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Chemical synapses comprise of 3 main parts: the presynaptic neuron (in all it's vessicles and glory), the synaptic cleft, and the post synaptic neuron. From basic neurobiology, we know that the presynaptic neuron fires, and the post synaptic neuron takes it like a bitch.The main function of a synapse is to cause changes in the membrane potential of the post synaptic neuron. But what is the mechanism behind it? It largely has to do with membrane carriers. Before a synapse can fire, it has to be depolarised enough to reach threshold, so that a large proportion of ion gate channels open, ions swoop in, change the action potential and trigger the secretion of neurotransmitters. But let's start from the beginning. Membrane carriers (ion channels) that sit in between the lipid bilayer of the neuronal cell membrane allow and control the ebb and flow of certain cations, anions and proteins. Some ion channels are gated, opening and closing in response to a change in voltage (voltage-gated channels) or in response to certain neurotransmitters (ligand-gated channels). The relative internal environment inside a neuron is slightly more negatively charged than its external environment. At rest, this difference of charge, or action potential, sits at about - (50 - 80) mV. At this stage, the diffusion into and out of the cell by K+ is at equilbrium. However, the cell's membrane is not perfectly impermeable to Na+, so Na+ slowly diffuses in. If this were uncontrolled, the internal environemnt would depolarize until it reached zero, and the neuron would be unable to fire. The sodium-potassium pump actively pumps out Na+ and pumps in K+, so the equilibrium is maintained. However, if the influx of Na+ exceeds that of the capacity of the sodium-potassium pump to expel the Na+, then the inside of the cell slowly depolarises. Once the internal environment of the cell reaches -40mV, then threshold is reached. At this point, voltage-gated Na+ channels open, and a rapid influx of Na+ changes the action potential of the cell to around +40 mV. The Na+ channels close in response to the change in action potential. K+ channels open tot he same change in action potential, increasing the cell membrane's permeabilty to K+. This repolarises, and hyperpolarises the cell. At this more, all the gated channels close, and the cell returns to it's resting potential. This action potential travels down the interior of the presynaptic axon, until it reaches the presynaptic terminal. In response to the sudden depolarisation, voltage-gated calcium channels open and Ca2+ enter the axon terminal. The Ca2+ causes synaptic vessels (filled with neurotransmitter goodness) to fuse with the pre-synaptic membrane, and burst, releasing it's gooey-goodness into the synaptic cleft. The post synaptic membrane have receptor sites specifically designed for particularly neurotransmitters. Depending on the neurotransmitter released, the receptor-neurotransmitter complex either indirectly or directly opens certain ligan-gated ion channels in the post synaptic membrane. For example, Ach is a neurotransmitter that can have either excitatory and inhibitory effects depending on the synapse. At an excitatory synapse, Ach will cause ligand-gated channels to open for Na+ and K+ ions. This causes depolarisation in the postsynaptic cell, and if the depolarisation is sufficient to reach threshold, the whole process is repeated in that neuron. At an inhibitory synapse, Ach will cause ligand-gated channels to open up for Cl-. This causes a hyperpolarisation in the cell, and takes it further away from firing threshold. The remaining neurotransmitter left in the synaptic cleft is either reuptaken by the presynaptic terminal via pinoctosis, or it is broken down by enzymes. This ensures that the transmissionis brief.

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