Seventy-Seven Opinions on Nervous System Related Health Disorders: Seventy-Seven Thought Provoking Q

on Nervous System Related Disorders: Seventy-Seven Thought-Provoking Q & As! health disorders that are related to the functioning of the nervous system, Questions and Answers/Opinions 61 through 77 (Note: Proper diagnosis and.
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However, the PMAT, despite its relatively low serotonergic affinity, has a considerably higher transport 'capacity' than SERT, "resulting in roughly comparable uptake efficiencies to SERT in heterologous expression systems. At present, no known pharmaceuticals are known to appreciably inhibit PMAT at normal therapeutic doses. Serotonin can also signal through a nonreceptor mechanism called serotonylation, in which serotonin modifies proteins. The effects of serotonin upon vascular smooth muscle tone this is the biological function from which serotonin originally got its name depend upon the serotonylation of proteins involved in the contractile apparatus of muscle cells.

The neurons of the raphe nuclei are the principal source of 5-HT release in the brain. Axons of neurons in the lower raphe nuclei terminate in the cerebellum and spinal cord , while the axons of the higher nuclei spread out in the entire brain. The serotonin nuclei may also be divided into two main groups, the rostral and caudal containing three and four nuclei respectively. The rostral group consists of the caudal linear nuclei B8 , the dorsal raphe nuclei B6 and B7 and the median raphe nuclei B5, B8 and B9 , that project into multiple cortical and subcortical structures.

The caudal group consists of the nucleus raphe magnus B3 , raphe obscurus nucleus B2 , raphe pallidus nucleus B1 , and lateral medullary reticular formation, that project into the brainstem. Serotonergic pathway are involved in sensorimotor function, with pathways projecting both into cortical Dorsal and Median Raphe Nuclei , subcortical, and spinal areas involved in motor activity.

Pharmacological manipulation suggest that serotonergic activity increases with motor activity, while firing rates of serotonergic neurons increase with intense visual stimuli. The descending projections form a pathway that inhibits pain called the "descending inhibitory pathway" that may be relevant to disorder such as fibromyalgia, migraine and other pain disorders, and the efficacy of antidepressants in them. Serotonergic projections from the caudal nuclei are involved in regulating mood, emotion and hypo [38] or hyperserotonergic [39] states may be involved in depression and sickness behavior.

When humans smell food, dopamine is released to increase the appetite. But, unlike in worms, serotonin does not increase anticipatory behaviour in humans; instead, the serotonin released while consuming activates 5-HT2C receptors on dopamine-producing cells. This halts their dopamine release, and thereby serotonin decreases appetite. Drugs that block 5-HT 2C receptors make the body unable to recognize when it is no longer hungry or otherwise in need of nutrients, and are associated with weight gain, [40] especially in people with a low number of receptors.

In macaques , alpha males have twice the level of serotonin released in the brain than subordinate males and females as measured by the levels of 5-Hydroxyindoleacetic acid 5-HIAA in the cerebro-spinal fluid. Dominance status and cerebro-serotonin levels appear to be positively correlated. When dominant males were removed from such groups, subordinate males begin competing for dominance.

Once new dominance hierarchies were established, serotonin levels of the new dominant individuals also increased to double those in subordinate males and females. The reason why serotonin levels are only high in dominant males but not dominant females has not yet been established. In humans, levels of 5-HT 1A receptor activation in the brain show negative correlation with aggression, [45] and a mutation in the gene that codes for the 5-HT 2A receptor may double the risk of suicide for those with that genotype. Serotonin has been implicated in cognition, mood, anxiety and psychosis, but strong clarity has not been achieved.

The gut is surrounded by enterochromaffin cells , which release serotonin in response to food in the lumen. This makes the gut contract around the food. Platelets in the veins draining the gut collect excess serotonin. If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5-HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting.

Drugs that block 5HT3 are very effective in controlling the nausea and vomiting produced by cancer treatment, and are considered the gold standard for this purpose. In mice and humans, alterations in serotonin levels and signalling have been shown to regulate bone mass. In humans, increased blood serotonin levels have been shown to be significant negative predictor of low bone density.

Serotonin can also be synthesized, albeit at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. There is very delicate balance between physiological role of gut serotonin and its pathology. Since serotonin signals resource availability it is not surprising that it affects organ development. Many human and animal studies have shown that nutrition in early life can influence, in adulthood, such things as body fatness, blood lipids, blood pressure, atherosclerosis, behavior, learning and longevity.

Human serotonin can also act as a growth factor directly. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic growth factor , to aid healing. Several classes of drugs target the 5-HT system, including some antidepressants , antipsychotics , anxiolytics , antiemetics , and antimigraine drugs , as well as the psychedelic drugs and empathogens.

