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Biochem 2 > 16. Glutamate, GABA neurotransmission > Flashcards

16. Glutamate, GABA neurotransmission Flashcards

1
Q

Neurotransmitters can not cross the BBB
=> Which amino acid can enter?

A

Essential AAs
Arginine
Tyrosine

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2
Q

Glutamatergic synapse
-> Characteristics of Glutamin transporters

A

System N/A transporters (Sodium-coupled neutral amino acid)

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3
Q

Describe Glutamate transporters

A

EAAT: 1 glutamate enter + 3 sodium enter➔
1 glutamate / 1 ATP

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4
Q

3 Glutamatergic ionotrop receptors

A

NMDA
AMPA
Kainate

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5
Q

List Glutamatergic metabotrop receptors:

A

mGluR -

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6
Q

Ionotropic glutamate receptors agonists and antagonists
-> What are some Specific agonists:?

A

NMDA – N-methyl-D-aspartate

AMPA – alpha-amino-3-hydroxy-5- methyl-4-isoxazole propionic acid

Kainate: 2-Carboxy-3-carboxymethyl-4- isopropenylpyrrolidine

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7
Q

Ionotropic glutamate receptors agonists and antagonists
-> What is 2 important antagonists?

A

1/ Phencyclidine
2/ Ketamine

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8
Q

Pharmacologic binding sites of the NMDA receptor
-> Identify

A
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9
Q

The synaptic AMPA & NMDA receptors are coincidence receptors
-> How do they work?

A

AMPA & NMDA receptors simultaneously present – ion channels

AMPA activation (Na+ permeability) → depolarization → Mg2+ detaches → Mg2+ inhibition on NMDA receptor ↓ → NMDA activation → [Ca2+]i rises

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10
Q

Dual-component Excitatory Postsynaptic Potential (EPSP)
-> What happen after activation of AMPA?

A

Activation of AMPA
➔ depolarisation
➔ Mg2+ inhibition of NMDA decreases
➔Activation of NMDA receptors

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11
Q

Characteristics of Metabotropic glutamate receptors

A

-mGluR- pre- and postsynaptic localization
-Various intracellular signalling pathways: Gq, Gi

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12
Q

Metabotropic glutamate receptors have the regulation of ___

A

Ion channels
1/ L-N type Ca2+ channels ↓
1/ K+-channels ↓

Receptors
(NMDA, AMPA, DA, GABA, NA) ↑or↓

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13
Q

How does Ca2+ homeostasis in neurons work?

A

Activation of Ca2+ -dependent enzymes

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14
Q

Ca2+ homeostasis in neurons
-> List 5 Ca2+ -dependent enzymes

A

1/ PKC
2/ NO synthase
3/ Ca2+-calmodulin dept. prot. kinases
4/ Calcineurin (phosphatases)
5/ Phospholipase A2

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15
Q

LTP (long-term potentiation: a model of learning
-> Identify

A

1/ NMDA receptor
2/ AMPA receptor

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16
Q

Mechanisms of long-term potentiation
-> What happen during normal transmission?

A

Only AMPA receptors activated

17
Q

Mechanisms of long-term potentiation
-> What happen after conditioning train?

A

1/ AMPA, NMDA, mGlu1 receptors activated
2/ Increased [Ca2+]I
3/ Activation of CaMKII, PKC, and NOS

18
Q

What is the role of CaMKII

A

calcium-calmodulin–dependent protein kinase II. (drugs that block CaMKII prevent LTP)

19
Q

Events that lead to cell death, including apoptosis and necrosis, after ischemia

A
20
Q

The role of GABA – γ-aminobutirate

A

major inhibitory neurotransmitter in the central nervous system (glycin: brainstem)

21
Q

2 Toxins that destroy synaptic SNARE proteins

A

1/ Tetanus toxin
2/ Botulinum toxin

22
Q

2 Toxins that destroy synaptic SNARE proteins

A

1/ Tetanus toxin
2/ Botulinum toxin

23
Q

Toxins that destroy synaptic SNARE proteins
-> The role of Tetanus toxin

A

1/ acts selectively to prevent glycine release
from inhibitory interneurons in the spinal cord, causing excessive reflex hyperexcitability
and violent muscle spasms (lockjaw)

24
Q

Toxins that destroy synaptic SNARE proteins
-> The role of Botulinum toxin

A

prevents acetylcholine release
- prevents contraction
- muscle relaxant
- toxin-induced paralysis

25
Q

What is GABA A channel receptor?

(γ-Aminobutyric acid, or GABA)

A

a heteropentamer that not only has a pore for Cl− but also separate binding sites for GABA and several classes of channel modulators

26
Q

Mechanism of GABA A channel receptor

A

Chloride equilibrium potential is more negative than
the resting membrane potential
→ chloride influx
→ hyperpolarization

27
Q

All drugs which increase inhibitory neurotransmission through positive allosteric modulation of the GABAergic neurotransmission
-> they can cause…. (in case of increasing dose)

A
  • anxiolytic action (unfortunately not fully distinguisable from sedation – lowest dose)
  • hypnotic action (moderate dose)
  • general anesthesia (still higher dose)
  • coma and death (toxic dose)
  • There is an additive synergism among the GABAergic or other sedatives and ethanol.
28
Q

Synthesis of GABA
-> Identify

A

γ-Aminobutyric acid, or GABA

29
Q

The role of GAD

A

– cytosolic, expressed only in GABAergic neurons (some in non-neuronal tissues?)
- (two isoforms with slightly different molecular weight (GAD65 and GAD67))
- inhibition → convulsion

30
Q

How does Degradation of GABA occur?

A
31
Q

What is GABA-T? How does it work?

A

GABA-T – mitochondrial
GABA analog – (Vibagatrin, γ-vinyl GABA)
→ irreversible covalent binding to GABA-T
→ elevation of synaptic GABA → antiepileptic effect

32
Q

GABA shunt
-> Identify

A

1/ gamma-Amino butyrate
2/ SSADH - Succinic semialdehyde dehydrogenase

33
Q

Neuron – glia interaction in the metabolism of GABA and glutamate
-> Where are GABA transporters (GATs)

A

neurons astrocytes (~ 20 % of released GABA is taken up by astrocytes)

34
Q

Characteristics of GABA transporters (GATs) – neurons
astrocytes

A
  • Na+-dependent
  • functions against a GABA concentration gradient
  • bidirectional
  • (GAT1 – primarily on presynaptic GABAergic terminals, GAT3 on astrocytic processes, GAT2
    extrasynaptic region)
35
Q

what are GAT inhibitors?

A

anticonvulsants

36
Q

What are the 2 types of GABA receptors

A

1/ GABAA receptor – ligand-gated chloride ion channels
2/ GABA B receptor – dimeric G-protein coupled receptor

37
Q

The role of GABAA receptor – ligand-gated chloride ion channels

A

1/ produce rapid phasic (synaptic) and
tonic (extrasynaptic) inhibitory currents
2/ targets of benzodiazepines (anxiolytics) anaesthetics, ethanol

38
Q

What are characteristics of GABA B receptor – dimeric G-protein coupled receptor?

A

coupled to a variety of effectors (some receptors activate certain K+ channels producing slow inhibitory synaptic currents, others decrease Ca2+ conductance and /or inhibit cAMP production)

Mediate pre and postsynaptic inhibition)

Biochem 2 (38 decks)

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