Serotonin, a naturally occurring substance functions as a neurotransmitter whose main function is to carry signals between neurons (nerve cells) throughout the body. A person with low levels of serotonin in the brain may experience anxiety or depression hence making it one of the most prescribed types of antidepressant. Serotonin is therefore considered an inhibitory transmitter as it aids in the regulation of mood, sleep, appetite, and blood clotting. Serotonin receptors, 5-hydroxytryptamine include a group of ligand-gated ion channels and g protein-coupled receptors which are found in the CNS. The serotonin-producing neurons make up the largest and intricate efferent system in the rain.
The nervous system utilizes two types of receptors, these are: metabotropic and ionotropic. Ionotropic receptors create an ion channel pore while metabotropic ion channels that are indirectly linked with g -proteins which are signal transduction mechanisms (Singh & Goel, 2016). There are fifteen known types of serotonin receptors, these are placed in specific groups. Most of these receptors are metabotropic except for 5-ht3 which is a Lingard-gated ion channel.
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Cocaine and alcohol are both responsible for the increase of serotonin in the brain. Cocaine however blocks the reuptake of serotonin as it broadly affects numerous parts of the brain (Volkow et al., 2010). On the other hand, alcohol is selective and produces subtle changes to the level of serotonin. Most drugs act as either agonists or antagonists at specific receptors that respond to neurotransmitters (Yeung et al., 2018). While agonists bind to the receptor and produce a reaction within the cell, antagonists bind to the receptor blocking it to a natural agonist. A serotonin antagonist, therefore, is any drug that inhibits the action of serotonin receptors. Antidepressants are functional antagonists at the serotonin 5-HT3.
References
Singh, T., & Goel, R. K. (2016). Evidence in support of using a neurochemistry approach to identify therapy for both epilepsy and associated depression. Epilepsy & Behavior , 61 , 248-257. https://doi.org/10.1016/j.yebeh.2016.05.005
Volkow, N. D., & Boyle, M. (2018). Neuroscience of addiction: Relevance to prevention and treatment. American Journal of Psychiatry , 175 (8), 729-740. https://doi.org/10.1176/appi.ajp.2018.17101174
Volkow, N. D., Wang, G., Fowler, J. S., Tomasi, D., Telang, F., & Baler, R. (2010). Addiction: Decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain's control circuit. BioEssays , 32 (9), 748-755. https://doi.org/10.1002/bies.201000042
Yeung, A. W., Tzvetkov, N. T., & Atanasov, A. G. (2018). When neuroscience meets pharmacology: A neuropharmacology literature analysis. Frontiers in Neuroscience , 12 . https://doi.org/10.3389/fnins.2018.00852
