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Understanding how a pulse is transmitted along the axon of a nerve cell is the first step in understanding how neurons communicate among themselves and ultimately how neuronal control is achieved. The axon of a neuron usually synapses with the dendrites of other neurons or the cell body. A single neuron can synapse with many other neurons because the last end of an axon normally has a large number of branches. Moreover, it usually synapses at multiple points with each of these neurons. Each of the thin branches of an axon ends with small bulges in the form of buttons. 


These structures are called synaptic ends. In a small number, there is sometimes a junction between the synaptic end membrane and the membrane of the cell in contact with the membrane. Such a region, it provides a direct electrical transmission between the two neurons and thus the impulse that travels along the axon of the first neuron passes through the second neuron without encountering any resistance. Because electrical synapses minimize the delay in impulse conduction, they occur in areas where the transmission rate in the nervous system is particularly important. They also substantially secure the impulse in the first neuron to create an impulse in the second neuron.
In contrast, the vast majority of synapses are chemical, not electrical. The space approximately 20 nm wide, which separates the synaptic end of the first neuron (presynaptic) and the membrane of the second neuron (postsynaptic), is called the synaptic range. Through this gap, transmission is required by transmitter chemicals that diffuse and diffuse from small synaptic vesicles located at the last end. Each of these thousands of vesicles has up to 10,000 transmitter molecules.
When the impulse that travels along the axon of the presynaptic neuron reaches the terminal, special voltage-gate calcium channels that are concentrated in the synapse region are opened and the membrane at the last end becomes more permeable to Ca ++ ions. Since they are found to be 10,000 times more dense than the cell, by stimulating the Ca ++ ions in some way, the synaptic vesicles at the last end move towards the membrane of the tip and fuse with it and disintegrate. Thus, the transmitter chemicals are exhaled into the synaptic space by exocytosis. Ca ++ ions play a similar role to initiate muscle contraction.
Transmitter molecules that are released into the synaptic space are transmitted by diffusion and weakly bound to highly specific receptors in the postsynaptic membrane of the second neuron. These receptors are specific to the neurotransmitter and function in a manner similar to that of hormone receptors.
When the transmitter is acetylcholine (chemical that allows vertebrate motor neurons to communicate with muscle cells), two donor molecules must be connected to activate the receptor. The molecules contained in a single vesicle activate approximately 2000 receptors. The binding of the transmitter to the receptor opens the gates of a channel and allows a specific ion to pass through the membrane. This ion movement results in a potential change in the membrane of the postsynaptic neuron, and a new impulse can be created in that cell. The channels carrying the acetylcholine receptors pass both K + and Na + ions and the regions around the cells are partially depolarized. Since transmission in a synapse requires a series of events ter the introduction of Ca ++ ions at the final end, the movement of the transmitter vesicles, exocytosis, The diffusion of the transmitter in the synaptic space and the diffusion of the ions in the postsynaptic channels at the end is much slower than the impulse being transmitted through the neuron. Therefore, the transmission time of a message will be longer than expected. In general, the more synapses a nerve path has, the slower the average transmission rate per unit length across the path.
The transfer of the transmitter to the postsynaptic cell diffusely in the synaptic space is not the end of the event. If the transmitter is persistent, the postsynaptic receptors are stimulated forever by the arrival of a single pulse. Then there must be a mechanism to eliminate the transmitter. For example, acetylcholine is rapidly inactivated by an enzyme called acetylcholinesterase after diffusing from the synaptic space and acting on the dendrite or cell body membrane of the postsynaptic cell. This enzyme eliminates the transmitter and allows the transmission of the next pulse with the new information. Many insecticides such as organophosphates (also known as nerve gases) cholinesteraseInhibitor. They prevent the abolition of acetylcholine, and as a result, the synapses of an insect exposed to them remain active as expected. If they are administered at high doses, cholinesterase inhibitors affect significant physiological events and the animal dies.
Acetylcholine, which acts as a transmitter other than the central nervous system, is also included in the growing list of transmitters in the central nervous system. In vertebrates, these include noradrenaline (also made as a hormone in the adrenal medulla), serotonin, dopamine, nitrous oxide and gamma amino-butyric acid (GABA). It is now known that various abnormalities such as schizophrenia and serious depression, previously thought to be caused by unclear mental disorders, are now caused by biochemical defects of CNS transmitters, receptors and previously unknown neural hormones. These discoveries have begun to lead to the relatively precise physiological treatment of some mental disorders.
Source: poxox blogs

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