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PSYC 475 > glutamate Chapter 8 > Flashcards

glutamate Chapter 8 Flashcards

1
Q

what is glutamate an ionized form of?

A

ionized form of glutamic acid (an amino acid)

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2
Q

how is glutamate formed?

A

formed from glutamine by glutaminase

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3
Q

what kind of neurotransmitter is glutamate?

A

Glutamate is an excitatory amino acid neurotransmitters.

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4
Q

what kind of neurons use glutamate as a transmitter?

A

Glutamatergic neurons

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5
Q

Is glutamate in all cells? yes or no? Why?

A

Glutamate is in all cells because of its multiple biochemical functions

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6
Q

what can you tell me about glutamatergic neurons concentration and neurotransmitter pool?

A

glutamatergic neurons have higher concentrations
and segregate their neurotransmitter pool, even though glutamate has multiple biochemical function.

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7
Q

how is glutamate synthesized?

A

This reaction, catalyzed by the enzyme glutaminase, requires energy provided by the breakdown of adenosine triphosphate (ATP) into adenosine diphosphate (ADP) and phosphate (PO4
3−).

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8
Q

what are the three transported responsible for moving glutamate into the synaptic vesicles?

A

Vesicular glutamate: VGLUT1,VGLUT2, and VGLUT3

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9
Q

What are special about vesicular glutamate transporters?

A

found only in cells that use glutamate as neurotransmitter.

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10
Q

What do DA-Glutamate co-expressing neurons of the VTA release do?

A

release the two transmitters from separate vesicles at different kinds of axon terminals

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11
Q

how many plasma membrane transporters have been identified for glutamate uptake? What are they called?

A

5 different membrane transporters have been identified

They are called excitatory amino acid transporters (EAATs)

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12
Q

Name the 5 different glutamate uptake transporters and where they are expressed.

A
  1. EAAT1: highly expressed in astrocytes in the cerebellum
  2. EAAT2: highly expressed in astrocytes (may account for about 90% of glutamate transport
    of total glutamate uptake in the brain)
    * EAAT3: major neuronal glutamate transporter; postsynaptic
    localization
    * EAAT4: expressed primarily by Purkinje cells in the cerebellum
    * EAAT5: present in bipolar cells in the retina.
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13
Q

What is mentioned about glutamate?

A

prolonged high levels of glutamate in the extracellular
fluid are very dangerous, producing excessive neuronal excitation and even cell death.

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14
Q

Think about knockout mice. Why is EAAT2 important?

A

knockout mice lacking EAAT2 developed spontaneous epileptic seizures, were more susceptible than wild-type mice to experimentally induced seizures and brain injury, and had a greatly shortened life span

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15
Q

what do astrocyte transporters do to glutamate?

A

Astrocyte transporters convert the glutamate they take up to glutamine using glutamine synthetase

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16
Q

After the production of glutamine. Where does is it transported?

A

Glutamine is then transported out of astrocytes and picked up by neurons, where it can be converted back into glutamate by glutaminase

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17
Q

what are some other functions of glutamine synthetase?

A

In addition to inactivation of glutamate, a second function of glutamine synthetase is to help in the metabolism and removal of ammonia that is either generated metabolically in the brain or taken up from the bloodstream

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18
Q

Explain the cycling of glutamate and
glutamine between glutamatergic neurons
and astrocytes

A

After neurons release glutamate, it can be transported into nearby astrocytes by EAAT1 or EAAT2, or less commonly it can be transported into the postsynaptic
cell by EAAT3. Inside the astrocyte, glutamate
is converted into glutamine by the enzyme
glutamine synthetase. The glutamine can be
later released by the astrocytes, taken up by
neurons, and converted back into glutamate
by the enzyme glutaminase.

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19
Q

What are glutamatergic pathways in the brain include?

A
  1. Projections of the pyramidal neurons of the cortex (projection tostriatum, thalamus, limbic system structures, and regions of the brainstem)
  2. Parallel fibers of the cerebrum
  3. Excitatory pathways in the hippocampus
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20
Q

With regards to function, what is important to note about glutamate?

