundary than those further from the boundary.
  • Explains Mach bands illusion
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49
Q

Neuronal networks

A
  • During feedforward excitation, an excitatory cell activates the next cell, which passes on that excitation
  • During lateral inhibition. excitatory cells activate inhibitory neurons that inhibit adjacent excitatory neurons.
  • Feedforward inhibition happens when an excitatory cell activates an inhibitory cell, producing inhibition on a subsequent excitatory cell.
  • Feedback inhibition occurs when an excitatory cell activates an inhibitory neuron which inhibits the cell’s own excitatory inputs - i.e. it is a negative feedback loop.
    (- Recurrent excitation is a positive feedback loop)
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50
Q

Sensation vs perception

A

Sensation - the capacity to detect a particular physical or chemical stimulus - (external or internal) sensory organs or afferent nerves

Perception - the conscious experience and interpretation of sensory information - CNS

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51
Q

Stimulus transduction

A

Each sensory organ deploys a specific mechanism to transform chemical or physical attributes of stimuli to neuronal activity.

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52
Q

Examples of animals using other senses

A

Electrolocation and communication in electric fish - Produce and detect small current flows around them. Use these currents to “see” objects
(electrolocation) and communicate with conspecifics (electrocommmunication)

Ultraviolet vision in bees - detecting a different spectrum of light may be advantageous for bees when looking for the right flowers to feed from

Asymmetric vision in the cockeyed squid - Large (yellow) eye looking upward: detects predators against the dim sunlight. Small eye looking downward to detect prey bioluminescent signals.

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53
Q

Sensory receptors

A
  • Photoreceptors - detect light for vision
  • Mechanoreceptors - detect movement - sound, texture, blood pressure, muscle stretch
  • Chemoreceptors - chemical compounds - smell and taste
  • Nociceptors - detect tissue damage - pain
  • Each sensory organ or receptor detects a specific part/quality of the world
  • transduce stimuli into neural activity
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53
Q

The retina

A
  • Fovea covered by densely packed cones (acute vision during the daylight) (blue green and red cones, each sensitive to a specific wavelength band)
  • periphery covered by rods, more sensitive to light but not as acute (sense very dim light)
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54
Q

the eye

A
  • The iris opens and closes to allow more or less light through the pupil
  • The cornea and the lens focus the light into the retina, where the image is recreated
  • The optic disc allows vessels going in and out, and the optic nerve to carry visual information to the brain
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54
Q

Transduction

A
  • Photoreceptors are depolarised in the dark, releasing glutamate.
  • Light makes them hyperpolarise, reducing glutamate release
  • Photoreceptors and bipolar cells do not fire action potentials, change their membrane potential, which affects the probability of neurotransmitter release.
  • In vertebrate retinas, there are two types of bipolar cells: ON and OFF.
  • In the fovea, one bipolar cell connect to only one photoreceptor, In the peripheral retina, one bipolar cell connects with several PR.
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55
Q

Neural routes to the brain (visual)

A
  1. Retinohypotalamic tract (regulate circadian rhythm, regulates light to retina)
  2. Geniculostriate pathway (dorsal = how, ventral = what)
  3. Tectopulvinar pathway (no colour, where of objects)
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56
Q

Sounds made up of:

A

Frequency, amplitude and complexity

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57
Q

Human ear:

A
  • Outer ear captures and amplifies sound waves.
  • Middle ear amplifies and transmit vibrations.
  • Inner ear translates vibrations into neural activity
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58
Q

Middle ear

A
  • Air filled cavity occupied by ossicles, the three smallest bones in the human body: Malleus, Incus and Stapes.
  • Ossicles vibrate in response to tympanic vibration. Amplify and transmit sounds to inner ear (oval window).
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59
Q

Inner ear

A

vestibular organs tell us which way up we are, sound detected in cochlea, nerves bring information

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60
Q

Organ of Corti and basilar membrane

A

sensitive to different frequencies, vibrations from oval window displace liquid and make the basilar membrane vibrate (high frequency base and lower frequency in apex)
- Pressure transmission along the canals
- Vibrations of the stapes push and pull the flexible oval window in and out of the vestibular canal at the base of the cochlea.
- Pressure waves deflect the basilar membrane in a frequency specific manner.
- All pressure ends up moving the round window and dissipates.

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61
Q

Inner and outer hair cells

A

If we lose hair cells they are gone forever (can stress hair cells and they can die - we lose them as we age)

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62
Q

Vibration to neural activity translation in inner hair cells:

A
  • Stereocilia: Hair-like extensions on the tips of hair cells. Molecular filaments (tip link) connect the tip of each cilia to neighbouring potassium channels.
  • In resting state (no sound, middle panel), there is a basal K+ influx and neurotransmitter release.
  • Basilar membrane vibration (right panel) induce bending of stereocilia which increase K+ influx, increasing neurotransmitter release at the cell base.
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63
Q

Coding of freqency and amplitude in the cochlea

A
  • Place code: Frequency information is coded by the place along the cochlea with the greatest mechanical displacement.
  • Amplitude code: louder sounds produce larger vibrations of the basilar membrane, making the inner hair cells release more neurotransmitter.
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64
Q

Auditory pathways:

A
  • Hair cell neurotransmitter release activates bipolar cells that form the auditory nerve (cranial nerve VIII).
  • The auditory nerve enters the medulla, making synapsis in a tonotopic manner
  • Axons from the cochlear nuclei ascend to the superior olivary complex in the pons. (Inputs from each ear are processed by both olivary nuclei)
  • A series of ascending projection along the midbrain ends up in the primary auditory cortex (A1). The tonotopic representation is preserved up to A1.
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65
Q

Hearing loss:

A
  • Hearing declines with age.
  • Or damage (permanent or transitory) to any components of the auditory pathway.
  • Transitory: (will recover)
    • Obstruction of the ear canal (i.e. excessive ear wax), damage to the tympanic membrane.
    • Conductive hearing loss: caused by problems in the ossicles (i.e. otitis media during ear infections).
  • Permanent:
    • Otosclerosis: excessive growth of ossicles. Requires surgery.
    • Sensorineural hearing loss (most common defect), due to defects in cochlea or auditory nerve. Damage to hair cells caused by toxicity or excessive exposure to noise.
      (worse in men)
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66
Q

Hearing Aids:

A

Cochlear implant bypass degenerated inner hair cells.

