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2402 Supp > Amino Acids as Neurotransmitters > Flashcards

Amino Acids as Neurotransmitters Flashcards

1
Q

GABA and aspartate are derived from

A

Glutamate

synthesised in the CNS

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2
Q

Glycine is derived from

A

Glutamate

synthesised in the spinal cord

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3
Q

Main NT classes:

A
  1. Amino acids
  2. Peptides
  3. Monoamines
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4
Q

Glial cells outnumber neurons at a ratio of

A

10:1

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5
Q

Neuromodulators:

A 
Cause complex responses/modulation;
Alter sensitivities of synapses;
Modify post synaptic responses;
Change pre-synaptic handling of NT;
Changes occur over minutes, hours or
days;
Associated with slower events,
e.g. growth, learning, protein synthesis
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6
Q

Agonistic drug effects:

A

Drugs bind to autoreceptors and block inhibitory effect

Drugs bind to postsynaptic receptors and either activates them OR increaes the effect on them via neurotransmitters

Drugs block the deactivation of NT molecules by blocking degregation or reuptake

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7
Q

Antagonistic drug effects:

A

Drug activated autoreceptors and inhibits NT release

Drug binds to postsynaptic receptor and blocks the NT

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8
Q

BBB

A

Blood-brain barrier, a system of tight
junctions between the endothelial cells
and surrounding astrocytes of the
capillaries.

Tightly regulated the CNS and prevents toxins entering the brain

May be compromised in diseased states

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9
Q

GABA and Glycine are

A

Inhibitory

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10
Q

Glutamate and aspartate are

A

Excitatory

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11
Q

Glutamate can be derived from

A

Glucose or glutamine

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12
Q

Glutamate receptors: Excitatory

A

NMDA, kainate and AMPA
Ionotropic

Permeable to Na+ and Ca+

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13
Q

Glutamate receptors: Inhibitory

A

Metabotropic receptors (MGluR)

coupled to
phosphatidylinositol metabolism

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14
Q

Glycine is an positive allosteric modulator of NMDA receptor glutamate responses. T/F

A

True

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15
Q

Positive allosteric modulators are:

A

Allosteric ligands that bind to a topographically distinct site
to the orthosteric agonist and enhance the affinity (cooperativity factor-α) and/or efficacy
(modulation factor-β) of the orthosteric agonist.

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16
Q

Orthosteric agonists:

A

bind to the G protein-coupled receptor (GPCR), which induces a
conformational change that results in the activation of downstream signaling, such as
glutamate

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17
Q

All ionotropic glutamate receptors are

A

tetramers

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18
Q

When located post-synaptically, these GPCR mGluRs are thought to be largely

A

excitatory

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19
Q

Group II and III receptors predominantly presynaptic, and activation actually
reduces neurotransmission and overall excitability. They can be considered to, in
some cases, function as

A

autoreceptors

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20
Q

It is difficult to selectively block glutamate because:

A

Glu is so generally used within the CNS

21
Q

Blocking the glycine site on NMDA

receptors effectively is

A

antagonistic to responsiveness

22
Q

Only two drugs in current
medicinal use, and they are lipid
soluble and can cross the BBB;

A

– Ketamine (anaesthesia,
analgesia, depression)

– Memantine (Alzheimer’s
Disease)

23
Q

PCP and Ketamine bind to:

A

The same deep site within the ion
channel of the NMDA receptor, where they block ion
movement into the neuron.

As they bind to an area other than the glutamate
binding site, they are considered to be noncompetitive antagonists of the NMDA receptor.

24
Q

Ketamine binds to:

A

NMDA and mu opioidreceptors

25
Q

Memantine is also a noncompetitive antagonist on the NMDA receptor. T/F

A

True

26
Q

Memantine is a clinically useful drug in treating:

A

moderate to severe confusion (dementia)
related to Alzheimer’s disease. It may improve
memory, awareness, and the ability to perform
daily functions

27
Q

very little
GABA is found outside of the
CNS because:

A 
GABA is synthesized from
glutamate by the enzyme
glutamic acid decarboxylase
(GAD), and only GABAergic
neurons have GAD
28
Q

GAT1 sit

A

Presynaptically

29
Q

GAT2/3 sit

A

Postsynaptically

30
Q

The function of GABA transaminase

(GABA-T):

A

Recycles GABA so it can be re-used or degradedto glutamine, which can
be transported without effect.

31
Q

GABAa receptor motif:

A

a-b-a-g-a motif.

arranged symmetrically around the central chloride anion conduction pore

32
Q

Benzodiazepines

A

Positive allosteric modulators,
potentiating the effects of GABA, giving the
receptors a greater affinity for GABA,

increasing the
inward Cl- current.

33
Q

Benzos increase inward Cl- T/F

A

True

34
Q

More GABAa receptors sit

A

Postsynaptically

35
Q

Activation of GABAa receptors lead to

A

HYPERpolarisation due to an influx of Cl- ions

36
Q

Activation of GABAa receptors make it LESS likely for an AP to occur due to

A

the inward movement of Cl- ions,

37
Q

Full GABA agonists within the CNS display

A

A large number
of effects including anti-anxiety (anxiolytic),
muscle relaxant, sedation, anti-convulsion,
and at high enough doses, anaesthesia.

38
Q

GABAb receptors

A

are dimers of two different proteins, bound together at the C-termini. B1 and B2 subunits have a GABA binding site linked to 7 transmembrane domain typical of all GPCRs; B2 is coupled to Gi protein.

39
Q

Activation of the heterodimer

A

inhibits adenylyl cyclase activity via G-proteins

40
Q

Activation of the heterodimer inhibits adenylyl cyclase and

A

Increases outward K+

Reduces inward Ca2+ conductance;

both
channel effects reduce post- and presynaptic excitability.

41
Q

Baclofen is a derivative of GABA,

and is an agonist of

A

GABAb

receptors.

42
Q

Baclofen treats spasicity due to

A

decreases
neurotransmitter release in
excitatory spinal pathways, and
increases inhibitory pathway activity

43
Q

GHB

A

is an agonist at GABAA receptors and a partial

agonist at GABAB receptors

44
Q

GHB may induce

A

nausea, dizziness,
drowsiness, agitation, visual disturbances, depressed
breathing, amnesia, unconsciousness, and death.

45
Q

Ionotropic Receptors:

A

Glycine receptors are pentamers of 5a, 3a:2b or 2a:3b
each with a chloride ion channel. There are 4 known a subunits and no
metabotropic forms.

46
Q

Synapse clearance:

A

via transporters with GlyT1 into astrocytes, and GlyT2 into

presynaptic neurons.

47
Q

Strychnine

A

a toxin obtained from seeds of an
evergreen tree, is a competitive antagonist for
glycine receptors, binding the blocking access
of glycine to its receptors.

48
Q

Tetanus

A

toxin blocks glycine release from inhibitory interneurons in the spinal cord,
resulting in reflex hyperactivity and violent muscle spasms

2402 Supp (5 decks)

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