Drugs in Neurophysiology
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Anesthetics inhibit an influx of sodium ions, preventing the propagation of an action potential. This means that there is no movement of sodium ions and then no voltage change at the voltage gated sodium channels.
Prolonged presence of serotonin in the synaptic cleft increases postsynaptic neuron activity because there is an abundance of serotonin in the cleft that can bind with the postsynaptic neuron.
Alcohol causes an increase in the release of the neurotransmitter GABA, which opens Cl channels causing an influx of negative ions, lowering the membrane potential and increasing IPSPs.
D.C.A.E.B
Positive. Sodium. Serotonin. GABA. Hyperpolarization. Less.
Just draw it
No because if voltage gated channels aren’t open then that means that there wasn’t enough sodium ions to change the resting potential of the cell membrane and propagate an action potential, and an action potential needs to be propagated for neurotransmitters to release. Local anesthetics will cause this effect.
This would generate an EPSP because because it would change the membrane potential and depolarize the soma, leading to an action potential. SSRIs would have this effect because SSRIs bind to sodium ions and then are more concentrated in the synaptic cleft and available to bind to the ligand gated channels in the cell membrane.
If ligand-gated chloride channels opened it would result in an IPSP because chloride has a negative charge and would hyperpolarize the cell lower membrane potential. Alcohol is the drug that produces this effect because it causes the release of the neurotransmitter GABA which opens ligand gated Cl channels.
Bonus: One example of manipulating neurotransmission for medical benefits is the use of SSRIs because they increase the amount of serotonin in synaptic clefts to be used by the postsynaptic neuron and cause an improvement in mood. But, SSRIs cause an increase of the presence of serotonin in the body as a whole, not just the brain which can lead to gastrointestinal issues & effects to libido.