  • Miniature flexible electrode array surgically implanted in the cochlea through the oval window.
  • A receiver/stimulator detects and process sound into radio signals, which are sent to the stimulator (implanted inside the skull during surgery).
  • Miniature electrodes positioned in frequency specific regions of the cochlea emit electrical signals, activating neighbouring bipolar cells and the auditory nerve.
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67
Q

Function of smell

A
  • Primary function of nose is to humidify and warm air going to the lungs
  • Secondary function is olfaction:
    • Air flows into the nose cavity.
    • Odorants interact with the olfactory epithelium.
    • Mucus in the epithelium captures odorants
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68
Q

In olfactory epithelium (cell types)

A

Three cell types:
- Supporting cells: metabolic and physical support.
- Basal cells: olfactory cell progenitors.
- Olfactory sensory neurons (OSN): detect odors and produce mucus.

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69
Q

Olfactory receptors

A
  • Odorants are recognised by specific receptors in the cilia of OSNs.
  • Olfactory receptors are G-coupled proteins whose activation opens Na+/Ca2+ channels.
  • OSN is depolarized by Na+/Ca2+ influx, firing action potentials.
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70
Q

Olfactory pathways

A
  • Axons from OSNs pass through the tiny holes in the cribriform plate (bone) to enter the brain.
  • Each type of OSN projects its axon to a single glomerulus within the olfactory bulb.
  • OSN axons make synapsis with mitral and tufted cells, that project to the primary olfactory cortex and other brain regions.
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71
Q

shape pattern theory

A
  • each scent—as a function of odorant-shape to OR-shape fit —activate unique arrays of olfactory receptors in the olfactory epithelium from each scent.
  • These various arrays produce specific firing patterns of neurons in the olfactory bulb, which then determine the scent we perceive.
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72
Q

Detection threshold of olfaction affected by

A
  • Gender - women have lower thresholds - heightened in ovulation but not heightened in pregnancy
  • Training - perfume and wine tasters can distinguish more
  • Age - 50% of population is anodmic (sense of smell loss) by 85
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73
Q

Olfactory fatigue:

A
  • Smell detection stops during continuous exposure, detector of changes
  • Receptor adaptation - makes the receptor stop responding - detection ceases
  • Mechanism - receptors internalisation or sodium or calcium channel inactivation in the olfactory sensory neuron
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74
Q

Purpose of taste

A

guides appetite and triggers physiological processes for absorbing nutrients and adjusting metabolism - identifying nutrients and avoiding chemical threats
- Bitter taste might signal poisonous food. While intense sour might be related to acidic substances, that might cause damage.
- Sweet and salty tastes normally induce seeking behaviour since such substances increase survival.

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75
Q

Taste sensors

A
  • Taste receptors are arranged in taste buds, distributed along the tongue, palate, pharynx, epiglottis, and upper third of the oesophagus.
  • Taste buds arranged in three kind of papillae, distributed in specific regions of the tongue.
  • Receptors for different tastes group together in the same bud.
  • Receptor activation sends neural signal through taste nerves
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76
Q

Retronasal olfactory sensation

A
  • perception of odourants while chewing and swallowing food - brain processes odours differently, depending on whether they come from nose or mouth
  • Flavour: taste (sweet, salty, sour, bitter, umami and fat) and olfaction (retronasal) combination.
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77
Q

Types of taste receptors

A
  • G-coupled protein receptors (like in olfactory neurons) T1R and T2R.
  • T1R detects sweet and umami taste.
  • T2R detects bitter taste.
  • Ion (Na+) channel ENaC detects salty taste.
78
Q

Three cranial nerves which collect taste information:

A
  • Chorda tympani
  • Glosso-pharyngeal
  • Vagus
  • Synapse at nucleus of the solitary tract (medulla) → hypothalamus → insula or gustatory primary cortex → orbitofrontal cortex.
79
Q

Taste classes

A
  • Salty - animals have an appetite for salt, high concentration is aversive - prevent hypernatremia and dehydration - ENaC deletion in rodents removes NaCl behavioural taste response in Na+ deprived mice.
  • Sour - from acidic substances, acids damage external and internal body tissues, associated with increased protein concentration, receptor cells names permeate H+ - contribute to cell depolarisation and active potential initiation
  • Sweet - sugars typically - T1R for all, G-coupled protein - cell depolarisation and action potentials - mice lacking T1R receptors lose preference for natural and artificial sweeteners
  • Bitter - large quanity and compounds are bitterm many poisionous - Quinine: Prototypically bitter-tasting substance, T2R bitter receptors. G-coupled protein. Induce cell depolarisation and action potentials. 30 different T2R genes suggest certain specificity in bitter senses
80
Q

different types of human skin

A

Humans have hairy skin and glabrous skin - no hair follicles but more receptors e.g palm of hand - sensitive to wide range of stimuli
- Two point discrimination test reveals differences in skin sensitivity across the body

81
Q

Nocioception receptor

A
  • pain and temperature
  • free nerve endings
  • sharp/dull pain and hot and cold
  • damage to dendrites pr surrounding cells release chemicals that stimulate dendrite and produces an action potential
  • Small axons with little or no myelination (slow)
82
Q

Hapsis receptor

A
  • fine touch and pressure (e.g grasp)
  • dendrite attached to hair, connective tissue or encased in tissue capsule
  • Distinguish touch, pull, vibration
  • Mechanical stimulation, produces an action potention
  • Composition of capsule determines the type of mechanical energy conducted
  • e.g. parcinian carpusle
  • Large, well-myelinated axons (fast)
83
Q

Proprioception receptor

A
  • location and movement of body e.g. dancing
  • Movements stretch receptors to mechanically stimulate dendrites and produces an action potential
    • muscle spindles (muscle stretch), Golgi tendon organs (tendon stretch), joint receptors (joint movement)
  • Large, well-myelinated axons (fast)
84
Q

