2.5: Neurotransmitters & pharmacology Flashcards

1
Q

What is synaptic transmission?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List 4 characteristics of synaptic transmission

A

Rapid timescale
Diversity
Plasticity
Learning and memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

4 basic structures of neurones

A

Dendrites
Soma
Axon
Synaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Purpose of spines present on surface of dendrites

A

Protein molecules that increase the surface area for information reception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What neuronal structure integrates all information coming into a neurone

A

Soma (cell body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 steps that occur when a dendrite of one neurone receives an electrical impulse form another neurone

A

Information reception at dendrites
Integration (occurs at soma)
Rapid transfer (AP) - impulse passed along axon towards synaptic terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What type of neurotransmission occurs at the synapse

A

Chemical neurotransmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What structures is neurotransmission restricted to?

A

Synapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 things synapse consists of

A

Presynaptic nerve ending/terminal
Gap(synaptic cleft) ~ 20-100nm
Postsynaptic regions (dendrite or cell soma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 stages of synaptic transmission

A

Biosynthesis, packaging and release of neurotransmitter stored in vesicles
Receptor action- activation of post-synaptic receptors
Inactivation - NT inactivated once it’s activated receptors on post synaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 types of molecules that can be neurotransmitters + examples

A

Amino acids - glutamate, gamma-aminobutyric acid (GABA)
Amines - noradrenaline and dopamine
Neuropeptices -opioid peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Single-most important excitatory neurotransmitter in the brain

A

Glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Single-most important inhibitory neurotransmitter in the brain

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is glycine most active (2)
Is glycine excitatory or inhibitory?

A

Spinal cord and brain stem
Inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 methods by which neurotransmitters are returned to the pre-synaptic terminal

A

Re-uptake via protein transport channel
Enzymatic degradation within synaptic cleft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the source of neurotransmitter

A

Synaptic vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Outline process of neurotransmitter release

A

Membrane depolarisation lead to opening of Ca2+ channels
Ca2+ influx leading to docking of synaptic vesicles onto pre-synaptic membrane
Neurotransmitter released by exocytosis in synaptic cleft
Vesicle buds off and recycles forming new vesicles that can be reused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 things required for neurotransmitter release

A

Calcium influx
Rapid transduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

SNARE proteins (vesicular proteins e.g. synapsin)

20
Q

Vesicular proteins are targets for

A

Neurotoxins (esp. those that interfere with NT release process)

21
Q

What does alpha larotoxin (neurotoxin) do?
(From black widow spider)

A

Stimulate NT release until depletion of NT leading to muscular paralysis

22
Q

Function of Zn2+ dependent endopeptidases

A

Inhibit transmitter release

23
Q

What does tetanus toxin cause ?
What bacteria produce it

A

Spasms and paralysis as GABA and glycine inhibited

Produced by Clostridium tetani

24
Q

What does botulinum toxin cause and how does this come about?

A

Flaccid paralysis - complete muscle relaxation

Cleaves peptide bonds of vesicular proteins leading to inactivation - docking, fusion, release of NT cannot occur

25
Q

What bacteria produces botulinum toxin (one of most powerful toxins)

A

Clostridium botulinum

26
Q

How can drug toxicity be measured

A

Minimum dosage required to kill a mouse

27
Q

What repossessed do ion channel linked receptors mediate?

A

All fast excitatory and inhibitory transmission

28
Q

What type of responses do G-protein coupled receptors mediate?

A

SLOWer than ion channel linked receptors

29
Q

What can the effectors of the response generated by G-protein coupled receptors be?

A

Enzymes or ion channels

30
Q

2 examples of responses where ion channel linked receptors are used

A

CNS - glutamate, GABA
NMJ - ACh at nicotinic receptors

31
Q

Give examples of responses where G-protein coupled receptors are used

A

CNS and PNS - ACh at muscarinic receptors (heart)
Dopamine, noradrenaline, serotonin and neuropeptides

32
Q

What does opening of Na+ channels via a glutamate molecule do to postsynaptic membrane potential

A

Increase for short time
repolarisation

33
Q

What postsynaptic potential does an inhibitory NT (e.g GABA A) cause ?

A

IPSP ( inhibitory postsynaptic potential) caused by GABA A receptor —> Cl- influx
hyperpolarisation

34
Q

2 types of ion-channel linked glutamate receptors and what they mediate

A

AMPA - FAST excitatory synapses, only Na+ permeable

NMDA - SLOW component of excitatory transmission, coincidence detectors which underline learning mechanisms - permeable to Na+ and Ca2+ (HIPPOCAMPUS high density )

35
Q

Outline the process that occurs at an excitatory glutamate synapse

A

1) Glutamate synthesised from glucose via TCA cycle and transamination
2)Loaded into vesicles- released into synaptic cleft via exocytosis
Glutamate reversibly binds postsynaptic receptors (AMPA and NMDA)
3) Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)
OR
4) Glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells

36
Q

What does an EEG (electroencephalogram) measure

A

Electrical activity in brain

37
Q

Abnormal cell firing associated with excess glutamate leads to

A

Seizures

Spikes on EEG

38
Q

What is epilepsy characterised by?

A

Recurrent seizures due to abnormal neuronal excitability

39
Q

Process that occurs at an inhibitory GABA synapse

A

1) GABA synthesised (pre-synaptic terminal) by decarboxylation of glutamate by glutamic acid decarboxylase [GAD]

2) GABA Reversibly binds to post-synaptic receptors (Cl- channels open, influx leading to hyperpolarisation)

3) Rapid uptake of GABA by GABA transporters (GATs)
OR
4) GABA enzymatically modified by GABA-T (GABA transaminase) to succinic semialdehyde (glial cells and GABA nerve terminals)

40
Q

6 drugs facilitating GABA transmission.

A

Barbiturates
Benzodiazepines
Steroids
Convulsants
Zn 2+
Ethanol

41
Q

4 properties of drugs facilitating GABA transmission

A

Antiepileptic
Anxiolytic
Sedative
Muscle relaxant

42
Q

How many subunits does the GABA A receptor have?

A

5 - pentameric

43
Q

4 examples of neurotoxins

A

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

44
Q

Two types of neurotransmitter receptors

A

Ion channel-linked receptors
G-protein-coupled receptors

45
Q

Two types of ion channel linked receptors

A

GABA receptor - Na+
glutamate receptor - Cl-