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NESC 3670: Genes, Brain & Behaviour > Cognition part 2 (lec 11/12) > Flashcards

Cognition part 2 (lec 11/12) Flashcards

1
Q

what are the 3 main classes of NT?

A

amino acids

amines

peptides

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2
Q

name the 3 amino acid NT

A

GABA

glutamate

glycine

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3
Q

list 6 amine NT

A

ACh

DA

epinephrine

histamine

NE

5-HT

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4
Q

list some (9) of the peptide NT

A 
CCK 
dynorphin 
Enk 
NAAG
neuropeptide Y
somatostatin 
substance P 
thyrotropin-releasing hormone 
VIP
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5
Q

the CA1 region has how many kinds of glutamate receptors? name them

A

2

NMDA

AMPA

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6
Q

describe the state or AMPA and NMDA receptors in normal synaptic transmission

A

AMPA: when activated it depolarizes cell, glutamate and Na bind

NMDA: inactive because block by Mg (glutamates tries to enter)

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7
Q

what occurs at the NMDA/AMPA rec in order to induce LTP?

A

with repeated activation of AMPA rec, the change in postsynaptic membrane potential drives Mg out of NMDA channel

  • inc in Ca (pos charge) =depolarization
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8
Q

describe how Na and Ca enter into cell

A

Na= through AMPA rec

Ca= through NMDA rec

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9
Q

what is the 1st mechanism of inc Ca?

A
  • Ca dependent signalling is important for activation of CaMKII = chaparoning of more glutamate rec to membrane surface
  • 3 kinds of receptors
  • goal: guide these AMPA rec that havent been embedded yet, and embed them to membrane, changing sensitivity of membrane to further glutamate exposure
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10
Q

what is 2nd mechanism of inc Ca

A
  • inc Ca= activate Ca-dependent pathways= inc in CREB
  • CREB is like transcription factor, can bind to promoter regions and inc amount of glutamate receptors
  • CREB important for activating more promoters to express more of the AMPA rec

*** gene expression is crucial for stability of LTP

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11
Q

what is the response/mechanism of inc Ca?

A
  • inc Ca through NMDA rec through retrograde signalling
  • NO and arachidonic acid and other retrograde messengers that can be sent through extracellular matrix to the cell that is stimulating the presynaptic cell, to stimulate more NT release
  • can be facilitated by NO and arachidonic acid
  • CREB is important mediator
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12
Q

stimulate more glutamate release results in…?

A

more representation of a receptor (like feedback loop)

more rec= have same effect whether have little or a lot of glutamate released

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13
Q

what occurs of 1+ AMPA rec have been repeatedly stimulated?

A

enough Na ions enter to largely depolarize the dendrites membrane

  • this displaces the Mg ions, enables glutamate to open the NMDA rec
  • Na and Ca enter

feedback= further release of glutamate, due to Mg that facilitates it

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14
Q

the large Ca influx activates certain ____ _____, which are ..?

A

protein kinases

enzymes that add P groups to protein molecules

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15
Q

what is an example of a protein kinase that is activated by Ca influx?

A

CaMKII (calcium-calmodulin kinase II)

  • important because involved in regions of brain that are involved with learning/memory
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16
Q

name 3 ways in which CaMKII affects AMPA rec

A

1) cause more AMPA rec to be produced and inserted in postsynaptic membrane
2) moves existing nearby AMPA rec into active synapse
3) inc conductance of Na and K ions in membrane-bound AMPA receptors

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17
Q

describe what happens to dendritic branches in response to LTP

A

more AMPA rec are built and dendritic branching is increased

in response to LTP get inc in structure of dendrite= more platforms for insertion of more AMPA

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18
Q

strong stimulation of a postsynaptic cell releases a ____ ____

A

retrograde messenger

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19
Q

what is a retrograde messenger?

A

often a diffusible gas like carbon monoxide or nitric oxide that travels across the synapse

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20
Q

a retrograde messenger alters the function of pre/postsynaptic neuron????

A

PRESYNAPTIC

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21
Q

how does retrograde messengers alter function of presynaptic neuron?

A

1) dec in AP threshold= inc release of NT

2) expansion of axons= transmitter release from additional sites

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22
Q

how do the changes of the retrograde messengers affect glutamate?

A
  • inc the synaptic sensitivity to glutamate and the synapse is strengthened (bc inc in rec)
  • inc later responsiveness of the dendrite to incoming glutamate
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23
Q

what is an enhanced synapse?

A

after induction of LTP

  • changes from LTP make synapse more responsive
  • synapse now ready to give more rapid and stronger response, because more transmitter is released and there are more AMPA receptors in the postsynaptic membrane
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24
Q

what are the 5 main steps in the neurochemical cascade during induction of LTP?