Rapid vs slow adapting receptors

A
  • Rapidly adapting receptor - body sensory receptor that responds briefly to the beginning and end of a stimulus on the body
  • Slowly adapting receptor - body sensory receptor that responds as long as a sensory stimulus is on the body
  • Nocioception all slow, hasps and proprioception slow and rapid
85
Q

Deafferentiation

A
  • Loss of incoming sensory input usually due to damage to sensory fibers; also loss of any afferent input to a structure
    • significant consequences - patient GO could not perform many daily tasks, afferent feedback is required for fine movements - had to see if they were making the right movements
86
Q
  1. Dorsal Spinothalamic Tract
A
  • Carries haptic and proprioceptive information
  • Axons from the dorsal-root ganglion neurons enter the spinal cord and ascend ipsilaterally until they synapse in the dorsal column nuclei (base of brain)
  • Axons from the dorsal column nuclei cross over to the opposite side of the brain and project up through the brainstem as part of a pathway called the medial lemniscus
  • Axons synapse with neurons located in the ventrolateral nucleus of the thalamus, which projects to the somatosensory cortex and motor cortex
87
Q
  1. Ventral (or anterior) Spinothalamic Tract
A
  • Carries nocioceptive information
  • Axons from the dorsal-root ganglion neurons enter the spinal cord and synapse onto neurons in the posterior horn. These ‘2nd order’ neurons, in turn send their axons to the contralateral side.
  • Axons from contralateral spinal cord then ascend to the brain where they join with other axons forming the medial lemniscus, eventually synapsing with neurons located in the ventrolateral nucleus of the thalamus
  • Neurons from the thalamus then project to the somatosensory cortex
88
Q

Spinal cord damage

A

results in distinctive sensory loses to both sides of the body below the injury - e.g. fine touch and pressure sensation lost on right side and loss of pain and temperature on the left side

89
Q

Monosynaptic reflex

A

reflex requiring one synapse between sensory information and movement (through motor neurons) eg. knee jerk reflex - more complex spinal reflexes involve multisynaptic connections

90
Q

Vestibular system

A

receptors in the inner ear that respond to body position and movement of the head - 3 semicircular canals, Otolith organs (utricle and saccule)

  • Tell us about position of body in relation to gravity and signal changes in the direction and speed of head movements
91
Q

Vestibular system - angular acceleration

A
  • When the head moves, fluid (endolymph) located within the semicircular canals pushes against hair cells, which causes bending of the cilia located on top of the hair cells
  • Responds to ‘angular acceleration’
  • Bending of cilia leads to receptor potentials in the hair cells and action potentials in the cells forming the vestibular nerve
  • The direction in which the cilia are bent determines whether the hair cell becomes depolarized or hyperpolarized
92
Q

Vestibular system - linear acceleration

A
  • The utricle and saccule also contain hair cells, which are embedded within a gelatin-like substance that contains small crystals of calcium carbonate called otoconia
  • Responds to ‘linear acceleration’
  • When the head is tilted, the gelatin and otoconia push against the hair cells, which alters the rate of action potentials in cells that form the vestibular nerve
93
Q

Primary somatosensory cortex

A
  • projections from the thalamus, Brodmann’s areas 3-1-2, constructing perceptions from somatosensory information
94
Q

Secondary somatosensory cortex

A
  • located behind primary, Brodman’s areas 5 and 7, continues constructions of perceptions, projects to frontal cortex
95
Q

Studies finding somatosensation

A
  • Wilder Penfield stimulated cortical surface with electrodes and recorded responses, wanted to find source of seizures, suggested there was a single ‘somatosensory homunculus’ - useful concept for understanding functional layout
  • Brain has no pain receptors
  • Jon Kaas - used small electrodes and precise recording techniques - better spatial resolutions - found 4 seperate somoatosensory homunculi -
    • Area 3a: Muscles
      Area 3b: Skin (slow)
      Area 1: Skin (fast)
      Area 2: Joints, pressure
96
Q

Effects of damage to somatosensory system

A

– impairment in pressure sensitivity, proprioception, hapsis (ability to identify objects by touch), and simple movements (e.g., reaching and grasping)
- Reorganization following damage is possible (Pons and colleagues 1991)
–Following damage to the arm, the cortex that was devoted to the arm becomes sensitive to the face →’plasticity’ - The ability of the brain to reorganize neural pathways following damage, new experiences, learning, memory formation, etc.

97
Q

Hierarchical control of movement

A

visual information -> frontal lobe motor areas -> spinal cord -> motor neurone -> sensory cortex -> basal ganglia and cerebellum to judge and correct -> spinal cord carries sensory information to the brain

98
Q

conscious and automatic areas of the brain

A

Neocortex (conscious) brainstem and spinal cord (automatic)

99
Q

Hughlings-Jackson (19th Century) - motor systems

A
  • Conceived of nervous system as organised in successive layers, with higher levels controlling complex behavior by acting through lower levels
  • Adapted from evolutionary theory
100
Q

1930s concept of motor systems

A

action → feedback (action successful) → action

101
Q

1950s karl lashley - motor systems

A
  • Movements for skilled actions are performed quickly to rely on feedback
  • Movement modules preprogrammed by the brain and produced as a unit or as ‘motor sequence’
  • Complex behaviours require selecting and executing multiple movement sequences
  • As one sequence is executed, the next sequence is being prepared
102
Q

frontal lobes for motor systems

A
  • Prefrontal cortex - planning of movements - specifying goal
  • Premotor cortex - organises motor sequences (movements appropriate to the context of the action)
  • Primary motor cortex - produces specific, skilled movement
103
Q

the motor cortex: Fritsch and Hitzig & Wilder Penfield

A
  • 1870: Fritsch and Hitzig
    • Electrical stimulation of a dog’s cortex produced movement of mouth, limbs, and paws
  • 1930s: Wilder Penfield
    • Used electrical stimulation to map the cortices of human patients who were about to undergo neurosurgery
    • Confirmed the role of primary motor cortex in producing movement in humans
104
Q