Drugs that alter serotonin levels are used in treating depression , generalized anxiety disorder and social phobia. Monoamine oxidase inhibitors MAOIs prevent the breakdown of monoamine neurotransmitters including serotonin , and therefore increase concentrations of the neurotransmitter in the brain.

MAOI therapy is associated with many adverse drug reactions, and patients are at risk of hypertensive emergency triggered by foods with high tyramine content, and certain drugs. Some drugs inhibit the re-uptake of serotonin, making it stay in the synaptic cleft longer.


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The tricyclic antidepressants TCAs inhibit the reuptake of both serotonin and norepinephrine. The newer selective serotonin reuptake inhibitors SSRIs have fewer side-effects and fewer interactions with other drugs. Certain SSRI medications have been shown to lower serotonin levels below the baseline after chronic use, despite initial increases. Extremely high levels of serotonin can cause a condition known as serotonin syndrome , with toxic and potentially fatal effects.

In practice, such toxic levels are essentially impossible to reach through an overdose of a single antidepressant drug, but require a combination of serotonergic agents, such as an SSRI with an MAOI. Some 5-HT 3 antagonists , such as ondansetron , granisetron , and tropisetron , are important antiemetic agents. They are particularly important in treating the nausea and vomiting that occur during anticancer chemotherapy using cytotoxic drugs. Another application is in the treatment of postoperative nausea and vomiting. Some serotonergic agonist drugs cause fibrosis anywhere in the body, particularly the syndrome of retroperitoneal fibrosis , as well as cardiac valve fibrosis.

These are the serotonergic vasoconstrictive antimigraine drugs ergotamine and methysergide , [83] the serotonergic appetite suppressant drugs fenfluramine , chlorphentermine , and aminorex , and certain anti-Parkinsonian dopaminergic agonists, which also stimulate serotonergic 5-HT 2B receptors. These include pergolide and cabergoline , but not the more dopamine-specific lisuride. As with fenfluramine, some of these drugs have been withdrawn from the market after groups taking them showed a statistical increase of one or more of the side effects described.

An example is pergolide.

Lecture11 Central Nervous System

The drug was declining in use since it was reported in to be associated with cardiac fibrosis. Two independent studies published in the New England Journal of Medicine in January , implicated pergolide, along with cabergoline , in causing valvular heart disease. Treatment for hyperprolactinemia requires lower doses than that for Parkinson's Disease, diminishing the risk of valvular heart disease. Several plants contain serotonin together with a family of related tryptamines that are methylated at the amino NH 2 and OH groups , are N -oxides , or miss the OH group.

These compounds do reach the brain, although some portion of them are metabolized by monoamine oxidase enzymes mainly MAO-A in the liver. Examples are plants from the genus Anadenanthera that are used in the hallucinogenic yopo snuff. These compounds are widely present in the leaves of many plants, and may serve as deterrents for animal ingestion. Serotonin occurs in several mushrooms of the genus Panaeolus.

Serotonin is used by a variety of single-cell organisms for various purposes. SSRIs have been found to be toxic to algae. Outside the gut of a host, there is nothing that the entoamoebas provoke to release serotonin, hence the serotonin concentration is very low. Low serotonin signals to the entoamoebas they are outside a host and they become less virulent to conserve energy. When they enter a new host, they multiply in the gut, and become more virulent as the enterochromaffine cells get provoked by them and the serotonin concentration increases.

In drying seeds , serotonin production is a way to get rid of the buildup of poisonous ammonia. The ammonia is collected and placed in the indole part of L - tryptophan , which is then decarboxylated by tryptophan decarboxylase to give tryptamine, which is then hydroxylated by a cytochrome P monooxygenase , yielding serotonin.

However, since serotonin is a major gastrointestinal tract modulator, it may be produced by plants in fruits as a way of speeding the passage of seeds through the digestive tract, in the same way as many well-known seed and fruit associated laxatives. Serotonin is found in mushrooms , fruits and vegetables. Moderate levels from 0.

Serotonin is one compound of the poison contained in stinging nettles Urtica dioica , where it causes pain on injection in the same manner as its presence in insect venoms see below. It is also naturally found in Paramuricea clavata , or the Red Sea Fan. Serotonin and tryptophan have been found in chocolate with varying cocoa contents. The highest serotonin content 2. The intermediate in the synthesis from tryptophan to serotonin, 5-hydroxytryptophan, was not found.

