pharmacology Flashcards
what is the role of Ca2+ in synaptic transmission?
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)
what happens to the neurotransmitter in the synaptic cleft?
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
what are the 3 ways of inactivating a neurotransmitter?
- diffusion: lost in inter-cellular space
- enzymatic degradation breaking down neurotransmitter
- re-uptake: recycled in either neuron (saves synthesis resources)
what do substances influence in the synaptic sequence?
- propagation of action potential
- release of transmitter
- modulate how transmitter interacts with post-synaptic receptors
- modulating inactivation and recylcing
example of drug which interferes with signals going through the axon?
TTX - blocks sodium channels in the axon’s membrane
example of 2 substances which interefere with release of transmitter and consequences?
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
example of an excitatory transmitter?
glutamate
example of an inhibitory transmitter?
GABA
example of mainly excitatory but also inhibitory transmitter?
acetylcholine
dopamine
example of neurotransmitters classified by structure?
e.g adrenaline and serotonin known as monamines as contain single amino group
example of substance which can enhance the release of transmitter?
amphetamine
enter dopamine releasing neuron through membrane or binding to dopamine transporter
facilitates release of dopamine from vesicles when they fuse to membrane
what are thet VTA and nucleus accumbens involved in?
pleasure, reward and motivation
dopaminergic pathways
example of substance which can alter how transmitter interacts with receptors?
curare occupies acetylcholine’s receptors in excitatory synapses
blocks them causing paralysis therefore antagonist
used as anaesthetic agent
what are antagonists?
blocks receptor at post synaptic cell and prevents neurotrasmitter from binding with it and opening the channels
reduces effects
what are agonists?
bind with receptor at post synaptic site but do open the channel hence increasing its effect
(mimics function of e.g heroin mimicing endorphines)
what is anandamide involved in?
emotion, pain, appetite and memory
marijuana contains THC which is an agonist of anandamide
example of drug influencing transmitter inactivation and recycling?
cocaine blocks the transporter (aiding reuptake into original cell) of noradrenaline and dopamine
interfering with re-uptake and boosting their effect
chocolate as a psychoactive substance?
contains small amounts of anandamide and phenylethylamine
in such small amounts that don’t cause noticeable effects
coffee as a psychoactive substance?
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)
alcohol as a psychoactive substance in low doses?
low doses: agonist of GABA (nhibitory synapses) so increases effect leading to relaxation
stimulates dopamine release which stimulates nucleus accumbens so feelings of pleasure
alcohol as a psychoactive substance in moderate doses?
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
what can anxiety disorders be characterised as?
and how may they be treated in this way?
deficits in GABA-ergic transmission
so benzodiazepines (GABA agonists) reduce anxiety
what is a non-competitive and competitive agonist/antagonist?
non- doesn’t bind to same receptor sites as the transmitter
competitive - bind to the same sites in the ion channel as the transmitter
what is depression associated with?
and how was it treated in this way?
but problems with treatment?
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)
what is the current treatment for depression?
serotonin most closely linked monoamine to depression
SSRIs inhibit transporter of serotonin without effecting other neurotransmitters (fewer side effects)
what is schizophrenia associated with?
how is it treated?
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
what does the opposite of neuroleptics?
how?
what are the effects?
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)