Topographical organisation

A
  • Neural spatial representation of the body or areas of the sensory world perceived by a sensory organ
  • The parts of the motor cortex that control the hands, fingers, lips, and tongue are disproportionately larger than parts of the motor cortex that control other areas
105
Q

Nudo and colleagues (1996) (motor systems)

A

–Damaged part of motor cortex that controlled the hand in monkeys

–Without rehabilitation: (relies on good hand)

  • The hand area of the motor cortex became smaller whereas the elbow and shoulder area became larger
  • Monkeys lost most ability to move the hand

–With rehabilitation: (forced to use bad hand)

  • The hand area of the motor cortex retained its size
  • Monkeys retained some ability to move hand
  • May explain recovery after stroke in humans → Brain Plasticity
106
Q

Corticospinal tract of motor systems

A
  • Bundle of nerve fibres connecting cerebral cortex to spinal cord
  • originates from layer 5 - pyramidal neurons
  • branches at the brainstem into opposite-side lateral tract that controls movement of limbs and digits, and a same-side ventral tract that informs movement of the trunk (middle of the body)- Also called the pyramidal tract
107
Q

different types of motors neutrons

A
  • Laterally located motor neurons project to the muscles that control the fingers and hands
  • Intermediately located motor neurons project to muscles that control the arms and shoulders
  • The most medially located motor neurons project to muscles that control the trunk
108
Q

control of muscles

A
  • Neuromuscular junction - motor neurons from spinal cords to muscles - acetylcholine
  • Extensor
    • Moves (extends) the limb from the trunk away
  • Flexor
    • Moves the limb from the trunk toward
  • Connections between interneurons and motor neurons ensure that the muscles work together so that, when one muscle contracts, the other relaxes
109
Q

Consequences of spinal cord damage:

A
  • Quadriplegia - Paralysis of the legs and arms due to spinal cord injury
  • Paraplegia –Paralysis of the legs due to spinal cord injury
110
Q

Basal ganglia

A
  • collection subcortical neurcli within the forebrain (Striatum (caudate, putamen, accumbens), globus pallidus, substantia nigra, subthalamic nucleus)
  • Receives input from all areas of the neocortex (e.g. motor cortex) and limbic cortex (e.g. amygdala, hippocampus)
  • Project back to the motor cortex
  • Allow us to adjust the force of our movements
111
Q

Volume hypothesis

A
  • the internal globus pallidus acts like a volume dial and projects to the thalamus, which projects to the motor cortex (two pathways to motor cortex)
    • Direct
      • Inhibitory effect on GPi: Too much activity leads to overactivity in the thalamus and force of movement amplified (turning up system)
    • Indirect
      • Excitatory effect on GPi: Too much activity leads to underactivity in the thalamus and force of movement reduced (turning down system)
112
Q

Damage to the basal ganglia can produce two main types of motor symptoms

A
  • Hyperkinetic Symptom –Symptom of brain damage that results in excessive involuntary movements, as seen in Huntington’s Chorea
  • Hypokinetic Symptom –Symptom of brain damage that results in a paucity of movement, as seen in Parkinson’s disease
113
Q

Huntington’s Chorea

A
  • Genetic disorder affecting muscle coordination
  • Symptoms: excessive spontaneous movements, irregularly timed, randomly distributed, and abrupt in characterdegeneration = blocking of indirect pathway from striatum → globus pallidus external
  • Atrophy of caudate nucleus and putamen (degeneration of indirect pathway neurons, direct pathway spared)
  • Treatment: Antipsychotics (e.g. clozapine) that block dopamine transmission, Anxiolytic/anticonvulsant GABAergic drugs (e.g.clonazepam) that increase inhibitory transmission (reduce anxiety)
114
Q

Parkinson’s disease (PD)

A
  • Slowly progressive disorder that affects movement, muscle control, and balance.
  • Symptoms: slowness of movement, resting tremor, stiffness of muscles, ‘gait’: small shuffling of steps
  • Loss of substantia nigra that sends dopamine projections to putamen that controls movement and coordination.
  • losing cell bodies- deficits when lost too many
  • Treatment - L-Dopa, dopamine precursor, boosts dopamine levels and increase transmission, less effective in many patients >5 years (Globus pallidus internal can be lesioned)
  • Dopamine normally increases activity in the direct pathway (DR1 expressing) and decreases in the indirect (DR2 expressing)
115
Q

Cerebellum: Acquiring a motor skill

A
  • Flocculus - Small but dense lobe involved in eye movements and balance – Inputs from vestibular (when head moves) system
  • Two hemispheres –Homuncular organisation (mid controls mid part of body and lateral part controls extremities)
    (Lateral parts - Controls movement of limbs, hands, feet, and digits, Medial parts - Controls movement of face and midline of body)
116
Q

Main motor functions

A

1) Timing of movements (Schlerf, 2007)
- Clock, pacemaker of body - controlled with timing

2) Maintaining Movement Accuracy (Thatch, 2007)
- Error Correction and accuracy

–Compares intended movement with actual movement and makes the necessary adjustments accordingly

117
Q

The monosynaptic stretch reflex:

A

(only one synapse needed)

  • stretch of the mechanoreceptors in the muscle increase firing rate of the afferent sensory neuron
  • Increased neurotransmitter release activates the motor neuron
  • Contraction of muscle
118
Q

Polysynaptic reflex and integration with CNS

A
  • Sensory neuron, intermediate neuron, motor neuron
  • CNS neurons can affect the sensory-motor relationship of polysynaptic reflexes - involves information from the brain
119
Q

Saccade

A
  • rapid movement of the eye between fixation points - visual attention content can be traced from saccades
    -Neurons in the posterior parietal cortex fire more vigourously when the visual stimulus are the target of saccades
  • lesions on the posterior parietal region cause attentional deficits in humans
  • keeps image in fovea where vision is most accurate
120
Q

movement vs visual neurons

A
  • Movement-related neurons: fire before saccades to specific locations.
  • Visual-fixation neurons: fire after the saccade, inhibiting movements away from the target.
  • Superior colliculus performs visuomotor integration.
  • This region form a map of potential eye movement. Each neuron within the map fires before the eyes move to the corresponding location in that map.
121
Q

