Cognitive neuroscience Flashcards

(133 cards)

1
Q

What is the principle of MRI

A

hydrogen is measured in the brain. The nucleus of a hydrogen atom is a single positively charged proton, a tiny spinning magnet. The huge magnet causes the external magnetic field is induced align the hydrogen in one direction. Second magnetic field is induced, direct the direction of the magnetic field for a short time. By switching off the b1 the hydrogen wants to go back to its original direction. The different tissue types have a different in time that the hydrogen goes back to the B0 direction -> this is how you see contrast.

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2
Q

how does fMRI work?

A

M0 recovers more slowly in oxygenated blood than in deoxygenated blood. To measure which brain area is active. Active brain areas are more oxygenated. You are measuring BOLD: Blood oxygen level dependent.

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3
Q

What is blocked design?

A

stimuli are often presented in quick succession in blocks between baseline periods, signal increases to plateau. -> only possible for simple tasks
o Multiple trials needed for good SNR
o No information about duration or time course of activation
o Only possible for simple tasks.

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4
Q

What is event related design?

A

between stimuli the signal goes back to the baseline.
o Complex tasks are possible.
o It gives information about duration and time course of activation.
o SNR can be worser: Small signal, less trials, more complex tasks have more conditions, fewer trials per condition.

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5
Q

Advantages of fMRI

A

o you can measure the whole active human brain
o it can be combined with many kinds of cognitive tasks
o Versatile: Anatomy, connectivity (DTI), Metabolites(fMRS), Neural activity (BOLD)

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6
Q

Disadvantages of fMRI

A

o You don’t measure neuronal activity but oxygen consumption (not all forms of neural activity consume the same amount of oxygen, action potential/ synaptic potential, excitation vs inhibition)
o Only correlational: you do not know the effect of the measured activity.
o Temporal and spatial resolution are limited.
o behavioural tasks are limited by scanner.
o expensive and time consuming: many subjects and many sessions are necessary for good signals.

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7
Q

LFP

A

combination of transmembrane currents from many neurons near the electrode: slow frequency, Excitation(sinks) and inhibition(source) occurs simultaneously at different locations of the neuron, such that the net transmembrane current is zero. Cortical LFP’s are so strong you can record them on EEG. Only possible because of elongated bipolar cells.

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8
Q

EEG

A

non invasive method to measure electric activity with electrodes on the scalp
- High temporal resolution
- Signal distortion and attenuation -> difficult to interpret the signals

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9
Q

ECoG

A

: electrocorticography: invasive, better signal. Placed surgically on top of cortical areas of brain.
- Utah array: Brain machine interface = electrical recording from motor cortex -> paralyzed patients can do some behaviour tasks by themselves.

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10
Q

Advantage extracellular recording

A

direct measure of neuronal activity, high temporal resolution

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11
Q

Disadvantages

A

invasiveness, a limited number of neurons can be studies, a limited applicability to neurons.

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12
Q

Optogenetics

A

Optogenetics is used to manipulate neuronal activity and verify the effects of such manipulations

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13
Q

Optogenetics principple

A

optogenetic and gated ion channels: light gated ion channels open when light is introduced -> initiates action potential. -> activates the constructed gene

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14
Q

Steps of optogenetics

A
  1. Piece together genetic construct: promotor + gene encoding opsin (light sensitive ion channel)
  2. Insert construct into virus.
  3. Inject virus into animal brain: opsin is expressed in targeted neurons
  4. Insert optrode plus electrode.
  5. Laser light of specific wavelength opens ion channels in neurons
  6. Record electrophysiological and behavioural results.
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15
Q

DREADDS principle

A

pharmacological on/off switch affecting only genetically modified cells.

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16
Q

Steps making DREADDS

A
  1. Make your desired receptor: activator or inhibitor
    a. Engineered G-protein coupled receptor
    b. Responding only to a specific drugs (CNO: clozapine-N-oxide)
    c. Responding only with a specific action
  2. Express that receptor in the brain(globally, locally or cell type specific
    a. Inject gene for the receptor via AAV(adeno-associated virus)
    b. With marker protein
  3. Inject ligand for the expressed receptor
    a. Inject the drug for the DREADD or via food, eye drops
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17
Q

Pro’s DREADDS

A

o The effect can be specific to one cell type or brain region
o The expressed receptors do nothing without CNO, only when CNO is provided, the receptors affect the cellular activity
o No need for light

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18
Q

Con’s DREADDS

A

o No strict timing control: slow the effect can be long lasting
o Side effect of injects drug?

