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PSYC 462 > CH 8 > Flashcards

CH 8 Flashcards

1
Q

Because glutamate is found throughout the brain, it is more difficult to assign specific ______ roles to these NTs. Glutamate is the ____ of everything that the brain does. All ______ cells in the cerebral cortex use glutamate, as well as projection neurons of the _____, ____ and _____. Glutamate projection neurons are _____ in other subcortical nuclei

A

functional, workhorse, pyramidal, thalamus, amygdala, hippocampus, embedded

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2
Q

To varying degrees, most other “classical” neurotransmitters ______ effects of glutamate on neural activity.

A

modulate

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3
Q

the non-ionized form of glutamate

A

glutamic acid

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4
Q

glutamate serves as a ____ and also a component of many _____ and has other metabolic roles

A

NT, proteins

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5
Q

the enzyme that converts glutamine to glutamate

A

glutaminase

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6
Q

A _____ substance containing ____ ____ was found to make cells fire, which led to the discovery of the use of glutamate as a NT by neurons

A

salty, glutamic acid

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7
Q

vesicular transporters that move glutamate into synaptic vesicles; only found in glutamatergic neurons

A

VGLUT1, VGLUT2, VGLUT3

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8
Q

____ neurons don’t use glutamate bu get many glutamate inputs from the cortex

A

striatal

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9
Q

Some cells will release a _____ NT such as DA or 5-HT and also glutamate togther. Neurons with different types of NT release will make different ____ _____ to release them (__). Sometimes, an axon may have different terminals that looks like either a _____ synapse or a ___ glutamate synapse. Moreover, ____ is sometimes expressed with markers of other transmitters

A

primary, axon terminals, collaterals, monoamine, wired, VGLUT

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10
Q

_____ of glutamate is usually fatal

A

knockout

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11
Q

Rapidly removes glutamate from the synapse and is on astrocyte glia (90% of glutamate reuptake)

A

EAAT1-2

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12
Q

removes glutamate from the synapse

A

EAAT1 - EAAT5

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13
Q

removes glutamate from the synapse; is on postsynaptic membrane

A

EAAT3

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14
Q

Because too much ____ can mess up the activity of neurons and is ____ to humans, there are many safety procedures to remove glutamate.

A

excitation, toxic

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15
Q

Majority of glutamate uptake is done by _____ that then convert glutamate to _____ by _____ _____. Storage of excess glutamate as ____ may protect the brain from excessive _______. This is then transported out of astrocytes and back to _____ to be turned back into glutamate

A

astrocytes, glutamine, glutamine synthetase, glutamine, excitation, neurons

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16
Q

The 3 glutamate receptors are _____, ____ and _____, and are all ______. They consist of ____ subunit proteins and an ion channel. They have different ____ of subunits, explaining the differences in their pharmacology

A

AMPA, kainate, NMDA, 3, combination

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17
Q

activation of _____/____ receptors allows entry of _____, depolarizing the neuron. These receptors are _____ activated when there is sufficient stimulation by glutamate. The _____ to glutamate is tightly regulated, as too much stimulation causes receptor _______. They may not _____ to glu as well, or ____ as wide, or pull receptors out of the membrane

A

AMPA, Kainate, Na+, always, sensitivity, desensitization, bind, open

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18
Q

A nonselective antagonist for AMPA, Kainate and NMDA receptors

A

kyunurenic acid

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19
Q

a competitive antagonist that blocks both AMPA and kainate receptors but not NMDA

A

NBQX

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20
Q

treatment with high doses of AMPA/kainate antagonists like NBQX exhibit ______, reduced _____ activity, _____ and protection against _______.