Eye saccade brain activation

A

The caudate nucleus inhibits the tonic inhibition of the substantia nigra pas reticulata (disinhibition) which allows the superior colliculus neurons to fire and produce a saccade

122
Q

Integration of visual information

A
  1. Geniculostriate pathway:
    - Perception of motion and depth by the dorsal visual stream (how).
    - Perception of contrasts, contour and colour by the ventral visual pathway (what).
  2. Tectopulvinar pathway:
    - Perception place by the pulvinar pathway (where).
123
Q

Trajectory projection

A
  • integration of information over time:
  • Prior information from experience
  • Sensorial integration produces a likelihood
  • using both the prior and likelihood the brain can estimate where a ball in a game of tennis will bounce and produce behaviour
124
Q

Movement controlled by basal ganglia:

A
  • Oculomotor loop controlling eye movement and tracking
  • Skeletomotor loop controls voluntary movements
  • Basal ganglia involved in:
    • action selection (as seen for the saccades before).
    • Initiation and terminating actions.
    • Relating actions with consequences.
125
Q

Cerebellum involved in …

A

involved in movement precision and outcome - some regions activated when eye tracking and hand movement require coordination

Reward system can modulate maintenance or modification of behavioural outcome

126
Q

Motor reaction:

A
  • The “motor homunculus” maps the areas of the motor cortex responsible for moving each part of the body.
  • Specific sections of the motor cortex will be active at different stages on the approach, racquet swing and ball hitting.
127
Q

learning in psychology vs neuroscience

A

Psychology - learning as a permanent change in behaviour due to experience
Neuroscience - learning as the response of the brain to environmental experiences involving adaptive changes in synaptic connectivity which will alter behaviour
- Not synaptic changes due to drugs ect.

128
Q

Limitations with innate responses:

A
  • stimulus must be physically present
  • behaviour fixed and little opportunity to modify
  • modification of innate responses does not occur within an individual’s life time (ontogenetic) but can in an evolutionary time scale (phylogenetic)

(can be maladaptive)

129
Q

Classical conditioning studies

A
  • Tinbergen’s Herring Gull experiments - dots on mother’s beaks which baby gulls would peck and then be fed - reduced pecking when position changed/colour changed
  • Edwin B. Twitmeyer - first experimental evidence of associative learning in humans - association between auditory stimulus an
130
Q

Terminology of classical conditioning:

A
  • Unconditioned stimulus (UCS or US): Stimulus that has biological relevance (e.g. food; loud noise; pressure on patellar tendon)
  • Unconditioned Response (UCR or UR): Innate behaviour/response triggered by unconditioned stimulus (e.g. salivation; startle reflex; patellar reflex)
  • Conditioned stimulus (CS): Neutral stimulus to begin with, but which elicits a behaviour/response through learning (i.e. through repeated pairings with the Unconditioned stimulus)
  • Conditioned response (CR) – Learned behaviour/response produced by conditioned stimulus
131
Q

Phenomena of classical conditioning

A
  • Extinction - no reinforcement/loss of contiguity - response loses strength
  • Spontaneous recovery - passage of time after extinction, retest conditioned stimulus
  • Reacquisition - conditioned response again reinforced by conditioned stimulus - ‘savings in relearning’ - learn faster than first time
  • Generalisation - a similar conditioned stimulus would elicit similar conditioned response
  • Discrimination - conditioned response reinforced and the opposite of the conditioned response not reinforced leads to a decrease in CS- (non-reinforced stimulus)
132
Q

Benefits of classical conditioning

A
  • Helps us to adapt to our environment beyond ‘simple’ reflexes - associations between stimuli/environment
  • Ontogenetic ‘adaptation’ (adaptation in our lifetime)
  • Ubiquitous (occurs in all species) and preserved by evolution (there is an evolutionary purpose to this type of learning)
  • All learning is classical conditioning (according to Pavlov – we know that this is not true)
  • Classical conditioning can shape our emotional life.
133
Q

Neuronal circuitry of conditioned fear

A

Somatosensory and auditory thalamus → auditory and somatosensory cortex → amygdala → motor output (e.g. freezing, blood pressure, hormones)

  • Pavlov hypothesised that, when (psychological) connection between the CS and US is conditioned, the area of the cortex activated by the CS becomes physically connected with the area activated by the US.
134
Q

Thorndike in operant conditioning

A

Thorndike’s puzzle pox - (wanted to turn psychology into a hard science), put cats inside box and cats would scratch to get out and would eventually scratch the pedal to open the door and get out, the cats got out quicker and quicker over trials

Thorndike’s laws of learning:
- Law of Effect - behaviour that leads to a positive outcome is more likely to occur in the future
- Law of Exercise – connections between responses and outcomes are strengthened by repetition
- Law of Readiness – learning is motivated by an internal state

135
Q

Operant behaviourism terms:

A

Reinforcer = Stimulus/event that increases the likelihood of the preceding behaviour to occur

Positive reinforcer = Stimulus (usually positive) produced by the behaviour that increases the likelihood of the preceding behaviour to occur

Negative reinforcer = Stimulus (usually negative) eliminated by the behaviour that increases the likelihood of the preceding behaviour to occur

Punishment = Negative stimulus/event that decreases the likelihood of the preceding behaviour to occur.