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19
Q

NMDA receptor

A

o GluN2 is the glutamate binding domain
 GLUN2B in immature hippocampal CA1 neuron
 After maturing you get GLUN2A subunits.
 Before birth almost all expression of GluN2B and after birth its more GluN2A
o GluN1 is the glycine binding domain
o If glutamate is released NMDA do not respond because of this. -> Depolarization of the membrane then the magnesium blockage is removed. Then NMDA receptors open their channels -> wiring of neurons
o Coincidence detector.
o Slow response

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20
Q

AMPA

A

AMPA is necessary for inflow of sodium
o LTP is an increase of AMPA receptors.
o AMPA has a faster response than NMDA receptors.
1 type contains GluA1 and GluA2
1 type contains GluA2 and GluA3?

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21
Q

CAMKII

A
  • Calcium/Calmodulin dependent kinase II(CAMKII) is always switched off normally
    o If calcium flows in and binds to calmodulin it binds to regulatory segment and it is phosphorylated.
    o Because it is in a ring structure in can phosphorylate itself. CAMKII can stay active for over a minute.
    o CAMKII can bind NMDA(GLUN2B) -> phosphorylation of AMPAs facilitates LTP -> causes the synapse to widen -> more room for AMPA receptors.
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22
Q

LTP

A

Early phase LTP: early phase is independent of protein synthesis
Late phase LTP: does require protein synthesis

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23
Q

Habituation

A

progressive decrease of the amplitude of frequency of a motor response to repeated sensory stimulation.
- Less glutamate released from presynaptic synapse= synaptic depression
- Fewer synapses : In the end there are fewer synapses between the sensory and the motor neurons but this only happens after days of continuing the stimulus.

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24
Q

Sensitization

A

repeated administration of a stimulus results in the progressive amplification of a response.
- Same number of action potential -> bigger excitatory response because of serotonin released by interneurons, changes the potassium channel causes a longer depolarization.

