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Neurobiology > Excitatory And Inhibitory AAs > Flashcards

Excitatory And Inhibitory AAs Flashcards

0
Q

What are the main inhibitory NTs:

a) in the brain
b) in the spinal cord

A

a) GABA

b) glycine

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1
Q

What are the two main excitatory NTs?

A

Glutamate and aspartate

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2
Q

Glut, aspartate, GABA and glycine are NON-ESSENTIAL AAs. What does this mean?

A

They are synthesized in the body not required in diet

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3
Q

Describe the glycolysis/oxidative metabolism of glucose pathway of synthesising excitatory AAs (glut)

A
  • Glucose converted to pyruvate in glycolysis
  • Pyruvate is decarboxylated to form acetyl-CoA
  • Acetyl-CoA enters the Krebs cycle
  • a-ketoglutarate is produced in cycle, undergoes transamination by aminotransferases to form glutamate
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4
Q

What is the preferred pathway in synthesis of glutamate?

A

Glutaminase catalyses glutamine –> glutamate

glutaminase undergoes product inhibition

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5
Q

What are the 3 paths of glutamate breakdown?

A
  • Glutamine synthetase - converts glutamate to Glutamine in glia
  • reversal of transamination - glutamate -> a-ketoglutarate
  • Glutamate dehydrogenase - glutamate -> a-ketoglutarate
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6
Q

How are EAAs stored?

A

In vesicles:
Highly specific transporter for L-glutamate
Proton antiporter system - actively moves H+ in, electrochem grad, transporter moves glut in and H+ out

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7
Q

Glutamate transporter concentrates glutamate in vesicles until it reaches a concentration of?

A

50mM

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8
Q

Describe release and uptake of EAAs (glutamate)

A
  • vesicular release and uptake by presynaptic transporters

BUT also release by TRANSPORTER REVERSAL

Transporters have high affinity and low specificity

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9
Q

How many glutamate transporter subtypes are there?

A

5

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10
Q

Where are glutamate transporters EAAT1-5 each found?

A 
EAAT1 - neurones an astroglia (esp Bergmann glia, cortex, hippocampus and cerebellum)
EAAT2 - astroglia
EAAT3 - neurones
EAAT4 - Cerebellar purkinje cells 
EAAT5 - retina
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11
Q

Which metabotropic glutamate receptor subtypes are in GROUP I? What do they stimulate?
What compounds are they activated by?

A

mGluR1 + mGluR5

Gq - stimulate PLC -> IP3 (Ca release)

Activated by trans-ACPD and quisqualate

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12
Q

Which metabotropic glutamate receptor subtypes are in GROUP II? What do they stimulate?
What compounds are they activated by?

A

mGluR2 + mGluR3

Gi - inhibit adenylyl cyc

Actuated by trans-ACPD and quisqualate

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13
Q

Which metabotropic glutamate receptor subtypes are in GROUP III? What do they stimulate?
What compounds are they activated by?

A

mGluR4, 6, 7, 8

Gi - inhibit adenylyl cyc

Activated by L-AP4 and L-SOP (no effect w trans-ACPD or quisqualate)

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14
Q

Which group of mGluRs act as autoreceptors?

A

Group III

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15
Q

What ions do AMPA, kainate and NMDA allow?

A

AMPA - Na, K (and some allow Ca)

Kainate - Na, K

NMDA - Na, K, Ca

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16
Q

Quisqualate is an agonist of which IONOTROPIC receptors?

A

AMPA and kainate

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17
Q

What is an agonist of NMDA receptor?

A

Aspartate

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18
Q

CNQX is an antagonist of which glutamate receptors?

A

AMPA

Kainate

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19
Q

AP5 is an antagonist of which type of glutamate receptor?

A

NMDA

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20
Q

How does a conditioning train result in long term potentiation?

A

= rapid stimulation
Changes efficiency of synapse, makes it stronger
Results in larger responses
Responsible for synaptic plasticity

Train -> sustained depolarization, NMDA block removed
Metabotropic glut receptors activated
AMPA phosphorylation, increased AMPA activity

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21
Q

How do EEA IONOTROPIC receptors cause stroke, Alzheimer’s and amyotrophic lateral sclerosis?

A

Sustained activation of AMPA, kainate and esp NMDA receptors
Leads to neuronal cell death due to Ca overload
=> neurodegeneration

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22
Q

What can provoke overstimulation of EAA receptors and consequently neurodegeneration?

Clue - restriction of blood supply

A

Ischemia

23
Q

What’s the main inhibitory transmitter in:
a) the brain?

b) the spinal cord?

A

a) GABA

b) glycine

24
Q

What is GABA synthesized from?

What enzyme catalyses it’s synthesis?

Where is this enzyme mostly found, what co-factor does it require, and what inhibits it?

A

Glutamate

Glutamate decarboxylase

Axon terminals of GABAergic neurones.
Pyridoxal phosphate derived from vitB
Inhibited by allylglycine.

