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BRS Bioregulatory Systems > Neurotransmitetrs Andpharmacology > Flashcards

Neurotransmitetrs Andpharmacology Flashcards

1
Q

Synaptic transmission

A

Information transfer across the synapse requiring the release of neurotransmitters from synaptic vesicles and their interaction with postsynaptic receptors

Electrical transmission through first neurone then chemical neurotransmission at synapse then electrical transmission at second neurone

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2
Q

4 characteristics of synaptic transmission

A
  • Rapid timescale
  • Diversity
  • Plasticity (brain can adapt)
  • Learning and memory
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3
Q

Structure of neurons

A
  • Soma (cell body)- involved in info reception through dendrites (extensions of soma)
  • Dendrites have spines
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4
Q

Purpose of spines on dendrites

A

Protein molecules that increase the SA for information reception

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5
Q

What neuronal structure integrates all the information coming into a neurone?

A

Soma (cell body)

  • Causes neurotransmitter release from synaptic terminal for the communication between neurones
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6
Q

Which specialised structures is neurotransmission restricted to?

A

Synapses
Consist of - Presynaptic nerve terminal
- Synaptic cleft → gap of around 20-100 nm
- Postsynaptic region (dendrite or cell soma)

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7
Q

What is the single-most important excitatory neurotransmitter in the brain?

A

Glutamate

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8
Q

What is the single-most important inhibitory neurotransmitter in the brain?

A

GABA

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9
Q

Where is glycine most active and is it excitatory or inhibitory?

A

spinal cord & brainstem

inhibitory

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10
Q

List 3 types of molecules that can be neurotransmitters and include examples of each

A

Amino acids - glutamate, gamma-aminobutyric acid (GABA), glycine

Amines - noradrenaline and dopamine

Neuropeptides - opioid peptides

  • These vary in abundance from nM to mM CNS tissue concs
  • May mediate rapid (microsecond to ms) or slower effects (secs/minutes/hours)
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11
Q

What does neurotransmitter release need

A

Calcium influx and RAPID transduction (electromechanical transduction - links the Ca2+ influx with NT release)

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12
Q

Describe what happens when a CNS synapse is activated by the arrival of an action potential+ (Outline process of neurotransmitter release)?

A

Arrival of action potential - spreads across pre-synaptic nerve terminal

Depolarisation of whole terminal (Na+ influx followed by a K+ efflux)

Activates VGCC to open allowing Ca2+ influx into presynaptic terminal (down its concentration gradient)

  • NT is loaded into vesicles
  • Vesicles then primed, then fuse with membrane

Activates exocytotic release of neurotransmitter into synaptic cleft ( → diffuses across synaptic cleft and makes contact with receptors (in this case excitatory receptors) on post-synaptic terminal

Depolarisation of post-synaptic terminal leading to generation of another action potential

Inactivation of neurotransmitter as it is returned to the pre-synaptic terminal back into its vesicle where it can be reused

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13
Q

Describe the 2 methods by which the neurotransmitter can be inactivated after depolarising the post-synaptic terminal?

A

Re-uptake of neurotransmitter via a protein transport channel, where it’s reloaded into synaptic vesicles

Enzymatic degradation within the synaptic cleft (e.g. acetylcholine broken down by acetylcholinesterase (which is bound to basolateral membrane in synaptic cleft))

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14
Q

What type of proteins on the vesicle and presynaptic membrane enable fusion and exocytosis of NT?

A

SNARE proteins (vesicular proteins e.g. synapsin, synaptobrevin, snap25)

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15
Q

What are vesicular proteins targets for?