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25
Priming
= nonconscious form of memory that involves a change in a persons ability to identify, produce or classify an item as a results of a previous encounter with hat item or a related item .
26
3 stages of skill learning
- Cognitive: what to do - Associative: how to do it - Autonomous : do it
27
Important structures for skill learning
Dorsal striatum, motor cortex, Cerebellum
28
Skill
= capacity to execute a motor/cognitive program Characteristics o Difficult to tell or transfer to others o The content cannot be retrieved consciously o Dependent on feedback during learning o Repetitions are necessary to learn
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Declarative memory
the ability to consciously remember personally experienced events and facts shared with others
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Episodic memory
personally experienced events
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Semantic memory
facts shared with others. Stored in anterior temporal cortex
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Recollection
memories of a past event that includes specific associations and contextual details
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Familiarity
the sense that we experienced an event at some point in the past even though no specific associations or contextual details come to mind
34
Hippocampus : in declerative memory
Hippocampus stores a summary of the whole event
35
Cognitive map theory
the role of Hippocampus is to mediate memory for spatial relations among objects in thew environment
36
Relational memory theory
hippocampus mediates memory for new associations in general not just spatial relations
37
Episodic memory theory
Hippocampus is critical for episodic memory but not for semantic memory
38
Memory consolidation
- After consolidation HP is no longer necessary to activate the solid memory - Place cells in HP and V1 were activated while rats were running a track, the same place cells were reactivated during slow wave sleep
39
Conciousness
State of being aware of and able to think about ones own existence, sensations, thoughts and surroundings
40
akinetopsia
Motion blindness
41
Global workspace theory
Hub from which imporant sensory infromation can be broadcasted via corticospinal fibers
42
Form blindness
You can still see colours and motion but you can not see any shapes.
43
Integrated information theory
take multiple theories and take the key points from it
44
Predictive processing
sensory input going in, Brain is trying to build a model of the world to predict: prediction on what’s going on in the present.
45
Concept cells
no sensory cells but they respond to the sensory input
46
Two ways to interpret neural responses in sensory cortex
- Brain responds to features in the world - Brain constructs explanation of what out there
47
Biological function of consciousness
- Reflex * habits - Goal directed behaviour: - Complex multifactorial decisions - Brain must take into account the whole situation & body
48
Visual attention
selective process
49
Inhibition of return
Cue delay from 0 - 200ms is facilitatory. After 200ms the cue delay causes a slower response
50
Central cue:
- Endogenous attention - Voluntary - Top down attention: slow
51
Peripheral cue
- Exogenous attention - Stimulus driven - Bottom up attention: Fast - Inhibition of return
52
Automatic vs serial processing
- Automatic o Search for specific features: colour, shape o Features are processing in separate brain areas - Selective attention o Searching for conjunctions ( combination of features) o Serial processing o All locations are examined
53
Behaviour effects of attention
1. focused attention speeds up reaction time. 2. attention increases contrast sensitivity. 3. attention increases spatial resolution
54
What are the effects of attention in visual cortex
1. increase signal to noice ratio 2. increase neuronal gain 3. increase contrast sensitivity.
55
Areas most consistently activated by attention to stimulus attributes include
Dorsal parietal cortex, Superior parietal lobule, Postcentral sulcus, Dorsal frontal cortex, Superior frontal sulci
56
Role of frontal eye field in visual attention
FEF microstimulation increases spiking rates in V4
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Pulvinar role during visual attention
coordinates multiple visual areas during attention by increasing synchrony at low frequencies
58
Thalamic nucleus role during visual attention
seem to amplify cortical connectivity between higher and lower areas, thus enabling efficient top down connectivity.
59
Balints syndrome lesion
Simultanagnosia, Optic taxia, Oculomotor apraxia
60
Simultanagnosia
inability to attend to and or perceive more than one visual object at a time
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Optic taxia
impaired ability to reach for or point to an object in space under visual guidance
62
Oculomotor apraxia
difficulty voluntarily directing the eye gaze towards objects in the visual field
63
Strengths of research with animal models in addiction
we can control the rats environment, manipulate and record different areas from the brain.
64
Weakness of research with animal models in addiction
less developed PFC, we cant talk to rats, hard to correlate to humans
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Punishment sensitive
Controlled alcohol use
66
Punishment resistant
Compulsive use
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Modeling drug relapse after abstinence
extinction, Home cage, negative consequence, alternative choice
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Relapse
Drug-induces, stress-induced, cue/context-induced
69
Identify active brain regions
Using fos, expressed after strong neuronal activation.
70
Compulsive alcohol use disorder
Lower activity in Nucleus Acumbens in punishment resistant alcohol use
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Nicotine relapse
Damage to insula cortex disrupts addiction to smoking
72
Electro convulsive therapy
resetting the circuit. Only used for o Severe or life-threatening depression and your life is at risk o Moderate to severe depression and other therapies haven’t helped you o Catatonia (staying frozen in one position/ making repetitive movements) o Severe or long-lasting episodes of mania
73
Lobotomy
Disconnection of the frontal cortex from the rest of the brain
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PFC ventro medial part
emotional and social control o Psychopaths have smaller connections between PFC and amygdala
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PFC dorsolateral
cognitive control
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Biological perspective of psychological disorder
o Medical/disease model o Disruption or imbalance of bodily processes o Brain disorder: genetic component involved, neurochemical , anatomical -> treatment with drugs
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Psychological perspective of psychological disorder
Behavioral perspective, cognitive perspective, psychoanalystical, cultural perspective
78
BioPsychoSocial approach of psychological disorder
mental disorders are seen as caused by the combination and interaction of biological, psychological and sociocultural factors
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Neuroses
- Anxiety - Unhappiness - Maladaptive behavior - Neurotic can function in society, though to a lesser degree - No hospitalization needed
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Psychosis
- Out of touch with reality - Cannot cope with demands of every day lives - Hospitalized
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Anxiety disorder
