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Yr 2: Pharmacology and Therapeutics (MGEM2016 UNUK) > Neuropharm 1: Neurotransmitters > Flashcards

Neuropharm 1: Neurotransmitters Flashcards

1
Q

Classification of CNS neurotransmitters

What are the 3 classification of CNS neurotransmitters by ROLE and give 2 examples of each?

A

Excitatory: (ACh, noradrenaline, dopamine, serotonin, glutamate, aspartate)

Inhibitory: ( GABA, glycine )

Modulatory: ( serotonin, dopamine, noradrenaline various peptides )

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2
Q

classification of CNS neurotransmitters

What are 3 classification of CNS neurotransmitters by chemical structure and give 2 examples of each?

A

Amino acids: (glutamate, aspartate, GABA, glycine)

Monoamines: (dopamine, serotonin, noradrenaline)

Peptides: ( somatostatin, CGRP, substance P, neurokinin)

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3
Q

Glutamate - excitatory neurotransmission

Briefly outline how glutamate is synthesized in neurons

A

Glutamine becomes glutamate via the enzyme glutaminase

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4
Q

Glutamate - excitatory neurotransmission

How is glutamate uptaken

think transporter proteins and glial cells

A

Uptaken via EAAT (excitatory Amino Acid Transporter) into neurons and astrocytes

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5
Q

glutamate - excitatory neurotransmission

Outline the process of glutatmate uptake if it happens in astrocytes

think conversion of molecules via an enzyme and transporter proteins

A
  1. Glutamate converted to glutamine via glutamine synthase
  2. Glutamine is transported out of astrocyte and into neuron via Glutamine transporter
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6
Q

Glutamate

what is one difference between NDMA and AMPA and Kainate ionotropic receptors regarding the ions they allow into the channel?

think types of ions

A

NMDA: allows Na+, K+ and Ca2+

AMPA/Kainate: only allows Na+ and K+, NOT Ca2+

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7
Q

Glutamate

what is the difference between NMDA and AMPA and Kainate in terms of function and speed and what is AMPA the prodominant receptor for?

think excitatory transmission, synapses, toxicity

A

NMDA:
- has SLOW excitatory transmission
also has functions in:
- Synaptic plasticity
- excitotoxicity

AMPA/ Kainate: both have FAST excitatory transmission

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8
Q

glutamate

where are group 1 metabotropic mGluR (G-protein coupled receptor) found, what are they linked to and what ion signal do they respond to and what type of function does the receptor have?

think synapses, G-proteins, ions in receptors, what functions receptors can have

A
  • they are found postsynaptic membrane
  • linked to Gq G-protein
  • they respond Ca2+ signalling
  • there function is to be excitatory
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9
Q

Glutamate

where are group 2 & 3 metabotropic mGluR (G-protein coupled receptor) found, what G-protein are they linked to and what type of function does the receptor have?

think synapses, G-proteins, glutamate

A
  • found in the presynaptic membrane
  • linked to Gi and Go G-proteins
  • function is to regulate glutamate release
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10
Q

Glutamate - NDMA receptors

What normally blocks Glutamate on NMDA receptors and what removes block?

think Ions and action potentials

A
  • NMDA receptors normally blocked by Mg2+
  • Depolarization removes block
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11
Q

Glutamate - NMDA receptors

What does activation of NMDA receptors require?

think amino acids and neurotransmitters

A

Activation requires action of glycine as well as neurotransmitter (glutamate)

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12
Q

NMDA receptors - Mechanisms of Long term Potentiation (synaptic plast)

What is the mechanism of action of infrequent synaptic activity in long term potentiation?

think action potentials/signals, receptors being activated, what this causes, and the result of these effects

A
  1. infrequent signal comes through
  2. only AMPA receptors activated
  3. Brief depolarization and thus brief excitation
  4. Signal just goes down into neuron cell with no structural alterations or altered gene expression
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13
Q

NMDA receptors - Mechanisms of Long term Potentiation (synaptic plast)

What is the mechanism of action of a conditioning train of stimuli in long term potentiation?

think stimuli, AMPA and NMDA receptors, ions involved and what the effects of one of these ions cause.