A

Neurotoxins
Neurotoxin alpha latrotoxin stimulates neurotransmitter releas until depletion of NT causing muscular paralysis

Zn2+ dependant endopeptides inhibit neurotransmitter release

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16
Q

Tetanus toxin

A

Causes spasms and paralysis as it inhibits release of GABA and glycine (both inhibitory NT in CNS)

Produced by Clostridium tetani

17
Q

Botulinum toxin causes

A

Flaccid paralysis (due to complete muscle relaxation)

Cleaves peptide bonds of vesicular proteins leading to inactivation hence docking, fusion and release of NT can’t occur
Prevents exocytosis

18
Q

2 main receptors on post synaptic membranes

A

Ion channel linked receptors
G protein coupled receptor

19
Q

Ion channel linked receptors

A
  • Give fast response (microseconds to ms)
  • mediate all fast excitatory and inhibitory transmission
  • Na+ channel linked receptors responsible for depolarisation, thus excitatory transmission
  • Cl- channel linked receptors responsible for hyperpolarisation, thus inhibitory transmission

Eg - CNS:
- glutamate receptor (GluR- linked to Na+ channel)
- GABA receptors (GABAR- linked to Cl- channels)
- glycine receptors (GlyR- linked to Cl- channels)
- NMJ:
- ACh acts at nicotinic cholinergic receptors (nAChR- linked to Na+ channels) on skeletal muscle fibres

20
Q

G protein coupled receptor

A
  • Give slow response (secs/mins)
  • NT binding causes binding of receptor to G protein which binds to effector

Eg - CNS & PNS → ACh at muscarinic receptors (e.g. in heart), DA, NA, serotonin (5HT) and neuropeptides like enkephalin

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21
Q

What post-synaptic potentials do we see following excitation vs inhibition, and explain how each occurs and give examples of each?

A
  • For excitatory NT receptors → we see excitatory postsynaptic potential (EPSP)- Na+ influx causes increase in Em from resting potential (-65mV) to around -50/-40mV → this then returns to normal over a few ms
  • e.g. Glutamate
  • For inhibitory NT receptors → we see inhibitory postsynaptic potential (IPSP)- Cl- influx causes decrease in Em from resting potential to more negative (hyperpolarised) → this then returns to normal over a few ms
  • e.g. GABA
22
Q

2 types of glutamate receptors

A

AMPA receptors

  • Fast excitatory synapses
  • Permeable to Na+ ions

NMDA receptors

  • Slow component of excitatory transmission
  • ## Permeable to Na+ and Ca2+ ions
23
Q

Outline the process that occurs at an excitatory glutamate synapse?

A

1) Glutamate synthesised from glucose via TCA cycle and transamination in presynaptic terminal

2) Loaded into vesicles, AP comes, depolarises membrane, Ca2+ influx, stimulates exocytotic release of Glu into synaptic cleft, Glu diffuses across

3) Glu reversibly binds to postsynaptic receptors linked to ion channels (AMPA and NMDA) which produces response

4) Glu inactivated by reuptake into presynaptic nerve terminal to be reused, but also rapid uptake by glial cells via excitatory amino acid transporters (EAATs) on their surface

5) Once in glial cell, glutamate converted to glutamine by glutamine synthetase

6) Glutamine released by glial cells and can be pumped back into presynaptic terminal to be recycled into glutamate → called ‘glutamine-glutamate cycle’

24
Q

EEG

A

Measures electrical activity in brain

25
Q

Abnormal firing associated with excess glutamate causes

A

Seizures
Shown by spikes in eeg

26
Q

What is epilepsy characterised by?

A

Recurrent seizures due to abnormal neuronal excitability
Due to excess glutamate in synapse

27
Q

Outline the process that occurs at an inhibitory GABA synapses?

A

1) GABA synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD) in presynaptic terminal

2) AP comes, depolarises membrane, Ca2+ influx, exocytosis of GABA into synaptic cleft, diffusion across cleft

3) GABA reversibly binds to post-synaptic GABA-A receptors (linked to Cl- ion channels, Cl- influx into postsynaptic cell, hyperpolarisation) → this is inhibitory effect

4) Rapid uptake of GABA by GABA transporters (GATs) into presynaptic terminal to be reused

OR GABA taken up by glial cells and modified by GABA-transaminase (GABA-T) to succinic semialdehyde (this process occurs in glial cells & in GABA presynaptic terminals)

28
Q

What 4 properties do drugs facilitating GABA transmission have?

A

Antiepileptic

Anxiolytic

Sedative

Muscle relaxant

29
Q

How many subunits does the GABA A receptor have?

A

5 (pentameric organisation)

30
Q

Glutamate to gaba

A

Glutamate decarboxylase

BRS Bioregulatory Systems (54 decks)

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