- Physiological symptoms: fight or flight response - Cognitive symptoms: believe something bad is going to happen - Behavioral symptoms: freezing, avoiding - Emotional symptoms: sense of dread and terror
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Panic disorders
- 30 to 40% genetic - hyper vigilent - Chronically aroused fight or flight response
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Depression
Noradrenaline/ serotonin : Reuptake blockers are used as medication. Genetic variation: chromosome 13
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Stress
Emotional arousing events are remembered well
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Stress alter behavioral strategies
- Stress reduces spatial strategy - Enhances stimulus responses strategy
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Corticosteroid receptors
o High affinity MR: cytosol membrane o Lower affinity GR: cytosol, membrane
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when stressed:
o HPA-axis release of corticosteroids o autonomic system: fast release of noradrenaline
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Do stress hormones regulate AMPA receptors?
Corticosteroid hormones regulate surface expression of AMPA receptor: Slowly more receptor to synapses: stronger synaptic connection
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Chronic stress causes
Less receptors in membrane
90
Less maternal care
Reduced hippocampal dendritic complexity, synaptic plasticity. - reduces spatial learning ability - Enhanced sensitivity of synapses for stress hormones
91
How to teach a rat to perform a task
- reverse day-night rhythm - food restriction/ deprivation ]- weight control every day
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Steps
1. habituation 2. shaping : teach them the task in small steps 3. ready for the complete task: Sessions until maximum performance
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TASC to study the effect of PFC
Neuron only fires if the task is done in a specific context
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How to research if there is information transferred from PFC to accumens during learning
- retrograde injection, disconnection lesions, cross correlation analysis
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Memorize proper goals : working memory
Dorsolateral PFC & SPL
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Select proper perceptual input and prioritize selection = attention
Frontal eye field & SPL
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Inhibition of irrelevant perceptual input & inhibit motor actions = inhibition
Pre SME & IFG
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Activate proper motor actions = motor action
BG, SMA, PREmotor, M1
99
Evaluate your actions, did they match the expectation = evaluative control
Anterior cingulate cortex
100
Adjust goals and the order for your actions
ACC to dIPFc
101
disinhibition syndrome
Damage to ventral medial PFC: o Constant movement o Euphoric or manic o Abnormal sense of humor o Fail to respond to normal social cues o Reveal embarrassing personal information
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dysexecutive syndrome
damage to lateral PFC: o Planning problems o Working memory problems o Leave tasks uncompleted if initiated at all o Limited attention Span o Lack of insight in own and other actions o Difficulties dealing with real world o Not able to problem solve anymore o Confabulate: create implausible explanations for problems
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Function Dorso lateral prefrontal cortex
the conscious choice in attention and thought
104
Function Orbito frontal Pfc
inhibition of behavior
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Function Ventro medial PFC
emotional and social control
106
Function anterior cingulate cortex
behavioral evaluation
107
Concious choice
Freedom of choice but bound to rules.
108
stimulus response learning
learn an appropriate action of each and every stimulus
109
Abstract learning
learn rules that connect stimuli to actions
110
reward based responses: lateral PFC
switching rules. o Keeping rules in memory or active o Neurons respond to matching rule o Independent of cues used
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What happens if you disconnect IT and PFC
Difficulty making the right choice based on information
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Inhibiting processes: lateral PFC
- Halting behaviors that are well trained - Preventing irrelevant information from interfering - Restraining actions that are inappropriate in social contexts - Removing irrelevant information from working memory
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Go - no go task in schrizophrenics
schizophrenics perform normal on GO trials, but severely impaired on No-go trials.
114
Rule shifting
Wisconsin card sorting task: shift of rules is impaired after frontal damage
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Contextual control : Anterior cingulate cortex
- Monitoring o Efficiency of own actions -> processing of feedback o Outcome of own actions o Outcome of actions of others o Outcome in general
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Working memory
- Attended information is stored in WM - Rehearsed information in WM is passed on and encoded as long term memory - Long term memory information can be retrieved and manipulated as working memory later.
117
Firing rate models
We can describe the activity of a neural network by looking at average properties such as the network average firing rate
118
Areas of Working memory
Are scattered across the cortex
119
DBS surigcal procedures
- Patient is often awake - MRI navigation - Electrophysiological navigation - Stimulation navigation - Only 25% of eligible patients choose DBSA increase in asleep DBS surgeries - Effects of sedation on neural activity in basal ganglia
120
Local effect of DBS
inhibition of the soma and excitation of dendrites and synapses
121
Function effect of DBS
information jam and mimics ablation
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DBS parameters
High frequency: tremor suppression Low frequency: speech improvement.
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DBS for psychiatric disorders
Depression, OCD: 40-60% success tourette's
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Targeting Thalamus with DBS
Restoring arousal and conciousness access: for locked in syndrom and COMA
125
Egocentric navigation
Follows stimulus response learning Strengthen the connection between stimulus and response, chain association together to make a path
126
Allocentric navigation
 Requires an internal cognitive map of the environment.  How to find short cuts, detours
127
path integration
Path integration starts with egocentric navigation and chance into allocentric navigation. Updating knowledge of its position in space
128
Cognitive map hypothesis of hippocampal function
a representation of relationships between entities that is used to perform a cognitive task
129
Place cells
can code a spatial localization, New environment -> global remapping
130
Grid cells
in m ediual entorhinal cortex. - A grid cell on its own does not indicate where the animal is: all cells together do - A grid cell help determine distance between locations
131
Head direction cells
subicular head direction cell: output region of the hippocampus
132
Border cells
fires always at the same border
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Hippocampal ensemble recordings: memory traces & replay
Replay: spontaneous reoccurrence of firing patterns previously evoked during an awake behavioral experience. - Sleep replay is forward but awake replay can be forward or backward