A

sedation, locomotor, ataxia, seizures

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21
Q

NMDA receptors allow flow of both ___ and ____ into the neuron and tends to cause a greater _____ that AMPA / Kainate receptors. To open the channel, both glutamate and ____ or _______ (co-agonists) must bind at the same time. The co-agonist binding site is ____ under most conditions because there is a lot of glycine in the CSF. In addition, when the neuron is at ___ ___, ____ ions are bound to a site in the channel, which blocks it. Repeated ____ receptor activation can depolarize the neuron enough to remove this block and allow NMDA receptor activation. This occurs with ____ firing

A

Na+, Ca2+, depolarization, glycine D-serine, occupied, resting potential, Mg2+, AMPA, burst

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22
Q

A competitive agonist for NMDA receptors that block glutamate from binding

A

AP-5 / APV

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23
Q

Drugs that block the NMDA channel when its open; independently of glutamate binding

A

Phencyclidine (PCP), ketamine, MK-801

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24
Q

Noncompetitive antagonists of the NMDA receptor can cause ____-like symptoms at lower doses such as _____ and _______. At higher doses, they can cause ____ and then anesthesia

A

SZ, hallucinations, delusions, ataxia

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25
Q

Certain noncompetitive antagonists target the _______ site. ____ agonists may act like a positive _____ _____

A

glycine-binding, glycine allosteric modulator

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26
Q

Activation of AMPA/Kainate vs NMDA receptors can have different ____ effects on postsynaptic neurons. NMDA receptors can induce _____/_____ lasting depolarization vs AMPA/Kainate. This can be tested by stimulating _____ glutamate inputs and using ____ to isolate the respective effects of each receptor. NMDA receptor activity can also alter _____ _____(e.g. promote burst firing)

A

excitatory, larger/longer, presynaptic, antagonists, firing patterns

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27
Q

Glutamate has ____ metabotropic receptors named ______. ______ and ______ are mostly postsynaptic, while other are mostly _______, which act as ____ or heteroreceptors. These receptors ____ glutamate or other transmitter release.

A

8, mGluR 1-8, mGluR1, mGluR5, presynaptic, autoreceptors, suppress

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28
Q

an agonist for mGluR 4,6,7, and 8 autoreceptors, which suppress glutamate release

A

L-AP4

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29
Q

mGluRs are ____ distributed and participate in many functions such as ____, motor _____, ___ and mood and ____ perception. Many mGluR drugs are being developed for treatment of many _____ disorders

A

widely, locomotion, coordination, cognition, pain, neuropsychiatric

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30
Q

The most studied function of glutamate receptors are their involvement in ____ ___ and ____/_____, which is measured by the activation of the _____ cell in response to stimulation. Alterations in the activity of ___ are thought to underlie learning as measured by changes in _____ strength. An increased strength means a larger ______ evoked in the postsynaptic neuron. The primary way this is measured is with _______ methods

A

synaptic plasticity, memory/learning, postsynaptic, synapses, synaptic, EPSP, electrophysiological

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31
Q

steps of LTP

A
  1. stimulate presynaptic axons at low frequency to get a subthreshold EPSP (no APs) and establish baseline, 2. stimulate axons at a very high frequency (ie. tetanus) and get lots of APs in the postsynaptic neuron, 3. stimulate axons at low frequency again, and get a much bigger EPSP than before, that is more likely to evoke an AP
32
Q

LTP can last for _____ and when the memory is recollected, same groups of ____ neurons that were activated when first forming the memory are activated

A

years, activated

33
Q

In the early phase of LTP, high frequency activation of postsynaptic neurons allow ____ receptors to be activated, and _____ entry into the neuron. This is the most essential step. Then kinases such as _____ are activated, which hits latent ____ receptors floating inside the cell and inserts it into the ______. Other kinases such as ______ _____ ____ and _______ ____ can induce formation of a _____ ______ such as ______. ____ _____ undergo structural changes that make them more excitable (thicker, bigger), resulting in more _____ channels.

A

NMDA, Ca2+, calcium-calmodulin (CaM), AMPA, membrane, protein kinase C, tyrosine kinase, retrograde messenger, NO, dendritic spines, Na+

34
Q

In early stage LTP, there is an increase in synaptic strength by both presynaptic (more _____ release) and postsynaptic (more _____) mechanisms

A

NT, receptors

35
Q

In late stage LTP, the cell synthesizes new ______ that make these changes _____ _____

A

proteins, longer lasting

36
Q

Injections of ____, ____ or ___ can lesion any brain nucleus. In _____ neurons, activating NMDA and non-NMDA receptors with high glutamate _____ most within a few hours

A

glutamate, kainate, NMDA, cultured, kills

37
Q

prolonged depolarization of neurons which leads to eventual damage or death

A

excitotoxicity

38
Q

fast death characterized by lysis due to osmotic swelling (blebs –> holes in membrane –> cellular disintegration)

