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Synapses
An action potential reaches the presynaptic neuron, causing Ca²⁺ channels to open and Ca²⁺ to enter.
This triggers vesicles to release NT into the synaptic cleft.
The NT binds to receptors on Na⁺ channels of the postsynaptic membrane, allowing Na⁺ in and possibly triggering a new action potential.
Enzymes then break down the NT, resetting the synapse for the next signal.
drugs that are stimulates by an agonist
increase NT synthesis & release
bind to receptors & activate them
stop NT from degrading or being taken up
drugs that are repressed by an antagonist:
blocking NT synthesis & release
blocks receptors & stops NT binding
nicotine (stimulant)
binds to ACh receptors on the postsynaptic membrane. It triggers an action potential but temporarily desensitizes the receptor to further stimulation. Nicotine also increases heart rate, blood pressure, and dopamine release.
lidocaine (anesthetics)
blocks voltage Na+ channels on the post synaptic neuron
stops action potential
no pain is felt
cobra venom (represent)
binds to post-synaptic receptors
stops transmission across synapses including at the NMJ
muscles don’t contract = paralysis