Omission = Elimination of positive reinforcer decreases the likelihood of preceding behaviour

136
Q

Schedules of reinforcement:

A
  • Continuous reinforcement = every behavioural response reinforced
  • Partial reinforcement = behaviour reinforced only part of the time
  • Ratio schedules = reinforcement given after every nth response
    • Fixed= response requirement always constant
    • Variable= response requirement varies around average
  • Interval schedules = reinforcement given after certain amount of time
    • Fixed = reward intervals constant
    • Variable= reward interval varies around mean time
137
Q

Classical and operant learning interact - dual-process - avoidance learning:

A
  • Rat placed in chamber with 2 compartments
  • Speaker delivers auditory stimulus (would-be CS)
  • Grid floor delivers mild footshock (US)
  • Barrier for escape/avoidance of footshock
  • Initially, rat escapes following US (i.e. footshock)
  • Eventually learns to escape following CS (i.e. auditory stimulus)

Classical conditioning – Tone (CS) leads to shock (US)
Operant conditioning – Escape/avoidance leads to safety

138
Q

Principles of associative learning (operant and respondant):

A
  • Learning through reinforcement
  • Association by contiguity
  • Co-occurrence in space and time
  • Arbitrariness – We can learn associations between any stimuli and between any response and outcome
  • Empty organism –Organism is black box – collection of associations
  • Passive organism - Learning happens TO the organism
139
Q

Taste aversion learning - Garcia and Koelling:

A
  • All rats learned to associate clicking sound and light with sweet taste from bottle
  • One group got a foot shock at the same time and another group had x-rays and so felt ill later (same time as experiencing the other sensations)
  • Rats then given the choice to lick 2 bottles (one with normal not sweet water and would hear the click and see the light and the other with just sweetened water) (contiguity useful for learning)
  • Would assume they would avoid both bottles but
  • Those that were ill avoided sweet water, those that received shock avoided bright/noisy water
140
Q

Edward Tolman’s latent learning effect:

A
  • latent = dormant learning
  • Placed rats in a maze, had to learn to navigate through and find way out
  • food reinforcement given to one group, other group not
  • group always reinforced showed fewer mistakes than group never reinforced
  • a group which started never being reinforced and then after day 10 given reward did best out of maze
141
Q

Non-associative learning

A
  • based on repeated experience with a stimulus
  • Habituation - decrease in effect
  • Sensitisation - increase in effect
142
Q

Karl Spencer Lashley - learning and memory

A

discrete lesions of cortical areas did not interfere with maze learning in rats, but large areas of damage did - no one physical location that you can remove to lose maze memory - engram

Principle of Equipotentiality: All cortical regions can mediate learning equally
Principle of Mass action: Ability to learn is proportional to the amount of cortex available

143
Q

Memory storage areas of the brain:

A
  • Hippocampus – declarative and spatial memories (e.g., review case of H.M.)
  • Cerebellum – procedural memories (simple Pavlovian associations)
  • Amygdala – emotional memories – Pavlovian associations
  • Frontal cortex – short-term/working memory
144
Q

Structural basis of memory

A

Golgi formed the Golgi silver stain (brain parts) - Ramon y Cajal

  • Cajal proposed that structural/morphological changes store memories
145
Q

Neurogenesis

Creating Novel Circuits

A
  • Predominant view prior to the mid-1990s:
    –The mammalian brain does not make new neurons in adulthood
  • There is now evidence that neurogenesis does occur in the mammalian brain
    –Olfactory bulb, hippocampal formation, and possibly the neocortex
    –Reason for neurogenesis is still unclear
146
Q

Environmental experiences alters brain morphology:

A
  • Raising rats in enriched enclosures increases brain weight, dendritic length and complexity (‘Sholl analysis’), Vascular volume (more blood vessels), Number of synapses per neuron (synaptic spine counting), Mitochondrial volume (marker of greater metabolic activity)
  • Being raised in an enriched enviroment leads to physical changes in neurons
147
Q

3 possibilities of synaptic basis of memory:

A
  • New synapses could be generated to store specific new memories.
  • Existing synapses could be modified to store the memories
  • A pool of new synapses could be continuously generated in the brain, learning and memory incorporates them into a functional storage network.
148
Q

Donald Hebb - ‘Hebbian synapse’

A
  • Donald Hebb’s original idea was that new synapses are continuously generated in the brain
  • Key points:
    • Simultaneous pre- and post synaptic activity
    • Some sort of change in the connection between the neurons
    • Increase in the influence that pre synaptic neuron has over postsynaptic activity
  • “cells that fire together, wire together”
  • Whole-cell electrophysiology as first evidence for ‘Hebbian learning and memory’
149
Q

Long-term potentiation (LTP)

A
  • long lasting changes in hippocampal synaptic efficacy following high frequency (tentanic) stimulation
  • Tetanic stimulation produced LTP in amygdala
  • Pavlovian conditioning produces LTP in amygdala
  • Neurochemical basis of LTP
150
Q

Motivation

A

an internal state that explain why we behave or why we learn to behave - science of motivation is understanding behavioural causation - motivational sates, desires and drives

151
Q

Drive reduction theory

A
  • Hull proposed that a reinforcer supports learning because it alleviates an internal state of deprivation
  • Imbalance in homeostasis creates ‘arousal’ that initiates action, The goal of homeostasis is to decrease the ‘arousal’ → Can achieve this goal by minimising the difference between an optimum ‘set-point’ and an ‘actual point’ of a physiological system
152
Q

Negative feedback

A
  • Walter Cannon - negative feedback as the primary mechanism by which we maintain homeostatic states - minimise difference between set point and actual point
  • Negative feedback = a process whereby the effect produced by an action serves to diminish or terminate that action.
153
Q

Body temperature:

A
  • Humans and other endotherms generate heat by metabolism
  • Sensors: Cells in the Pre-Optic Area of the Hypothalamus sense brain temperature & we have thermal sensors throughout our periphery
  • The Hypothalamus controls physiological & behavioural responses to regulate temperature
154
Q

Thirst and homeostasis

A
  • Water comprises 70% of our lean body mass, as water is lost cellular processes become inefficient and eventually excessive water loss is fatal, drinking behaviour is the primary means of replenishing water
  • 2/3 of body water is inside cells, direct water loss occurs primarily from extracellular compartment
  • Intracellular and intravascular (plasma) fluid volume and composition must be kept in precise limits. Intracellular - relative concentration solutes between intracellular and interstitial compartments (isotonic)
155
Q

Osmometric thirst/cellular dehydration

A
  • Water loss causes concentration of salts to increase in extracellular fluid, causes an osmotic imbalance between extra- and intra - cellular compartments and water leaves cells to restore balance (by osmosis)
  • Artificial increasing extracellular salt (NaCl) content stimulates drinking (Gilman, 1937), Drinking is directly proportional to additional salt load, Microinjection of small amounts of NaCl into certain brain areas induces drinking.
  • Changes in osmolarity are monitored by cells (osmoreceptors) in the Organum Vasculosum of the Lamina Terminalis (OVLT).
156
Q