A

1) activated protein kinases trigger protein synthesis
2) kinases activated CREB (cAMP responsive element-binding protein)
3) CREB binds to cAMP responsive elements in DNA promoter regions
4) CREB changes the transcription RATE of genes
5) regulated genes then produce proteins that affect synaptic function and contribute to LTP (e.g. AMPA and NMDA rec)
- CREB recruits and binds to histone acetylase transferase and targets it for further gene activation

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25
Q

gene expression is crucial for ….

A

LTP stability

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26
Q

what is role of actinomycin D in LTP?

A
  • inhibits transcription by binding DNA at the transcription initiation complex
  • prevent elongation of RNA chain by RNA polymerase
  • inhibited the maintenance of LTP in rat hippocampal neurons ex vivo and in vivo

–> study concluded that gene transcription was required for maintenance of LTP

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27
Q

3 experiments that show evidence that LTP may be a part of learning and memory formation

A

correlational observations

somatic intervention experiments

behavioural intervention experiments

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28
Q

what are correlational observations for LTP?

A

time course of LTP is similar to that of memory formation

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29
Q

what are somatic intervention experiments?

A

pharmacological treatments that block LTP impair learning

  • if lack function of NMDA rec= learn slowly
  • extra expression of NMDA rec= faster learning

—> NMDA rec must be important in learning

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30
Q

behavioural intervention experiments

A

training an animal in a memory task can induce LTP

  • e.g. water maze
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31
Q

explain the model for role of histone acetylation in long term memory formation

A
  • glutamate acting at AMPA and NMDA rec
  • results in Ca-dependent activation
  • series of phosphorylations (PKC) which result in huge cascade
  • MEK-ERK pathway is general signalling cascade results in activation of CREB and CRB binding= histone acetylation and transcription iniation
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32
Q

name 3 drugs that are HDAC inhibitors

A

sodium butyrate

valporate

TSA

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33
Q

what is the suggestion of role of histone acetylation in long term memory formation???

A

if we can regulate amount of histone acetylation MAYBE we can regulate LTP and MAYBE improve the memory formation in animals

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34
Q

HDAC inhibitors (enhnace/inhibit) LTP????

A

ENHANCE

  • they do not create LTP
  • promote acetylation, enhance induction of LTP
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35
Q

describe the contextual fear conditioning behavioural paradigm

A
  • animal placed in training chamber (novel context)
  • exposed to foot shocks, then removed from box
  • flash a light
  • frequency of freezing behaviour measured during 1-24hr after trial
  • condition these animals to freezing behaviour if in box and shock them and flash a light while giving shock
  • if place in box and shine light (no shock), look at frequency of freezing behaviour
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36
Q

contextual fear memories are stored where??? for how long???

A
  • amygdala
  • area CA1 of hippocampus
  • at least 24 hr after contextual fear conditioning
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37
Q

explain how HDAC inhibitor activity enhances formation of long term memory in vivo

A
  • animals injected with HDACI or vehicle 1hr prior to one-shock contextual fear conditioning
  • HDACI did not effect animals ability to perceive and respond to foot shock
  • HDACI increased histone H3-acetylation, enhanced the formation of long-term contextual fear memory
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38
Q

what is the effect of a DNMT inhibitor on long term memory?

A

inhibitor of DNMT activity in hippocampus blocks formation of LTM in vivo

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39
Q

explain the experiment of using DNMT inhibitor to block LTM formation

A
  • inject with DNMT inhibitor (Zebularine/RG108) or vehicle 1h prior to one-shock contextual fear conditioning
  • DNMT inhibitor did not effect animals ability to perceive and respond to foot shock
  • DNMT inhibitor specifically blocked formation of long-term contextual fear memory
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40
Q

what occurred if animals injected with HDACI and then inject with DNMT inhibitor

why??

A

DO NOT show memory impairment

bc methylation pattern is already laid down, changes have occurred

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41
Q

enhance or block LT contextual fear memory??

  • HDAC inhibitor
  • DNMT inhibitor
A

HDAC= enhance formation

DNMT= block formation

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42
Q

is DNA methylation involved in LT memory formation??

A

observations suggest that DNMT activity is not only necessary for memory and plasticity but

DNA methylation works in concert with histone modifications to regulate plasticity and memory formation in the hippocampus

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43
Q

with age, we tend to show some memory impairment int asks of conscious recollection that … (2)

A

1) require effort

2) rely primarily on internal generation of the memory rather than on external cues

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44
Q

as we age, experience decreases in ____ memory and ______ skills

A

spatial memory

navigational skills

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45
Q

name 2 causes of memory problems in old age

A

1) impairments of coding and retrieval (less cortical activation in some tasks)
2) loss of neurons and/or neural connections (some parts of the brain lose a larger proportion of volume)

46
Q

deterioration of which pathways provide input to hippocampus and cortex?

