pharmacology Flashcards

1
Q

what is the role of Ca2+ in synaptic transmission?

A

action potential reaches axon terminal and opens voltage-gated Ca2+ channels

higher conc outside so gradient pushes into cell

interact with neurotrasmitter vesicles pushing them towards the membrane (so they can be released into synaptic cleft)

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

what happens to the neurotransmitter in the synaptic cleft?

A

binds to receptors in postsynaptic neuron :
if ion channels then open when neurotransmitter interacts with them
if not ion channels, interact with specific ion channels and eventually open them

results in post-synaptic potential

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

what are the 3 ways of inactivating a neurotransmitter?

A
  1. diffusion: lost in inter-cellular space
  2. enzymatic degradation breaking down neurotransmitter
  3. re-uptake: recycled in either neuron (saves synthesis resources)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do substances influence in the synaptic sequence?

A
  1. propagation of action potential
  2. release of transmitter
  3. modulate how transmitter interacts with post-synaptic receptors
  4. modulating inactivation and recylcing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

example of drug which interferes with signals going through the axon?

A

TTX - blocks sodium channels in the axon’s membrane

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

example of 2 substances which interefere with release of transmitter and consequences?

A

tetanospasmin toxin interferes with vesicles of transmitter GABA

reduces amount of gaba released into synapse

imbalance between excitation and inhibition neural signals

strong muscle contractions

also botulinum toxin used in BOTOX by reducing effectiveness of meuromuscular junction in facial muscles

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

example of an excitatory transmitter?

A

glutamate

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

example of an inhibitory transmitter?

A

GABA

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

example of mainly excitatory but also inhibitory transmitter?

A

acetylcholine

dopamine

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

example of neurotransmitters classified by structure?

A

e.g adrenaline and serotonin known as monamines as contain single amino group

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

example of substance which can enhance the release of transmitter?

A

amphetamine
enter dopamine releasing neuron through membrane or binding to dopamine transporter

facilitates release of dopamine from vesicles when they fuse to membrane

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

what are thet VTA and nucleus accumbens involved in?

A

pleasure, reward and motivation

dopaminergic pathways

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

example of substance which can alter how transmitter interacts with receptors?

A

curare occupies acetylcholine’s receptors in excitatory synapses

blocks them causing paralysis therefore antagonist

used as anaesthetic agent

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

what are antagonists?

A

blocks receptor at post synaptic cell and prevents neurotrasmitter from binding with it and opening the channels

reduces effects

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

what are agonists?

A

bind with receptor at post synaptic site but do open the channel hence increasing its effect
(mimics function of e.g heroin mimicing endorphines)

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

what is anandamide involved in?

A

emotion, pain, appetite and memory

marijuana contains THC which is an agonist of anandamide

17
Q

example of drug influencing transmitter inactivation and recycling?

A

cocaine blocks the transporter (aiding reuptake into original cell) of noradrenaline and dopamine

interfering with re-uptake and boosting their effect

18
Q

chocolate as a psychoactive substance?

A

contains small amounts of anandamide and phenylethylamine

in such small amounts that don’t cause noticeable effects

19
Q

coffee as a psychoactive substance?

A

caffeine competes with adenosine for its receptors

so blocks adenosine and reduces its inhibitory effect

also increases glucose metabolism in cell so increases fuel levels (depeletes sources that already exist)

20
Q

alcohol as a psychoactive substance in low doses?

A

low doses: agonist of GABA (nhibitory synapses) so increases effect leading to relaxation

stimulates dopamine release which stimulates nucleus accumbens so feelings of pleasure

21
Q

alcohol as a psychoactive substance in moderate doses?

A

moderate: increases release of endorphines
high: binding to GABA leads to powerful inhibition and sedation

very high: destruction of cell membranes so brain cell death

22
Q

what can anxiety disorders be characterised as?

and how may they be treated in this way?

A

deficits in GABA-ergic transmission

so benzodiazepines (GABA agonists) reduce anxiety

23
Q

what is a non-competitive and competitive agonist/antagonist?

A

non- doesn’t bind to same receptor sites as the transmitter

competitive - bind to the same sites in the ion channel as the transmitter

24
Q

what is depression associated with?

and how was it treated in this way?

but problems with treatment?

A

reduced monoamine transmission (dopamie, serotonin and noradrenaline)

MAO inhibitors as breaks down these monoamines

tricyclic antidepressants inhibit transporter of these monoamines

(both treatments increase levels which effects many other systems so many side effects)

25
Q

what is the current treatment for depression?

A

serotonin most closely linked monoamine to depression

SSRIs inhibit transporter of serotonin without effecting other neurotransmitters (fewer side effects)

26
Q

what is schizophrenia associated with?

how is it treated?

A

surplus of dopamine

neuroleptics block transmission of dopamine by binding to dopamine receptors without opening ion channels (dopamine antagonists)

but too little dopamine can lead to parksinsons

27
Q

what does the opposite of neuroleptics?

how?

what are the effects?

A

cocaine, metamphetamines and amphetamines

reduce transport of monoamine neurotransmitters back into original cell

attach to enzymes which break down neurotransmitters

so boost neurotransmitter transmission (can induce schizophrenia symptoms)