A

Glutamate is found throughout the brain; important functions include synaptic plasticity, learning and memory, possibly in psychopathologic disorders

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21
Q

What do ionotropic and metabotropic receptors do to glutamate?

A

Both ionotropic and metabotropic receptors mediate the synaptic effects of glutamate

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22
Q

What specifically does ionotropic glutamate receptors do? Explain the functions of the 3 subtype glutamate receptors.

A

Ionotropic glutamate receptors depolarize the membrane of the postsynaptic cell (excitatory) (fast signaling):

  1. AMPA receptor, named for selective agonist AMPA; most fast excitatory responses to glutamate are mediated by stimulation of AMPA receptors

2.Kainate receptor, named for selective agonist kainic acid

  1. NMDA receptor, named for the agonist NMDA; allows both Na+ and Ca2+ to pass; then we have Ca2+ acting as a second messenger
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23
Q

what are the ion permeabilities(what ions are let into the cell) of ionotropic glutamate receptor channels?

A

All three ionotropic glutamate receptor
channels conduct Na+ ions into the cell. NMDA receptor channels additionally conduct Ca2+ ions, which can activate several important second-messenger functions

24
Q

How many subunits do ionotropic glutamate receptors have? What does the subunits identify about the receptors?

A

Ionotropic glutamate receptors have 4 subunits; each subtype is composed of a different set of subunits.

Due to all 3 receptors having different subunits explains why they differ in pharmacology

25
Q

What is NBQX, and what does it do?

A

Antagonist NBQX blocks AMPA and kainate receptors but not NMDA receptors

26
Q

what happened to the mice with NBXQ?

A

In mice, NBXQ leads to sedation, ataxia, reduced locomotor activity, and protection against seizures

27
Q

What are unique characteristics that NMDA receptors have?

A
  1. Flow of both Na+ and Ca2+. Where the other receptors only release Na+

2.Activated by simultaneous binding of glutamate and a co-agonist: glycine or D-serine

  1. Binding site for Mg2+ in the ion channel; blocks channel at resting potential; dissociates during depolarization of the membrane and opens channel
28
Q

What is the importance of phencyclidine(PCP)?

A

phencyclidine (PCP) is a abused drug. Which acts in the same manner as Mg2+. Such that, it blocks the passage of ions during resting potential.

29
Q

To open NMDA channels. What two events must occur?

A

1.glutamate is released onto the NMDA receptor
(assuming that a co-agonist is also bound to its site on the receptor complex),

  1. the cell membrane is depolarized by stimulation of a
    different excitatory receptor. Meaning that the other two receptors enable NMDA to activate
30
Q

In the NMDA receptor, what other purpose does the second binding site have?

A

Second binding site in the channel recognizes NMDA receptor antagonists that block the channel

31
Q

what are three examples of NMDA receptor antagonists. What do they do practically?

A
  1. Abused drugs phencyclidine (PCP) - disrupt normal cognition
  2. ketamine - also disrupt normal cognition
  3. Memantine (Namenda) used to treat Alzheimer’s disease - cognitive enhancer
32
Q

what type of antagonists drug that bind to NMDA receptor. how does that antagonist function?

A

the drugs are uncompetitive antagonists: require the receptor to be activated (open) by an agonist

33
Q

what are three ways to explain the effects of the antagonist NMDA drug?

A

(1) by the dose (recreational versus medicinal),

(2) by the subtle but significant differences in how each drug influences functioning of the NMDA receptor

(3) by the effects of each drug on other pharmacological targets besides the NMDA receptor

34
Q

where is metabotropic glutamate receptors located, and what are their functions?

A

Metabotropic glutamate receptors: widely distributed throughout the brain, involved in locomotor activity, motor coordination, cognition, mood, and pain perception.

35
Q

name the metabotropic glutamate receptors in group 1 and give a location of them and their function.

A

Group I (mGluR1 and mGluR5) – located postsynaptically; use the phosphoinositide second-messenger system

36
Q

name the metabotropic glutamate receptors in group 2 and 3 and give a location of them and their function.

