lecture 21 LOs Flashcards

1
Q

what receptors in the PFC mediate working memory

A

PFC D1 but not D2

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2
Q

how can manipulating PFC DA D1 activity change baseline levels of performance

A

poor performance: extra D1 stimulation will improve functioning
good performance: D1 receptors antagonist impairs functioning

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3
Q

which receptors mediate congnitive flexibility

A

D1 and D2 receptors

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4
Q

what does supranormal stimulation of D1 or D2 do to cognitive flexibility

A

does not affect it

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5
Q

what does D4 receptor stimulation impair

A

set shifting
S shaped function

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6
Q

what does the Val/Val polymorphism of COMT do in the brain

A

produces an enzyme that is more effective at metabolizing DA
leads to lower PFC DA levels vs the Met/Met version

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7
Q

what else is the Val/Val COMT gene associated with

A

poorer cognitive performance
may exacerbate cog dysfunction in schizophrenia

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8
Q

what is the glutamate hypothesis of schizophrenia

A

non competitive NMDA antagonists can induce psychotic symptoms and cognitive deficits resembling schizophrenia in healthy individuals

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9
Q

what does the degeneration of glutaminergic PFC/hippocampal neurons do in the brain

A

disrupts the functioning of these cells and leads to less glutamate transmission

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10
Q

what is the broad glutamate hypothesis

A

schizophrenia is caused by decreased glutamate transmission

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11
Q

what do studies using primate/rat models show regarding acute or repeated PCP

A

decreased DA levels in the PFC
cog deficits on PFC dependent tasks

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12
Q

how does the use of PCP cause symptoms

A

imbalance of DA transmission in PFC (too little) and striatum (too much)

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13
Q

what does the PCP model in animals show that is similar to schizophrenia

A

the model encompasses some of the positive and negative symptoms of schizophrenia

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14
Q

what can perturbed glutamate contribute to

A

increases in mesolimbic DA and reduced PFC DA transmission

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15
Q

what do descending PFC projections affect

A

both DA pathways

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16
Q

where do excitatory PFC projections synapse

A

directly onto mesocortical DA neurons (PFC excites these cells)

17
Q

where else do PFC input to

A

VTA GABA neurons that in turn synapse onto mesolimbic DA neurons (PFC activity can inhibit these cells)

18
Q

what can reduced PFC glutamate do to DA release

A

reduce DA release in PFC further causing more negative cog symptoms
also provide less excitation on VTA GABA neurons which could lead to excess NAc DA release causing more positive symptoms

19
Q

what can NMDA antagonists that induce psychosis/cog deficits do to activity of GABAergic interneurons

A

can reduce the activity of the GABAergic interneurons (and produce a ‘noisy’ cortex)

20
Q

where do NMDA receptors reside

A

on pyramidal cells and GABA interneurons

21
Q

what can lower doses of PCP/ketamine do to NMDA receptos

A

block them
they have a greater effect on interneurons to reduce their activity
this can cause disinhibitory increases in pyramidal neuron firing

22
Q

what is the net effect of PCP/ketamine on cells

A

disruption of the excitatory/inhibitory balance, with reduced signal combined with aberrant hyperactivity (aka noise)

23
Q

animal model of schizophrenia pharmacologically

A

high doses of amphetamine
produces stereotyped behaviours like sniffing/licking/gnawing like the compulsive repetitions of behaviour seen in schizophrenia
often used to identify potential antipsychotic drugs but does not reproduce the negative/cog symptoms very well

24
Q

neurodevelopment method to induce schizophrenia like symptoms

A

early insults (poor diet, viral infections, stressors, hypoxia) to pregnant rodents or young offspring induce neural/behavioural abnormalities later in life

25
Q

lesion method to induce schizophrenia like behaviours

A

neonatal ventral hippocampal lesion
well characterized model where a single, early life defect produces physiological/behavioural abnormalities in adulthood
show beh changes in adolescence that reflect symptoms of schizophrenia
neg/cog deficits show in early adulthood and can be potentiated by stress