Neurotransmission

Question 1

What is synaptic transmission?

Answer 1

Information transfer across the synapse requires release of neurotransmitters and their interaction with postsynaptic receptors

Question 2

What is the general process of synaptic transmission?

Answer 2

1. Transmitter released from 1st cell
2. Synaptic activation of 2nd cell
3. Signal integration and signal conduction by 2nd cell
4. Signal transmitted to effectors or subsequent neurones

Question 3

What are the 3 main processes of synaptic transmission?

Answer 3

1. Biosynthesis, packaging and release of neurotransmitter
2. Receptor action at post synaptic terminal
3. Inactivation of neurotransmitters

Question 4

What ion is neurotransmitter dependent on?

Answer 4

Calcium 2+

Question 5

What is the process of neurotransmitter release?

Answer 5

1. Membrane depolarisation
2. Ca2+ channels open
3. Ca2+ influx
4. Vesicle fusion with membrane
   S. vesicle exocytosis

Question 6

What allows for the rapid transduction?

Answer 6

Special proteins on the vesicle and pre-synaptic membrane enable fusion & exocytosis

Question 7

What is a vesicular protein?

Answer 7

membrane protein that regulates or facilitates the movement of specific molecules across a vesicle’s membrane

Question 8

What can reticular proteins be targets for?

Answer 8

Neurotoxins

Question 9

What are some examples of vesicular proteins + pre-synaptic proteins?

Answer 9

Vesicular:
→ SNARE proteins
→ synaptobrevin
Pre-synaptic:
→ syntaxin
→ SNAP25

Question 10

What are some examples of neurotoxins and their effects?

Answer 10

• Alpha latrotoxin (from black widow spider) stimulates transmitter release to depletion
• Zn2+ dependent endopeptidases inhibit transmitter release
• Tetanus toxin C tetani causes paralysis
• Botulinum toxin C botulinum causes flaccid paralysis

Question 11

What is the purpose of ion channel-linked receptor?

Answer 11

• FAST response (msecs)

* Mediate all fast excitatory and inhibitory transmission

Question 12

What are some examples of ion channel-linked receptors?

Answer 12

• nicotinic cholinergic receptors (nAChR)
• glutamate (GluR)
• gamma amino butyric acid (GABAR)
• glycine (GlyR) receptors

Question 13

What is the purpose of G-protein-coupled receptors?

Answer 13

• Slow response (secs/mins)

* uses effectors (enzymes or channels) to get the job done

Question 14

What neurotransmitters do ion channel-linked receptors interact with?

Answer 14

CNS: Glutamate, y-aminobutyric acid
NMJ: Acetylcholine (ACh) at nicotinic receptors

Question 15

What neurotransmitters do G-protein-coupled receptors interact with?

Answer 15

CNS + PNS: Ach at muscarinic receptors, dopamine, noradrenaline, serotonin + neuropeptides

Question 16

What neurotransmitter can produce an excitatory post synaptic potential? How?

Answer 16

Glutamate → causes influx of Na ions → causes post synaptic membrane depolarisation

Question 17

What neurotransmitter can produce an inhibitory post synaptic potential? How?

Answer 17

GABA or glycine → influx of Cl ions → causes hyperpolarisation of post synaptic membrane

Question 18

How does an excitatory CNS synapse work?

Answer 18

1. Glutamate is synthesised from glucose in the Krebs cycle & transamination
2. Glutamate reversibly binds post-synaptic receptors (linked to ion channels)
3. Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)
4. Glutamate is enzymatically modified by glutamine synthetase to glutamine in glial cell

Question 19

What are 2 examples of glutamate receptors?

Answer 19

• AMPA

* NMDA

Question 20

What are AMPA receptors?

Answer 20

• Majority of FAST excitatory synapses

* Rapid onset, offset and desensitisation

Question 21

What are NMDA receptors?

Answer 21

• Slow component of excitatory transmission

* Serve as coincidence detectors which underlie learning mechanisms

Question 22

How does an inhibitory CNS synapse work?

Answer 22

1. GABA is formed by decarboxylation of Glutamate by glutamic acid decarboxylase (GAD)
2. GABA reversibly binds to post-synaptic receptors (linked to ion channels)
3. Rapid uptake of glutamate by GABA transporters (GATs)
4. GABA is enzymatically modified by GABA- transaminase to succinate semialdehyde in glial cell

Question 23

What are 2 mechanisms of neurotransmitter inactivation?

Answer 23

° Reuptake into pre-synaptic terminal to be reused

° Enzymatic degradation in the synaptic cleft

Question 24

How can normal brain activity be described?

Answer 24

Non-synchronous

Question 25

How can brain electrical activity be described during seizures?

Answer 25

group of neurones begin firing in an abnormal, excessive, + synchronised manner, resulting in a wave of depolarisation.

Question 26

What causes the wave of depolarisation in seizures?

Answer 26

• influx of Ca2+ from outside of the cell → extended opening of Na+ channels + repetitive action potentials.
→ hyperpolarisation facilitated by γ-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the type of cell.

Question 27

What is abnormal cell firing in seizures associated with?

Answer 27

Excess glutamate in the synapse

Question 28

What can excess glutamate in synapses cause physically?

Answer 28

Convulsions

Question 29

What machine can be used to measure brain electrical activity?

Answer 29

Electroencephalography (EEG)

Question 30

What drugs facilitate GABA transmission?

Answer 30

• Anti-epileptic
• Anxiolytic
• Sedative
• Muscle relaxants