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Both electrical and chemical synapses can rapidly change the membrane potential of a postsynaptic cell. In electrical synapses, there is a direct electrical coupling that allows current flow to flow between cells with only negligible delay. While this provides a speed and synchronization advantage, there is low plasticity and directionality within these synapses. In chemical synapses, on the other hand, a presynaptic neuron releases a neurotransmitter, which diffuses across a synapse and binds to the postsynaptic receptor, causing a postsynaptic potential. While generally slower than the electrical synapse, the advantage of chemical synapses is their high plasticity, which gives them the ability to integrate neuronal functions.
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The two types of acetylcholine receptors were first characterized many years ago by their pharmacological response. The acetylcholine receptor in skeletal muscle is stimulated by nicotine and was hence named a nicotinic receptor. The acetylcholine receptor on the heart muscle is stimulated by muscarine and was thus named a muscarinic receptor.
Serotonin acts via a G protein to upregulate cAMP, which activates cAMP-dependent protein kinases to phosphorylate the K+ channel. This leads to a decrease in the repolarizing K+ current, allowing Ca2+ channels to stay open longer, mediating a greater release of neurotransmitter per action potential.
Although the acetylcholine channel has similar permeabilities to Na+ and K+, most of the synaptic current underlying the EPSP is created by Na+ movement. This is because the driving force for Na+ to enter the cell is far greater than the driving force for K+ to leave the cell.
Whether the PSP is excitatory or inhibitory depends on what kinds of ions flow through the ion channels when the channels open. A particular neurotransmitter can act at different receptors, and they may produce similar effects or different effects.