Hypovolemic thirst

A
  • Loss of extracellular fluid (ECL) levels can induce thirst without salt changes
  • Arises in the kidneys and the heart - stimulates brain sites leading to drinking
157
Q

Angiotensin and drinking

A
  • Hypovolemia causes the release of the enzyme renin from the kidneys
  • Renin converts a blood-borne molecule (angiotensinogen) into angiotensin
  • Angiotensin stimulates pituitary and kidneys to release hormone to conserve water and salt
  • Increase blood pressure by vasoconstriction
  • Stimulates drinking by binding on receptors in the Subfornical Organ (SFO)
158
Q

Atrial baroreceptor

A
  • Atria of heart contain neurons that detect stretch (baroreceptors)
  • Volume of return blood through veins detected by baroreceptors
  • Information from baroreceptors to nucleus of the solitary tract
  • Information to median preoptic area
159
Q

The body using energy

A

1 - Basal Metabolism (BMR) - 55% - normal resting functions e.g body heat
2 - Food digestion - 33% - processing and breaking down food
3 - Active Behavioural processes - 12-13% - other behaviours - varying on activity levels

  • Remaining energy stored in energy reserves
160
Q

Sources of energy: - glucose primary fuel

A
  • Carbohydrates (saccharides) - broken down to glucose for brain and muscles - stored as glycogen in liver and muscles (not essential)
  • Amino acids (proteins) - essential - building blocks for cell - can be converted to glucose
  • Lipids (fats) - long term energy store - source of glucose - converted to free fatty acids
  • Vitamins and minerals - needed to assist in bodily functions - sourced from diet - not a glucose source
161
Q

Glucostat theory - Mayer

A

absolute blood glucose as variable that needs to be at equilibrium (glucose main source of energy, lack of glucose = nutrient deficit → drive to eat)

162
Q

Two basic types of set-points are thought to regulate food intake:

A

Glucostatic Set-Point Theory: Eating is controlled by deviations from a hypothetical blood glucose set-point (Glucostat receptors)

Lipostatic Theory: Eating is controlled by a hypothetical body-fat set-point (long-term homeostatic maintenance).

163
Q

Dual-centre hypothesis

A
  • hunger/satiety dedicated brain areas - in lateral hypothalamus (LH) and ventromedial hypothalamus (VMH)
  • Ventromedial Hypothalamus lesions increase feeding and weight - Satiety centre&raquo_space; Stop eating centre? (hyperphagia)
  • Lateral hypothalamus lesions decrease feeding and weight Hunger centre&raquo_space; Start eating centre? (can be activated via optogenetics) (aphagia)
164
Q

Problems with dual centre hypothesis:

A
  • Rats chose to press a lever that activated lateral hypothalamus, rats would press this more than for heroin - why would the rat want to feel hungry, the animal would eat but also involved in other behaviours
  • So not a dedicated hunger centre but generally involved in motivation behaviours (such as eating)
  • Could be dedicated hormones (below)
165
Q

Hormones for hunger?:

A
  • Ghrelin and orexins are peptide hormones secreted in the gut and from adipose tissue + hypothalamus
  • Orexin and Ghrelin administration increase hunger
  • These peptides could be dedicated hunger signals?
166
Q

Hormones for satiety?:

A
  • Cholecystokinin (CCK) is a hormone released in the intestines in response to fat
    –CCK injections inhibit subsequent feeding
  • Peptide YY (PYY) is also released in the gut in response to food
    –Injections of PYY inhibit eating. PYY may be abnormally low in obese individuals.
167
Q

Leptin

A
  • Leptin discovered in obese mice, produced by adipose tissue, acts with receptors, present in some hypothalamic nuclei, binds to receptors in the ventromedial nucleus of the hypothalamus, genetic leptin deficiency associated with obesity
168
Q

Babies and rats feeding

A
  • Prior to 3 months babies as homeostatic machines - larger breast feeds first thing in the morning to relieve hunger
  • Around 3-6 months they switch to a large feed last thing at night - this large meal anticipates the relative difficulty of obtaining night-feeds - in anticipation of possible hunger
  • Rats feed in the same way depending on whether lights are on or off - related to own body clock - anticipatory feeding before sleeping
169
Q

Learning effects in eating

A
  • Certain associations can increase feeding - cue-potentiated feeding in satiated (full) rats
  • Played a tone when hungry, associate with delivery of food, and control group with association of not food, satiate with free feeding, when played conditioned stimulus it produces overeating
    • Due to the influence of the amygdala on the hypothalamus
  • Found cue potentiated feeding in humans - Birch - food specific cues enhance feeding of children
170
Q

Eating for pleasure

A
  • One main motivator for eating is for pleasure - emotions influence behaviour
  • Kent Berridge measuring pleasure - tongue protrusions for pleasure, opening mouth for when not pleasurable - both babies and animals - taste hedonics
171
Q

Dopamine for eating

A
  • Role of dopamine in pleasure - results from selective lesions of dopamine neurons: (low dopamine)
    • No dopamine means animal didn’t eat/drink, but still showed liking for sweet solutions if forced
  • Genetic mutation that increases dopamine activity makes mice want more sucrose - doesn’t change their liking - high dopamine levels want food more (run faster for it) but ‘like’ it just as much
172
Q

Dissociation between liking and wanting in nucleus accumbens

A

Liking mediated by opioid and GABA systems in the nucleus accumbens. And cannabinoid systems – Wanting mediated by dopamine

173
Q

Evolutionary ideas

A
  • William Bateson - bodies don’t have continuity - we all temporary atoms - if you break a stone in half you get 2 small stones but you can’t break an animal in half without getting a dead animal - permanence is an illusion
  • Plato - idealism/essentialism - perfect things exist and all the imperfect variations are an illusion - essential kinda of things - There exists a perfect world and what we see is an illusion - so species cannot change over time
  • Aristotle - great chain of being - humans at the top, going down to things, later god and angels above us - empiricism led to change - senses perceive reality
174
Q