25
Q

How is GABA broken down?

A

Converted in succinic semialdehyde by GABA aminotransferase

Succinic semialdehyde converted to succinate by SSADH (succinic semialdehyde dehydrogenase)

(Succinate = intermediate in Krebs)

26
Q

Where is GABA aminotransferase found?

What inhibits it? What are it’s inhibitors used for?

A

Mostly in mitochondria (in neurones and Astrocytes)

Inhibitors: aminooxyacetic acid and vigabatrin
Vigabatrin used to treat epilepsy

27
Q

Which GABA receptors are IONOTROPIC?

A

A + C

B is metabotropic

28
Q

Where is GABAc mainly located?

A

In retina

29
Q

Why is there huge diversity in GABAa receptors?

A

6 classes if subunit: a, B, y, d, E, p

19 different polypeptides

30
Q

What domain of GABAa is thought to line the pore?

What controls permeation?

A

M2

Charged rings

31
Q

What forms the GABA binding site on GABAa receptor?

A

Cys (cystine) loop

32
Q

GABA has 5 distinct binding sites for what molecules?

What do agonists of these sites do? (In brackets)

A

1) GABA
2) benzodiazepine
3) barbiturates (depressants)
4) steroids (anaesthetics)
5) picrotoxin (convulsants)

33
Q

Why do benzodiazepines and barbiturates decrease anxiety?

A

Potentiation GABA

34
Q

What 3 agonists of GABAa?

A

Muscimol, THIP, isoguvacine

35
Q

What is a competitive antagonist of GABAa?

A

Bicuculline

36
Q

What are non-competitor antagonists of GABAa?

A

Metrazol (phentylenetrazol)
and
Picrotoxin

(Both bind to picrotoxin site)

37
Q

How do benzodiazepines and barbiturates affect channel openings of GABAa?

A

Benzodiazepines: increase FREQUENCY of openings

Barbiturates: increase DURATION of openings

38
Q

What is the most common subunit composition if GABAa (40%)?

Where is this isoform located and what are it’s properties at these locations?

A

a1B2y2

Most brain areas, hippocampus - common coassembly

Cortical interneurones - BZ type I

Cerebellar purkinje cells - Zn insensitive

39
Q

What subunit is required for GABAa to respond to benzodiazepines?

A

Y

40
Q

How does GABAb bring about synaptic inhibition of NT release?

A

Coupled to Gi, inhibits adenyl cyclase

Stimulates PLA2

Activates VG K+ channels
Inhibits Ca channels
=> hyperpolarisation, no NT release

41
Q

What are agonists of GABAb? What are they used for?

A

Baclofen, saclofen

Muscle relaxants, anti spastic agents

42
Q

Phaclofen-2-hydroxysaclofen does what to which GABA receptor?

A

Antagonist of GABAb

43
Q

What five places are glycine receptors found?

A 
Spinal cord grey matter
Mindbrain (lower levels)
Medulla
Thalamus 
Hypothalamus

NB: absent from higher brain levels

44
Q

What is glycine synthesised from? Using what enzyme?

A

Serine

Serine hydroxymethyltransferase

45
Q

How is glycine stored?

A

In vesicles

Vesicular transporter hasn’t been found, most likely uses GABA transporter

46
Q

How is glycine taken up from synapse?

A

Na dependent transporters

Specific (GLYT1, GLYT2)

47
Q

How many subunits make up a glycine receptor?

What classes of subunit? What type of protein are these subunits?

A

5

a (a1,a2, a3) and B
Glycoproteins

48
Q

How many transmembrane domains make up each subunit if GlyR?

A

4

49
Q

What subunit composition of glycine receptor is found in adults? And in fetus?

A

Adult: 3a1/2B

Fetus: 5a2 (homomer)

50
Q

What other protein is associated with glycine receptor? Why is it’s role?

A

Gephrin
Cytoplasmic protein

Binds B subunit to cytoskeleton
Responsible for GlyR clustering at inhibitory synapse

51
Q

What is an allosteric modulator of glycine receptor?

A

Zinc

52
Q

Which of the following: B-alanine, cyanotriphenylborate, taurine, strychnine

are a) agonists b) antagonists and c) channel blockers of glycine receptor?

A

a) B-alanine, taurine
b) strychnine
c) cyanotriphenylborate

53
Q

How does tetanus toxin affect glycine receptor?

A

Causes Glycine release

=> over activation of muscles

54
Q

What role do glycine receptors have in whole organism?

A

Reflex responses- reciprocal and recurrent inhibition

Sensory processing

Voluntary muscle control

55
Q

Hyperekplexia (exaggerated reflexes) is caused by mutation of glycine receptors, decreases glycine signalling.

How is it treated?

A

With benzodiazepines (increase GABA activity in SC)

Neurobiology (9 decks)

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