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An autoreceptor is a receptor which is situated in the terminal of a presynaptic nerve cell, sensitive to neurotransmitters released by the neuron in whose membrane the autoreceptor sits.

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How do nerve signals travel from nerve to nerve?

This is a very long and hard 1-2 weeks of worth of work and studying to understand but ill try my best. A neuron consists of the following structures in the following order:dendrites, soma, axon, myelin sheath, and the axon terminal. Then the synapse. The dendrites on a cell recieve a chemical signal potential from recieved neurotransmitters. The potential changes the polarity within the soma by stimulating and opening the sodium ion channels. The cell either hyperpolarizes or depolarizes If it depolarizes an electrical impulse is sent down the axon. The axon is protected by the myelin sheath. The myelin sheath increases the conductivity of the axon allowing the electrical impulse to carry all the way down the axon. When it reaches the end of the axon it travels into the axon terminal, and the terminal buds. The vesicle sacs are then stimulated, which releases neurotransmitters into the synapse. The neurotransmitters then float across the synapse and stimulate the dendrites of the postsynaptic cell, starting the whole process over again with that cell. When enough neurotransmitters have been released, the autoreceptor on the presynaptic cell will be stimulated. Then the neurotrasmitters reuptake into the terminal buds, where they will either be returned to the vesicle sacs for use at a later time (next time the neuron fires), or else they will be destroyed by the MAO enzyme This is a very simplified version of it and will most likely confuse you but in this limited amout of space it about the best i can do. sorry.


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How do nerve signals travel from nerve to nerve?

This is a very long and hard 1-2 weeks of worth of work and studying to understand but ill try my best. A neuron consists of the following structures in the following order:dendrites, soma, axon, myelin sheath, and the axon terminal. Then the synapse. The dendrites on a cell recieve a chemical signal potential from recieved neurotransmitters. The potential changes the polarity within the soma by stimulating and opening the sodium ion channels. The cell either hyperpolarizes or depolarizes If it depolarizes an electrical impulse is sent down the axon. The axon is protected by the myelin sheath. The myelin sheath increases the conductivity of the axon allowing the electrical impulse to carry all the way down the axon. When it reaches the end of the axon it travels into the axon terminal, and the terminal buds. The vesicle sacs are then stimulated, which releases neurotransmitters into the synapse. The neurotransmitters then float across the synapse and stimulate the dendrites of the postsynaptic cell, starting the whole process over again with that cell. When enough neurotransmitters have been released, the autoreceptor on the presynaptic cell will be stimulated. Then the neurotrasmitters reuptake into the terminal buds, where they will either be returned to the vesicle sacs for use at a later time (next time the neuron fires), or else they will be destroyed by the MAO enzyme This is a very simplified version of it and will most likely confuse you but in this limited amout of space it about the best i can do. sorry.


How do SSRI's work?

Selective serotonin reuptake inhibitors (SSRIs) achieve their therapeutic effect by modifying synaptic availability of the neurotransmitter serotinin. This is accomplished, first of all, by blocking the proteins that normally transport serotonin back into the cells that release them (presynaptic cell). In doing so, synaptic levels of serotonin are temporarily boosted. This phase is normally associated with an acute increase in anxiety. However, this subsides over several days as subtypes of postsynaptic5-HT receptors down-regulate in response to the excess serotonin. During this time another kind of protein called an autoreceptor (in this case 5-HT1 autoreceptors) located on the presynaptic cell begins to desensitize. Normally these types of receptor proteins provide a kind of feedback mechanism that limits the production of neurotransmitters.With these desensitized, the cell receives less feedback and the rate of serotonin synthesis and release increases. Since not all postsynaptic 5-HT receptors down-regulate in response to increased synaptic levels of serotonin - the ones that don't are able to bind more serotonin and this is thought to account for the longer term effects of SSRIs. Similar processes occur as 'secondary effects' on cells that release noradrenaline - as these express 5-HT2a heteroceptors - and this also is thought to contribute to their therapeutic efficacy. The reason serotonin is targeted by SSRIs in the first place is that the same regions of the brain that contain a high density of serotinin-releasing neurons (Raphe nuclei) are known to regulate mood directly as well as indirectly via interactions with other brain areas and neurotransmitter systems (like noradrenaline and dopamine in other parts of the limbic system as well as frontal cortex). However, because it's so complex, and no two brains are the same, responses to SSRIs can vary. In most cases of mild to moderate depression they offer a benefit .