A

cholinergic pathways

47
Q

which medical condition is associated with lost cholinergic pathways

A

Alzheimer’s disease

48
Q

name 3 ways to improve cognitive function

A

nootropics

lifestyle factors

epigeneotype

49
Q

what are nootropics?

A
  • class of drugs, enhance cognitive function
50
Q

name 3 types of nootropics

A

1) cholinesterase inhibitors (enhance memory and cognition)
2) AMPAkines- bind AMPA rec, enhance hippocampal LTP
3) protein kinase (PKM-zeta)- needed for LT maintenance of hippocampal LTP and cortical memory traces

51
Q

list 3 ways in which lifestyle factors can help reduce cognitive decline

A
  • living in favourable environment (reduce stress)
  • involvement in complex and intellectually stimulating activities (education)
  • having partner of high cognitive status (think-pair-share)
52
Q

how does epigeneotype improve cognitive function

A

epigeneotype is shaped by lifestyle (diet, exercise, infection, environment)

  • epigenetic mechanisms (inc ncRNA) involved in memory formation
  • aging associated with disruption of memory-triggered epigenetic changes
53
Q

what is Yerkes-Dodson law?

A

certain stimulants will enhance cognition in the general population, but only when used at low (therapeutic) concentrations

  • relatively high doses of stimulants will result in cognitive deficits
  • with inc amount of arousal there is relationship with inc performance (only to a point), when systems become stressed there is a DEC in performance
54
Q

Yerkes-Dodson law:

  • simple task outcome vs difficult task
A

simple: inc arousal= inc performance

difficult: performance inc when arousal is weak and increasing
- hits point where performance dec as high arousal

55
Q

what are the 3 temporal stages of memory??

A

short
intermediate
long

56
Q

what is learning?

A

process of acquiring new information

57
Q

what is memory?

A

ability to store and retrieve information

specific information stored in the brain

58
Q

what did Donald Hebb discover? (LTM/STM)

A

LTM

59
Q

what did Baddeley/Hitch discover??? (LTM/STM)

A

STM

60
Q

what is iconic memory (IM)

A
  • briefest memories

- store sensory impressions that only last a few seconds

61
Q

what is short-term memory also called?

A

working memory

62
Q

what is STM?

A
  • only lasts up to 30 seconds, or throughout activity

- retained with rehearsal

63
Q

what are the 3 components of STM?

A

1) phonological loop– auditory info
2) visuospatial sketch pad – visual impressions
3) episodic buffer–integrated, sensory info

64
Q

what is ITM

A

intermediate-term memory

  • outlasts STM
  • not permanent (fade without rehearsal)
  • limited capacity
65
Q

what is LTM?

A

long-term memory

  • lasts for days to years
  • large capacity
  • stimulated with cue/hint
66
Q

how did we determine that memories of different durations form by different neurochemical mechanisms

A

use drugs and different agents

  • appear to affect different stages of memory formation
67
Q

what were the results and timing effects of different amnestic (memory impairing) agents

A
  • agents that caused memory failure by 5 mins after training= blocked STM
  • agents that caused memory failure by about 15mins after training= blocked ITM
  • agents that caused memory failure by about 60 minutes after training= blocked LTM
68
Q

experiments to test the hypothesis that the formation of LTM requires protein synthesis have employed both ___ & ____

A

behavioural intervention (form of training)

somatic intervention (form of agents that inhibit protein synthesis)

69
Q

what is behavioural intervention

A

training enriched experience

  • inc the branching of dendrites and number of synaptic contacts
70
Q

what is somatic intervention

A

antibiotic anisomycin is very effective at inhibiting protein synthesis (no toxic side effects)

  • prevents LTM storage in mice, without affecting STM
  • stronger the training was, longer the inhibition has to be maintained to cause amnesia
71
Q

when does protein synthesis that is involved in formation of LTM appear???

A
  • occur in 2 successive waves
  • first 1hr after training
  • second 5-8 hrs after training
72
Q

what was effect of protein synthesis inhibitors?

A

prevent formation of LTM by preventing the structural changes in the neurons that would normally encode the memory trace

73
Q

what is primacy effect?

A

higher performance for items at the beginning of a list

74
Q

what is recency effect?

A

shows better performance for the itms at the end of a list

75
Q

a functional memory system incorporates what 3 aspects?

A

1) encoding (sensory info passed into STM)
2) consolidation (STM info transferred to LT storage)
3) retrieval/recall (stored info is used)

76
Q

what are the 3 main divisions of the brain?

