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psyc 462 > lecture 8 LOs > Flashcards

lecture 8 LOs Flashcards

1
Q

what can high levels of glutamate do

A

lesion any brain nucleus

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2
Q

what is excitotoxicity

A

prolonged depolarization of neurons leading to eventual damage or death

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3
Q

what is necrosis

A

fast death characterized by lysis due to osmotic swelling

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4
Q

what is apoptosis or programmed necrosis

A

a slower death triggered by a series of biochemical events. lysis does not occur

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5
Q

how can apoptosis/programmed necrosis happen

A

by lower concentration and longer exposure time to glutamate, cell death takes several hours and depends on NMDA receptor activation

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6
Q

how can brain damage occur

A

brain ischemia (interruption of blood flow from stroke/heart attack etc)

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7
Q

when a brain ischemia occurs, how does it happen

A

massive glutamate release occurs in the affected area
abnormally high Ca2+ levels inside the neuron overloads the Ca2+ buffers so they cant compensate
extremely high Ca2+ levels activate certain enzymes that kill cells

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8
Q

what is GABA the primary transmitter for in the brain

A

inhibition

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9
Q

which neurons use GABA

A

all medium spiny neurons in the striatum and other nuclei in the basal ganglia
projection neurons intermixed with monoamine cell groups (DA and serotonin)
interneurons in the cerebral cortex, hippocampus, amygdala, and most other brain regions

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10
Q

what does GABA transmission do for brain function

A

filter for info coming into neurons
regulates different patterns of firing in cortex
reduced GABA activity promotes seizures
many brain circuits are set up as a series of inhibitory GABAergic connections

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11
Q

how is GABA synthesized

A

from glutamate by glutamate decarboxylase (GAD)

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12
Q

where is GABA synthesized

A

in GABA neurons

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13
Q

where does the vesicular GABA transporter (VGAT) move GABA to

A

vesicles

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14
Q

how is GABA removed from the synpatic celft

A

reuptake transporters GAT1 to GAT3

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15
Q

where can GAT1 be located

A

on presynaptic terminals

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16
Q

how is GABA metabolized

A

it is metabolized to glutamate and succinate by GABA aminotransferase (GABA-T)

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17
Q

in astrocytes how is glutamate converted to glutamine

A

by glutamine synthesis

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18
Q

glutamine can be released by ___, taken up by ___, converted back to ___, and used to remake ___

A

astrocytes
neurons
glutamate
GABA

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19
Q

GABA-A GABA receptor subtype

A

ionotropic
allows Cl- to move from outside to inside the cell, aka hyperpolarization

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20
Q

each GABA receptor consist of ___ subunits

A

five
various combinations of the four types (alpha, beta, gamma, delta)

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21
Q

GABA binding site agonist and competitive antaonist

A

agonist: muscimol
competitve antagonist: bicuculline

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22
Q

inside GABA channel pore non competitive antagonist

A

picrotoxin

23
Q

what do benzodiazepine (BDZ) and barbiturates do

A

bind to receptor sites distinct from GABA binding site
increase the potency of GABA to open receptor channel, does not open channel if GABA is not also bound
positive allosteric modulator

24
Q

example of benzodiazepine (BDZ)

A

diazepam (vallium)

25
Q

barbiturate example

A

phenobarbitol

26
Q

what does benzodiazepine only bind to

A

the gamma subunit (which most receptors have)

27
Q

neurosteroid binding site

A

some neurosteriods act like BDZ but bind to different part of the receptor

28
Q

what do inverse agonist or negative allosteric moculators do at the BDZ site

A

no affect itself, but attenuates the ability of GABA to open channel, promoting anxiety, arousal, seizures

29
Q

GABA-B receptors

A

metabotropic (G-proteins and second messenger)
require two different subuits to assemble in the membrane and work properly

30
Q

what does activation of GABA-B receptor do

A

inhibitory effect on post synaptic cells by K+ channel opening and inhibiting CAMP formation

31
Q

where else can GABA-B reside and serve as

A

can reside presynaptically and serve as autoreceptors or heteroreceptors

32
Q

GABA-B agonist

A

baclofen, used as muscle relaxant, and experimental treatments for alcoholism

33
Q

GABA-B antagonist

A

saclofen, convulsant primarily used for research

34
Q

NTs that are catecholamines

A

dopamine, norepinephrine, and epinephrine

35
Q

where are NE and EPI released from

A

adrenal medulla

36
Q

what are the behavioural functions from DA and NE

A

motor (primarily DA)
learning and memory
attention
motivation and emotion
reward

37
Q

what diseases are linked to catecholamine transmission

A

parkinsons, schizophrenia, depression, ADHD, drug addiction

38
Q

what does catecholamine synthesis begin with

A

the amino acid tyrosine

39
Q

where are tyrosine hydroxylase (TH) and dopamine decarboxylase found

A

in neurons that make DA
used as markers for DA neurons

40
Q

what do NE-synthesizing neurons have

A

dopamine beta-hydroxylase (DBH)

41
Q

what is activity of TH and catecholamine production regulated by

A

high catecholamine levels inhibit TH activity (neg feedback)
rate of cell firing (increased firing during stress stimulates TH to accelerate catecholamine synthesis)

42
Q

what does L-Dopa do

A

terminals take up precursor and quickly transform it to DA/NE
increases transmitter levels

43
Q

what does AMPT do

A

blocks TH, preventing synthesis
induces sedation, depression, reduced blood pressure (systemic effect)
effects can be reversed w L-Dopa

44
Q

what happens to DA/NE after synthesis

A

packaged into vesicles via vesicular monoamine transporter (VMAT)

45
Q

what does reserpine do

A

blocks VMAT, prevents DA/NE from being packaged (irreversible)

46
Q

if DA/NE are not protected in vesicles, what happens and what is the effect of that

A

they are broken down by enzymes in terminal and levels drop
results in sedation and depression and systemic effects (reduced blood pressure and heart rate)

47
Q

what have reversible VMAT inhibitors been developed for

A

reducing uncontrolled movements associated w huntingtons disease

48
Q

what are catecholamines metabolized by

A

monoamine oxidase (MAO) and/or catechol-O-methyltransferase (COMT)

49
Q

what is the primary mechanism of clearing catecholamines

A

reuptake

50
Q

what is the main DA metabollite

A

HVA (homovanillic acid)

51
Q

what are NE metabolites in the brain

A

MHPG
enter CSF and bloodstream, eliminated via urine

52
Q

what can levels of HVA compounds in CSF provide

A

rough indication of catecholamine activity

53
Q

MAO inhibitor

A

phenelzine, used to treat clinical depression

54
Q

COMT inibitors

A

tolcapone, enhances the effecitveness of L-DOPA in treating parkinsons

psyc 462 (21 decks)

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