A

Group II (mGluR2 and mGluR3) and Group III (mGluR4 and mGluR6–8) – located presynaptically; reduce transmitter release by inhibiting cAMP formation

37
Q

what is l-AP4?

A

selective agonist at group III glutamate autoreceptors;
suppresses transmission

38
Q

Knowing the functions of the brain that metabotropic glutamate receptors are involved in. With respect to treatment, Why is mGluR drugs important?

A

Increasing interest in the development of mGluR drugs for the treatment of numerous neuropsychiatric disorders such as depression, anxiety disorders, disorders characterized by cognitive
deficits, and drug addiction

39
Q

what do AMPA and NMDA receptor receptors play a key role in?

A

learning and memory

40
Q

What modulators of AMPA are cognitive enhancers?

A

Positive allosteric modulators of AMPA may be cognitive enhancers

41
Q

how are Positive allosteric modulators of AMPA cognitive enhancers?

A

most reduce the rate of receptor deactivation allowing glutamate can exert a more prolonged excitatory effect

42
Q

how does AMPA receptors enhance memory and learning?

A

Increase time that AMPA receptor channel remains open

43
Q

What kind of experiments have they done, with respect to positive allosteric modulators of AMPA receptor?

A

AMPA receptor positive allosteric modulators have been shown to enhance learning and memory in experimental animals but not in clinical trials.

44
Q

What is occurring at the synaptic level during associative learning.

A

at the synaptic level, for associative learning, repeated pairings of the Conditioned stimulus and the Unconditioned stimulus theoretically strengthen the synaptic connections between the Conditioned stimulus input neurons and the postsynaptic cells

45
Q

Connect the synaptic level understanding with classical pavlovian conditioning. Explain the step in (A),(B), and (C) order.

A

(A)The bell (condition stimulus) would be the neuron with the weak synaptic connection. The food would be the neuron with the strong synaptic connection

(B)Paring is considered when both bell and food are shown. meaning that the weak synaptic neuron and the strong synaptic neuron fire the same time. paring each other.

(C) then the paring causes the conditional stimulus, the bell, to have a stronger synaptic connection.

46
Q

What is long-term potentiation(LTP)?

A

persistent increase in synaptic strength produced by a burst of activity in the presynaptic neuron

47
Q

What is long-term potentiation(LTP) experimentally produced by?

A

experimentally produced by tetanic stimulus( a brief train of electrical stimuli. about100 stimuli over a
period of 1 second)

48
Q

what was the purpose of long-term potentiation?

A

experiments aimed at elucidating its underlying
mechanisms and behavioral functions.

49
Q

What part of the brain LTP elicited on?

A

hippocampus, specifically the CA1 hippocampal

50
Q

what to phases are in LTP?

A

early LTP (E-LTP) lasts a few hours

late LTP(L-LTP) lasts days or months

51
Q

What is E-LTP studied using?

A

E-LTP is studied using hippocampal slices

52
Q

What receptor is necessary hippocampal LTP work on?

A

activation of NMDA receptor is necessary for induction of hippocampal LTP

53
Q

What are the two phases involved in E-LTP?

A
  1. induction phase
  2. Expression phase
54
Q

when does the induction phase happen and what is critical for it to happen?

A

during and immediately after tetanic stimulation; NMDA receptors have a critical role

55
Q

what happens in expression phase?

A

the resulting increase in synaptic strength can be
measured. AMPA receptors are critical (AMPA receptor-mediated EPSP(increase action potential) is facilitated in LTP)

56
Q

What is a form of receptor trafficking?

A

Postsynaptic Ca2+ influx and CaMKII activation cause rapid expansion of dendritic spines and insertion of more AMPA receptors into the spine
membrane(basically getting rid of AMPA receptors)

57
Q

What happens to the synapse when E-LTP is done?

A

E-LTP converts silent synapses to functional by trafficking AMPA receptors into the spine

PSYC 475 (12 decks)

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