A

forebrain

midbrain

hindbrain

77
Q

what is the 2 subdivisions of the forebrain

A

diencephalon (Thalamus, hypothalamus)

telencephalon (cortex, limbic system, basal ganglia)

78
Q

what is the subdivision of the midbrain?

A

mesencephalon

79
Q

what are the 2 subdivisions of the hindbrain??

A

myelencephalon (medulla)

metencephalon (cerebellum, pons)

80
Q

brain regions responsible for recalling pictures

A

RIGHT prefrontal cortex

para-hippocampal cortex (both hemi)

81
Q

brain regions responsible for recalling pictures

A

LEFT prefrontal cortex

LEFT para-hippocampal cortex

82
Q

LH/RH for language?

A

LH

83
Q

LH/RH for spatial ability?

A

RH

84
Q

what is an engram?

A

memory trace

physical changes (several different synapses within a neural circuit) in the brain that underlie a LTM

85
Q

consolidation involves which part of the brain?

A

hippocampus

86
Q

LTM storage occurs where???

A

cortex

near where the memory was first processed and held in STM

87
Q

what is retrieval?

A

process of reconstruction/reactivation of various elements of past experiences from all parts of the brain

88
Q

explain PTSD and reinforcing memories

A

characterized as reliving and being preoccupied by traumatic events

  • memories produce stress hormones that further reinforce the memory
89
Q

which 3 types of transmission can enhance memory formation in animal models?

A

GABA
ACh
opioid

90
Q

explain how treatments/drugs can reduce stress responses in PTSD

A

can block chemicals acting on the basolateral amygdala

  • may alter effect of emotion on memories
91
Q

what is reconsolidation of memories?

A

return of a memory trace to stable long-term storage after its temporarily volatile during recall
- can distort memories

92
Q

what is hypnosis or ‘guided imagery’

A

patient encouraged to imagine hypothetical abuse scenarios can inadvertently plant false details during reconsolidation

  • planting false memories clouds issue of ‘recovered memories’
93
Q

explain what happened to Phineas Gage

A
  • railroad foreman, blasting rock
  • pointed end of rod shoots through left cheek bone, through top of head
  • full possession of reason, free from pain
94
Q

what was the end result of the accident for Phineas Gage

A
  • personality, reasoning, capacity to understand and follow social normals had been diminished/destroyed \
  • unable to consider what happens beyond his actions
95
Q

name the 2 major functions of the prefrontal cortex

A

emotion

cognition

96
Q

frontal lobe is responsible for … (3)

A
  • regulating temperament
  • personality
  • expressing personality
97
Q

what does primary motor cortex do?

A

controls voluntary body movements

98
Q

how is prefrontal cortex (PFC) divided?

A

lateral (divided into dorsal and ventral)

medial
ventral
dorsal

99
Q

prefrontal cortex accounts for __% of total cortex in humans

A

29%

100
Q

prefrontal cortex role

A
  • forming goals/objectives
  • devising plan of action required to attain those goals
  • selects cognitive skills to implement plans, coordinate skills, applies in correct order
  • evaluate actions as success or failure relative to our intentions
101
Q

Gage’s injury inspired what??

A

development of frontal lobotomy

102
Q

goal and results of frontal lobotomy

A
  • to diminish aggression and rage in patients

- drastic personality changes, inability to relate socially

103
Q

describe delayed response: working memory task

A
  • monkey sees well baited with food
  • delay- animal retrieves food
  • location food random
  • WM is required because at time animal responds, there is no external cues indicating location of food
104
Q

monkeys with what lesion have problem with WM task?

A

dorsal lateral PFC lesion in chimps

105
Q

describe delated non-matching-to-sample task

A
  • reward placed under item, monkey finds reward
  • delay and novel object
  • success: pick up novel object and find new location where reward is
  • monkeys attracted to novelties
106
Q

describe oculomotor spatial delayed response task

A
  • look at general activity
  • monkey fixate central fixation point in center
  • cue light was flashed on one of 1 locations
  • delay, monkey can respond by moving eyes to remembered cue location
107
Q

task shifting aka…

A

deficit perseveration

  • training individuals to do procedure then change the procedure
108
Q

good/bad at task shifting with PFC damage?

A

issue with re-ordering

  • unable to successfully do this task
109
Q

PFC damage and Wisconsin Card sorting task

A
  • damage to lateral PFC= difficulty with task
110
Q

name 3 functions related to cognition in PFC

A
  • working memory
  • task shifting
  • organization of goal directed behaviour
111
Q

good/bad with recency memory- temporal order of events with patients with PFC damage

A

impaired

  • asked to learn cards and remember which one they saw first
112
Q

lesions ____ ____ PFC in humans produce a selective impairment on the recency task, but not the item recognition task

A

dorsal lateral

NESC 3670: Genes, Brain & Behaviour (12 decks)

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