Serotonin physiological mechanism

Four principal mechanisms have been cited to explain the diverse physiological mechanisms of ginger. Broadly, these are (1) eicosanoid inhibition, (2) serotonin antagonism, (3) substance P release, and (4) Ca2-i-/ATPase activity. 

My guess is that serotonin will be found to be part of the equilibrated system of chemical controls of smooth muscle and that the gross effects most of us study with present crude methods bear little relationship to the physiological mechanisms of the circulation. The story may well have a parallel with norepinephrine. Until von Euler got the idea that norepinephrine was a transmitter, and then distinguished between exogenous and endogenous stores, the understanding of this catecholamine was pretty muddy as well. 

Serotonin is an indolamine related to the amino acid tryptophan. In evolutionary terms it is considered to be one of the oldest neurotransmitters, and several lines of evidence show that it is involved in more physiological mechanisms, behaviors and brain processes than any other neurotransmitter. In addition to its role as a neurotransmitter, 5-HT has morphogenic properties and can alter the cytoskeleton of cells. It also acts as a regulator of cell proliferation, migration, apoptosis and maturation in a variety of tissues and cell types, including lung, kidney, endothelial cells, mast cells, astrocytes and neurons [1]. 

First, you will learn about the human nervous system and how it works when it is healthy. This will include an introduction to the structure (anatomy) of the nervous system and the function (physiology) of the nervous system. Next, we ll describe the things that can go wrong. We ll look at how the system breaks down and malfunctions. Then we ll show you how these breakdowns can result in psychiatric illness. Finally, we ll introduce you to the medications used to treat psychiatric illness. You will learn where these medications work and our best guess of how they work. The presumed mechanism of action of many medications is just that, presumed. In contrast to antibiotics, in which we know quite a lot about the ways that they kill bacteria or stop them from reproducing and how these mechanisms ultimately effect a cure for an infectious disease, less is known about how psychotropic medicines work. Oh, we pretty well understand what psychotropic medicines do when they reach the nerve cell. For example, most of the antidepressants used today block the reuptake of serotonin at the nerve cell, but we re still not sure why blocking serotonin reuptake gradually improves mood in someone with depression. This will lead to a tour, if you will, of what happens to a medication from the time the pill is swallowed, until it exerts its therapeutic effect. 

Serotonin mediates many central and peripheral physiological functions, including contraction of smooth muscle, vasoconstriction, food intake, sleep, pain perception, and memory, a consequence of it acting on several distinct receptor types. Although 5-HT may be metabolized by monoamine oxidase, platelets and neurons possess a high-affinity mechanism for reuptake of 5-HT. This mechanism may be inhibited by the widely prescribed antidepressant drugs termed selective serotonin re-uptake inhibitors (SSRl), e.g. fluoxetine (Prozac ), thereby increasing levels of 5-HT in the central nervous system. 

Some regulatory mechanisms have been revealed for the TPHs, such as activation by phosphorylation-dependent interaction with 14-3-3 proteins (71,72). Catecholamines are also reported to be inhibitors of TPH (73). l-DOPA and L-DOPA-quinone derivatives, but not the end product serotonin, have also been shown to be inhibitors of TPH activity (see Martinez et al. 2001 (74) for the physiological and pharmacological implications of the inhibitory effects by catechol derivatives). 

Despite the recent advances in molecular biology, the mechanisms of action and the physiological functions of the anandamide system remain obscure. It would appear that the cannabinoid receptors and the anandamides reside within the neurons. Thus unlike the classical neurotransmitters noradrenaline and serotonin, the anandamides are not released into the synaptic cleft and are not involved in intemeuronal communication. Instead the anandamides modulate the excitability and inhibitory responsiveness of neurons by acting on cannabinoid hetero-ceptors located on inhibitory and excitatory terminals. In this way, the... 

In general, diverse TA are known to bind to (a) muscarinic receptors (MR), (b) 5-hydroxytryptamine (serotonin) receptor 3 (5-HT3R), (c) al-adrenoreceptors (al-AR), or (d) a7-nicotinic receptors (a7-nAChR) thus causing different physiological effects. The corresponding mechanisms of action should briefly be addressed below. 

Since the discovery of 5-hydroxytryptamine (serotonin, enteramine, thrombocytin) (VII), and the demonstration of its physiological activity and its important function as a neurohormone, the possibility of its occurrence in plants has attracted much attention. It was first shown to be present in Mucuna pruriens DC. (cowhage), and is probably responsible for the intense irritation which results when cowhage comes into contact with the skin (94). This irritation could be a mechanical effect due to the trichomes, but it is more likely to be the result of liberation of... 

Summary - Many diverse novel compounds that inhibit different platelet functions show great promise, not only for potential anti-thrombotic agents, but also for more specific effects on prostaglandin and/or thromboxane A2 synthesis, and serotonin or calcium uptake and release. Many active compounds can be used as tools in the search toward a more complete understanding of the physiologic interactions of the hemostatic mechanisms. This better understanding would lead to the development and use of more potent and selective synthetic compounds in the inhibition of platelet aggregation and fibrin formation, and in the enhancement of fibrinolysis for the control of both arterial and venous thrombosis. It is hoped that some of these new compounds will be evaluated clinically in the near fu ture. 

Early behavioral and neurochemical studies suggested the involvement of L-tryptophan in the mechanisms of analgesia. These studies were followed by many experiments on the possible involvement of serotonin in this phenomenon. At present, the physiological role of serotonin in pain and analgesia still remains to be fully explained. During the last decade, a number of studies have suggested that another route of metabolism of tryptophan, the kynurenine pathway, was involved in the control of neuronal activity. Some of the experimental studies are cited here. 

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