A
  1. if repeated stimuli occurs, sustained depolarisation occurs
  2. AMPA receptors that are excited continuously allow for NMDA receptors to be relieved of their Mg2+ block, so Na+ and Ca2+ (especially) can enter the postsynaptic membrane.
  3. ca2+ signalling causes 3 outcomes:
    - changes in gene expression
    - structural alterations
    - allows for the phosphorylation and insertion of more AMPA channels.
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14
Q

NMDA receptors - Role in excitotoxicity

what is excitotoxicity in issues such as ischemia ?

ischemia is the cause of strokes

think NMDA, AMPA and mGluR receptors

A

excessive activation of NMDA, AMPA and mGluR receptors

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15
Q

NMDA receptors - role in excitotoxicity

Outline the features of the Large influx of Ca2+ in excitotoxicity that ultimately lead to cell death

think glutamate release, enzyme activation, NO and ROS, arachidonic acid and what the effects of arachidonic aacid lead to

A
  1. larger influx of Ca2+ leads to:
  • Increased glutamate release
  • Activation of proteases and lipases
  • Activation of NO synthase leading to activation of Reactive oxygen species
  • Release of arachidonic acid (which is used to make prostaglandins and leukotrienes), which leads to the production of free radicals and the inhibiton of glutamate uptake
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16
Q

GABA - inhibitory neurotransmission

how is GABA synthesised?

A

GABA is synthesised in neurons from glutamate via glutamic acid decarboxylase

Glutamate -> via glutamic acid decarboxylase -> GABA

17
Q

GABA – inhibitory neurotransmission

how is GABA uptaken?

think transporter proteins in neurons and astrocytes

A

GABA is uptaken by GAT (a GABA transporter protein), into neurons, via GAT1, and astrocytes, via GAT3

18
Q

GABA – inhibitory neurotransmission

what drug can inhibit GAT from uptaking GABA?

drug begins with T

A
  • can be inhibited by tiagabine
19
Q

GABA – inhibitory neurotransmission

what is GABA broken down by in astrocytes and what drug can inhibit GABA breakdown?

drug begins with V

A
  • broken down by GABA transaminase
  • GABA tansaminase can be inhibited by Vigabatrin
20
Q

GABA receptors

waht are the 2 GABA receptor subtypes and what type of receptors are each of them

A

GABA(A):
- ionotropic

and GABA(B):
- g-protein coupled receptor

21
Q

GABA receptors

how does GABA(A) act as an inhibitory receptor?

think Cl- and membrane potentials

A
  1. Cl- channels in GABA(A) have influx of Cl- ions, causing hyperpolarisation.
  2. this decreases membrane potential making cell less responsive
22
Q

GABA receptors

what drug is an agonist for GABA(B) receptors and what is it used for?

think muscles for second part

A
  • Baclofen
  • used as a muscle relaxant
23
Q

GABA - inhibitory neurotransmission

outline how GABA can activate both GABA(A) and GABA(B) receptors

think glutamate and GABA and what GABA is packaged in, think what action potential would do to this, what receptors GABA activates, what happens if GABA activates one receptor versus the other, what 2 things occur if GABA activates one of the receptors

A
  1. glutamate in pre-synaptic membrane converted to GABA via glutamic acid decarboxylase, which is then packaged into vesicles
  2. signal that travels down pre-synatic neurone causes vesicles containing GABA to release GABA into synaptic cleft
  3. GABA activates GABA(A) and GABA(B) receptors.
  4. GABA(A) receptor stimulation causes influx of Cl- ions due to opening of Cl- ion channels, decreasing membrane potential (more negative)
  5. GABA(B) receptor stimulation causes 2 things:
    - efflux of K+ ions due to opening of K+ ion channels
    - G protein on the receptor to inhibit Adenylate cyclase from converting ATP to cAMP.
24
Q

what is the important functional associations for GABA?

think sex and focus, learning, being nervous, the “Zzz” and buff gym bros

A
  • arousal and attention
  • memory formation
  • anxiety
  • sleep
  • muscle tone
25
Q

GABA agonists

waht are GABA agonists and antagonists good for and what is an example of GABA agonist and GABA antagonist?

think killing people for first part

A
  • very good poisons
  • GABA agonist: muscimol
  • GABA Antagonist: Bicuculline
26
Q

Benzodiazepines

what are Benzodiazepines and when is the only time they have effects?

think GABA receptors and GABA itself

A
  • Allosteric modulators at GABA(A) receptors
  • Only have effect at receptor if GABA is present
27
Q

Benzodiazepines

what are barbiturates and why are they not used anymore clinically?

A

barbiturates are also Allosteric modulators of GABA(A) receptors by enchancing the effect of GABA however not used anymore because it can have direct activation at higher doses, so stopped usaged to prevent overdose.

28
Q

Benzodiazepines

outline 5 clinical uses of Benzodiazepines

think muscles, anxiety ,involuntary muscle contraction, forgetting things and sleep

M.A.A.A.S

A
  • muscle relaxant
  • anxiolytic
  • anticonvulsant
  • Amnesia
  • sedative (form insomnia for examples)
29
Q
A

Yr 2: Pharmacology and Therapeutics (MGEM2016 UNUK) (20 decks)

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