A

necrosis

39
Q

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

A

apoptosis/programmed necrosis

40
Q

Apoptosis / programmed necrosis results in death in _____ hours. It can be induced by lower ______ and longer exposure time to glutamate, and depends on ____ receptor activation. The excess ____ causes ____ enzymes to be activated which stripes down the cells and kills them

A

18-24, concentration, NMDA, Ca2+, killer

41
Q

interruption of blood flow from stroke or heart attack; excitotoxic brain damage may occur

A

brain ischemia

42
Q

Excitotoxic brain damage may occur with brain ischemia because a lack of _____ means the Na+/K+ _______ stops working, and neurons depolarize, resulting in a massive glutamate release in the affected area. Eventually, the high ____ levels overloads ____ and they cannot compensate, resulting in _____ enzyme activation. NMDA _____ may not work because once the process has already started, the _____ are already activated even if the ____ is stopped. This results in a degradation of _____ within the dying cells. However, treatment may be effective if we can deactivate the enzymes before ____ ___ occurs

A

O2, pump, Ca2+ buffers, killer, antagonists, enzymes, excitation, function, cell death

43
Q

when a stroke occurs, a ____ ____ stops the flow of blood to a brain region. Drugs that ___ them may restore flow to avoid further damage. Without ___ and ___, neurons begin to depolarize and produces APs. Drugs that inhibit the ____ ____ ____ may reduce the number of APs generated. Many of these neurons release _______. In addition, the lack of energy in the ____ neuron causes the glutamate ______ to stop working. Drugs that block _____ ____ may combat the excessive stimulation. Postsynaptic neurons also produce action potentials, so excess amounts of ____ and ____ enter the cell. This causes ____ ____. Drugs that block _____ _____ may avert the intracellular buildup of Ca2+

A

blood clot, dissolve, oxygen, glucose, voltage-gated Na+ channels, glutamate, presynaptic, transporters, glutamate receptors, Ca2+ Zn2+, cell death, Ca2+ channels

44
Q

the primariy inhibitory transmitter in the brain

A

GABA (gamma-aminobutyric acid)

45
Q

Secondary inhibitory transmitter found mostly in the back of the brain

A

glycine

46
Q

all ___ ______ neurons in the striatum and other nuclei with the ____ ____ use GABA. ____ neurons intermixed within monoamine cell groups also use GABA. ______ in the cerebral cortex (_____% of all neurons) such as in the ____, ___ and other brain regions also use GABA.

A

medium spiny, basal ganglia, projection, interneurons, 30, hippocampus, amygdala

47
Q

GABA acts like a ____ for information coming into neurons. It regulates different _____ of firing in the ______ (e.g. burst firing). One GABA neuron can make connections with up to _____ other neurons in the cortex

A

filter, patterns, cortex, 80

48
Q

Reduced GABA activity promotes ______. Many brain circuits are set up as a series of inhibitory ______ connections, and works through a processes of _______.

A

seizures, GABAergic, disinhibition

49
Q

_____ cells can fire without excitation and fires at _____Hz on _____ ____ cells. These cells fire at ____Hz back to pallidum cells which lower in firing and _____ the ventral striatum to produce _____

A

pallidum, 70, ventral striatum, 0-3, disinhibit, movement

50
Q

the enzyme that converts glutamate to GABA; only in GABA cells

A

glutamate decarboxylase (GAD)

51
Q

the transporter that moves GABA into vesicles

A

vesicular GABA transporter

52
Q

There are examples where GABA is contained in the same ____ and possibly even the same ____ as other NTs. The effect depends on the number of _____ receptors

A

terminals, vesicles, postsynaptic

53
Q

GABA reuptake transporters

A

GAT1 - GAT3

54
Q

GAT-1 is located on ________ _______, whereas all 3 transporters are on _____ that mop.up GABA in a similar manner to _____

A

presynaptic terminals, astrocytes, glutamate

55
Q

the enzyme that converts glutamate to glutamine in astrocytes

A

glutamine synthase

56
Q

glutamine can be released by astrocytes, taken up by ______ and converted back to ______ and used to remake ______. Some therapeutic drugs target ____ to elevate GABA levels; this is used for _____ treatment which causes more _____ to offset the excitation