Darwins voyage of the HMS Beagle - 1831-6

A
    • wrote a book about it and collected new species e.g. giant sloth fossils in dry environments (could not exist in these areas but animals in africa can - thinking of continuity)
  • Native people of Tierra del Fuego - people could survive in harsh conditions
  • Galapagos finches - different varieties in different areas (beaks) - influenced his thinking
175
Q

uniformitarianism (James Hutton)

A
  • geographical events happening all the time, differs from catastropism - geographical events only happening in great cataclysmic upheavals - both are true
176
Q

Thomas Malthus

A
    • power of population greater than that of producing food - human mortality exists to control the population
  • led darwin to think that some animals would be better at getting food and reproducing
177
Q

Terms of Darwin’s theories

A

1) species are not immutable (unchanging)
2) natural selection (struggle for existence, inherited variability, some variations more successful and more likely to leave offspring, descent with modification/evolution

178
Q

Problems with Darwin’s theory

A
  • medium or variable of heredity unknown
  • altruistic behaviour not explained
  • elaborate costly appendages
179
Q

the theory of sexual selections - the descent of man

A
  • Darwins other book
  • intrasexual selection - eg. male competition
  • intersexual selection - eg. female choice
  • Males must compete to reproduce with females - a successful male can mate with many females - Bateman’s Principle - intrasexual
180
Q

Human mate preferences

A
  • women seek resource gathering potential in mates, men should seek more fertile (younger) women
  • lower hip to waist ratios more attractive - Singh
  • hard to judge attractiveness to determine evolution as changes through history
181
Q

Darwinian Anthropology

A

Measures behaviour/babies, eschews mental causation, domain-general learning, humans as flexible opportunists
impacted by Darwin

182
Q

Evolutionary Psychology

A

Surveys/questionnaires, posits cognitive adaptations, domain-specific cognitive modules natural selection shapes psychology not behaviour
impacted by Darwin

183
Q

Gene-culture coevolutionary theory

A

cultural change, culture and genes co-evolve, domain-general biases, culture influences genetic adaptations and vice versa

184
Q

William James and John B Watson

A

William James - father of psychology - extreme nativist theory - instincts for sucking, biting, pointing, crying ect. (nature over nurture)

John B Watson - little albert associations - black box psychology (stimulus response psychology)

185
Q

Margaret Mead

A

easier transition to adulthood through adolescence in Samoa than Western Cultures, looked at 3 different cultures in New Guiniea in second book - culture moulded to be - a person is shaped by social cultures

186
Q

Axioms of the standard social science model - Cosmides and Tooby

A
  • Psychic unity of human kind
  • biological endowment is irrelevant to the manifestation of culture
  • Adult behaviours absent from infants - must be acquired from outside
  • outside source is social environment
  • social environment shapes individuals
  • culture operates on the rudimentary drives of the unformed infant to produce a cultural being
187
Q

Criticisms of the SSSM - Tooby and Cosmides

A
  • The fact that many adult characteristics are absent at birth foes not implicate the social environment as their source
  • Nature/Nurture is a false dichotomy
  • A domain-general learning capacity is a psychological impossibility
188
Q

Significant adaptive milestones

A

bipedal locomotion (7 million years ago), stone tool manufacture (3 million years), and big brains (last few million years)

189
Q

Humans adapted for bipedal locomotion:

A
  • Gorilla and human pelvis very different (gorilla tall and blade shaped, human is short and bowl shaped) - allowing for bipedal locomotion
  • Apes’ femur hangs straight down, they can walk biped-ally for short bursts (”knucklewalking” → african great apes), human femur hands down with a sharp angle
  • Our angled thighs allow for us to walk almost in a straight line - dated footprints from 3.7 million years ago walking almost in a straight line
  • This became more useful as the world cooled (less jungle more grassland in Africa)
190
Q

Theories for bipedal locomotion:

A
  • carrying e.g. weapons and tools
  • travelling between trees
  • feeding from bushes - reaching higher
  • feeding on grass seeds (walking along and stripping seeds at the same time)
  • provisioning a family
  • thermoregulation (sun on less area of body)
  • predator-avoidance - can see further
  • wading in water - to get resources (aquatic ape hypothesis)
191
Q

Brain expansion

A

Brains expanding consistently over the last couple million years - peaking with modern humans
- Masseter and Temporalis muscles allow us to chew - ours are smaller than gorillas and older humans - we no longer have a zygomatic arch (an arch on the head to accomodate these muscles - smaller muscles and larger skulls)

192
Q

Stone tool use

A
  • Core (rock you are hitting and hammerstone (rock you hit it with)
  • Stone tool increases don’t improve much as the brain expands
  • Human’s hands adapted for tool making - large size and strength of thumbs
193
Q

Oldowan stone tools - Lower Oaleolithic - 2.5 mya - 1.6 mya

A

Oldest tool in Oldowan - used the flakes not the core
- H.habilis and H.erectus

194
Q

Aucheulean - Lower Paleolithic - 1.7 mya to 200 kya

A
  • Aucheulean - two methods existing at the same time (still Oldowan use) - Aucheulean had hand axes and cleavers
  • Acheulean is associated with Africa, Europe, and southern Asia, whereas the non-handaxe technology, Developed Oldowan, is associated with southeast Asia. This is the first time the archaeological records shows cultural variation in technology.
  • Mix of core and flake uses
195
Q

Mousterian - middle paleolithic - 200 kya - 40 kya

A
  • A new approach - lasted 160,000 years
  • Step change in cognitive resources
  • Greater variety of modified flakes
196
Q

Aurignacian, Solutrean, Chatelperronioan ect. - Upper Paleolithic, 40 kya - 10 kya

A
  • Significant cultural/geographical variation in Europe
  • More cutting edge per unit stone
  • Production of blade tools
  • Could make thin and fragile stones - showcasing skill
  • First evidence of art
    Finding of art in South Africa further back than first thought (70kya)
197
Q

The frame problem

A
  • advantage to framing aa situation rapidly - responses biased to appropriate ones in different circumstances