Neurotransmitters

Question 1

What is the speed of chemical neurotransmission?

Answer 1

Takes 2ms to pass on AP over a 20-100 nm synapse

Question 2

What is an assymetrical synapse?

Answer 2

Dense pre-synaptic neurone contains vesicles. Post synaptic neurone has no vesicles but does have receptors

Question 3

What do neurotransmitters do?

Answer 3

Provide diversity in transmitters and receptors, mediating rapid (us-ms) or slower (ms) effects and varying in abundance from mM to nM in CNS

Question 4

Give 3 examples of groups of neurotransmitters

Answer 4

Amino acids
Amines
Neuropeptides

Question 5

Give examples of amino acids that are used as neurotransmitters

Answer 5

Glutamate (CNS excitatory NT)
Gamma amino butyric acid (GABA - CNS inhibitory NT)
Glycine (tends to be found in spinal cord)

Question 6

Give examples of amines used as neurotransmitters

Answer 6

Noradrenaline

Dopamine

Question 7

Give examples of neuropeptides

Answer 7

Opiods

Question 8

How are neurotransmitters prepared for rapid release?

Answer 8

Vesicles filled with NT are docked in the synaptic zone and “primed” for release, with vesicle proteins to allow fusion and rapid release due to Ca2+ sensor activation

Question 9

What is required for the rapid release of neurotransmitters?

Answer 9

• NT vesicles docked on presynaptic membrane
• protein complex formation between vesicle and membrane and cytoplasmic proteins to allow rapid response to Ca2+
  ATP and vesicle recycling

Question 10

What are examples of neurotoxins?

Answer 10

Tetanus toxin: C tetani
Botulinum toxin: C botulinum
Zn2+ dependent endopeptidases
Alpha latrotoxin

Question 11

What does C tetani do?

Answer 11

Tetanus toxin: C tetani causes paralysis due to tetanic contractions

Question 12

What does C botuliunum do?

Answer 12

Botulinum toxin: C botulinum membrane and vesicular proteins causing flaccid paralysis

Question 13

What do Zn2+ dependent endopeptidases do?

Answer 13

Inhibit transmitter release

Question 14

What does Alpha latrotoxin do?

Answer 14

Produced by black widow spider to stimulate transmitter release to depletion

Question 15

What is the difference in speed of ion channel receptors and G protein coupled receptors?

Answer 15

Ion channel receptors are faster (m-secs) compared to G protein coupled receptors (secs/min)

Question 16

What do ion channel receptors do?

Answer 16

Mediate all fast excitatory/inhibitory transmission

Question 17

What do g protein coupled receptors do?

Answer 17

Effectors can be enzymes such as adenyl cyclase/phospholipase C or channels such as Ca2+ and K+

Question 18

Where are ion channel receptors found?

Answer 18

CNS: glutamate/GABA
NMJ: ACh @ nicotinic

Question 19

Where are G protein coupled receptors found?

Answer 19

CNS/PNS: ACh at muscarinic receptors, dopamine, noradrenaline, 5-hydroxytryptamine, neuropeptides eg enkephalin

Question 20

Where is glutamate found and what does it do?

Answer 20

Found on dendritic cells

Opens Na+ channels and cause an excitatory response - depolarisation

Question 21

What do GABA receptors do? Where are they found

Answer 21

Open chloride channels therefore causing hyperpolarisation - inhibitory as raising threshold for response and typically found on soma

Question 22

What do glycine receptors do?

Answer 22

Produce an IPSP by opening chloride ion channels

Question 23

Give two examples of glutamate receptors?

Answer 23

AMPA receptor

NMDA receptor

Question 24

What does the AMPA glutamate receptor do?

Answer 24

Rapid onset, offset

fast excitatory response to open sodium ion channels on already depolarised cells

Question 25

What does the NMDA glutamate receptor do?

Answer 25

Opens sodium and calcium ion channel to serve as a coincidence detector - changes response to AMPA with calcium induced phosphorylation and changes of transcription to promote synapse formation

Question 26

Synthesis and affects of glutamate EPSP

Answer 26

1. produced from alpha ketoglutarate from TCA cycle 2. stored in vesciles with fuse on calcium influx 3. binding to GLURs on post synaptic cleft occurs in the pre -synaptic neurone and to glial cells using excitatory amino acid transporters 5. glutamate converted into glutamine using glutamine synthetases in glial cells

Question 27

What is excess glutamate in the synapses associated with?

Answer 27

Abnormal cell firing/seizures

Question 28

What is a treatment for epilepsy?

Answer 28

Damping down excitatory activity by facillitating inhibitory transmission (targeting GABA synapses)

Question 29

What drugs facilitate GABA transmission?

Answer 29

Anti epileptic sedatives that also relax muscle

Question 30

What do GABA receptors look like?

Answer 30

Pentameric structure with binding sites for steroids, GABA, barbiturates, benzos, ethanol, zinc and convulsants

Question 31

How is GABA made?

Answer 31

Produced from glutamate using glutamic acid decarboxylase to remove carboxylic acid group

Question 32

What are the effects of GABA?

Answer 32

Binds with GABA A receptors to hyperpolarise post-synaptic membrane, increasing excitation threshold (IPSP) GABA transporters on glial cells take up cleft GABA to allow conversion to succinate semialdehyde using GABA transaminase