A

neurons, glutamate, GABA, GAT, epilepsy, inhibition

57
Q

GABA-A is _____, allowing ___ to move from the outside to the inside of the cell, causing ______. This subtype has multiple ____ where drugs and other molecules can bind to affect its function. Each receptor consists of ____ subunits of various combinations of _____, _____, _____ and _______ types. Most have ___ of each and 1 _____. This makes the receptor more or less _____ to GABA depending on the subtypes

A

ionotropic, Cl-, hyperpolarization, sites, 5, alpha, beta, gamma, delta, 2, gamma, sensitive

58
Q

GABA-A competitive agonist (at GABA binding site)

A

muscimol

59
Q

GABA-A competitive antagonist

A

bicuculline

60
Q

GABA-A non competitive antagonist that binds inside the channel pore

A

picrotoxin

61
Q

where the endogenous ligand binds

A

orthosteric binding site

62
Q

_____ and ______ bind to receptors at sites distinct from the GABA binding site. These drugs increase ____ of GABA to open the receptor channel but do not open the channel is GABA is also not bound (ie. act as _____ _____ _____). Benzodiazepines only bind to receptors containing the _____ subunit (most receptors have them). _____ acts in a similar manner at the BDZ site, causing more ____ when mixed with them

A

benzodiazepines, barbiturates, potency, positive allosteric modulators, gamma, alcohol, inhibition

63
Q

a benzodiazepine that is used for sleep but reduces sleep quality because REM sleep is reduced over the sleep cycle

A

diazepam (valium)

64
Q

barbiturate

A

phenobarbital

65
Q

some drugs at like the BDZ, but bind to different parts of the receptor, not just the beta subunit

A

neurosteroids binding site

66
Q

Some drugs can act as ____ agonists at the BDZ site. They do not have an effect on their own, but _____ ability of GABA to open the channel, by stabilizing an _____ form of the channel. This promotes ____, ____ and _____.

A

inverse, attenuates, inactive, anxiety, arousal, seizures,

67
Q

GABA-B receptors are _____ and require ____ different subunits to assemble in the membrane and work properly. Activation of these receptors has an _____ effect on postsynaptic cells by _____ channel opening and inhibiting _____ formation. They also reside _____ where they serve as ______ or heteroreceptors.

A

metabotropic, 2, inhibitory, K+, cAMP, presynaptically, autoreceptors

68
Q

a GABA-B reveptor agonist used as a muscle relaxant and experimental treatment for alcoholism

A

baclofen

69
Q

a GABA-B receptor antagonist that is a convulsant and is primarily used for research

A

saclofen

70
Q

Blockade of ____ receptors impairs many forms of learning mediated by ______, ____ and _____. This is shown in rats given a _____ _____ ______ which severely impairs learning to find the platform quickly in the _____ _____ ______.

A

NMDA, hippocampus, amygdala, striatum, NMDA receptor antagonist, morris water maze

71
Q

NMDA antagonists that impair learning also impair the formation of _______. If you block the NMDA receptors during the high ___ activation of the ____ pathway, no ____ occurs. Enhancing glutamate activity can ____ learning/memory

A

LTP, frequency, glutamate, improve

72
Q

positive allosteric modulators of AMPA receptors

A

ampakines

73
Q

ampakines do not _____ AMPA receptors, but prolong _____ ____ and reduce _______. Ampakines can improve ____ in animals performing the _____ ____ ____ _____ task

A

activate, open time, desensitization, cognition, delayed match to sample

74
Q

ampakines do not _____ AMPA receptors, but prolong _____ ____ and reduce _______. Ampakines can improve ____ in animals performing the _____ ____ ____ _____ task

A

activate, open time, desensitization, cognition, delayed match to sample

75
Q

A task in which an animal is trained to move a cursor to the center of a shape, experience a 1-30s delay, then must select the shape that the animal first saw out of 3 other stimuli

A

delayed match to sample task

76
Q

GABA is metabolized to _____ and ____ by _____ ______. In astrocytes, then glutamate is converted to _____

A

glutamate, succinate, GABA aminotransferase (GABA-T), glutamine

77
Q

The enzyme that metabolizes GABA to Glutamate and succinate

A

GABA aminotransferase (GABA-T)

PSYC 462 (16 decks)

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