Serotonin functions as a neurotransmitter in the nervous systems of most animals. For example, in the roundworm Caenorhabditis elegans , which feeds on bacteria, serotonin is released as a signal in response to positive events, such as finding a new source of food or in male animals finding a female with which to mate. This mechanism increases the amount of time animals spend in the presence of food.

If lobsters are injected with serotonin, they behave like dominant individuals whereas octopamine causes subordinate behavior. Serotonin inhibits the fleeing reaction in subordinates, but enhances it in socially dominant or isolated individuals. The reason for this is social experience alters the proportion between serotonin receptors 5-HT receptors that have opposing effects on the fight-or-flight response.

Serotonin is evolutionarily conserved and appears across the animal kingdom. It is seen in insect processes in roles similar to in the human central nervous system, such as memory, appetite, sleep, and behavior. Invertebrate drug response has been far less characterized than mammalian pharmacology and the potential for species selective insecticides has been discussed.

Wasps and hornets have serotonin in their venom, [] which causes pain and inflammation. If flies are fed serotonin, they are more aggressive; flies depleted of serotonin still exhibit aggression, but they do so much less frequently. In the nematode C. In the fruit fly insulin both regulates blood sugar as well as acting as a growth factor. Thus, in the fruit fly, serotonergic neurons regulate the adult body size by affecting insulin secretion. Serotonin is known to regulate aging, learning and memory.

The first evidence comes from the study of longevity in C. The observation does not contradict with the notion that the serotonin level goes down in mammals and humans, which is typically seen in late but not early [ vague ] phase of aging. In animals including humans, serotonin is synthesized from the amino acid L - tryptophan by a short metabolic pathway consisting of two enzymes: The TPH-mediated reaction is the rate-limiting step in the pathway.

TPH has been shown to exist in two forms: Serotonin can be synthesized from tryptophan in the lab using Aspergillus niger and Psilocybe coprophila as catalysts. The first phase to 5-hydroxytryptophan would require letting tryptophan sit in ethanol and water for 7 days, then mixing in enough HCl or other acid to bring the pH to 3, and then adding NaOH to make a pH of 13 for 1 hour.

Asperigillus niger would be the catalyst for this first phase. The second phase to synthesizing tryptophan itself from the 5-hydroxytryptophan intermediate would require adding ethanol and water, and letting sit for 30 days this time. The next two steps would be the same as the first phase: This phase uses the Psilocybe coprophila as the catalyst for the reaction. Serotonin taken orally does not pass into the serotonergic pathways of the central nervous system, because it does not cross the blood—brain barrier. These agents are available as dietary supplements , and may be effective serotonergic agents.

One product of serotonin breakdown is 5-hydroxyindoleacetic acid 5-HIAA , which is excreted in the urine. Serotonin and 5-HIAA are sometimes produced in excess amounts by certain tumors or cancers , and levels of these substances may be measured in the urine to test for these tumors. Consuming purified tryptophan increases brain serotonin whereas eating foods containing tryptophan does not. In , Italian Vittorio Erspamer showed an extract from enterochromaffin cells made intestines contract.

Some believed it contained adrenaline , but two years later, Erspamer was able to show it was a previously unknown amine , which he named "enteramine". Rapport , Arda Green, and Irvine Page of the Cleveland Clinic discovered a vasoconstrictor substance in blood serum , and since it was a serum agent affecting vascular tone, they named it serotonin. In , enteramine was shown to be the same substance as serotonin, and as the broad range of physiological roles was elucidated, the abbreviation 5-HT of the proper chemical name 5-hydroxytryptamine became the preferred name in the pharmacological field.

Medications used to treat drug addiction include drugs that antagonize the action of addictive substances. For example, Naltrexone helps prevent relapse to alcohol and heroin abuse, although many side effects exist. In addition to drug therapy, behavioral treatments are also used but with limited success. Because of the complexity and environmental attributions to neuropsychiatric disorders, despite the strong underlying genetic basis, definitive genetic factors remain to be identified in most cases.

While the novelty induced diving is shown to be affected by nicotine and nicotinic antagonists, implicating the involvement of both alpha7 and alpha4beta2 receptors , rigorous pharmacological validations of other behavioral paradigms remain to be carried out. The psycho-stimulatory 48 , 49 and reinforcing 50 , 52 — 54 effects of alcohol and drugs of abuse have been examined in zebrafish. These studies show that zebrafish readily respond to addictive substances, and neural substrates such as dopamine, serotonin, opioid systems, and acetylcholine systems are involved. Behavior-based approaches to neuroactive drug discovery have a long history with much serendipity.

For example, many psychoactive substances such as ethanol, caffeine, and opium have been discovered due to their rapid perceptual and behavioraleffects on humans and other animals. However, is it feasible to use behavior as a read out in a small molecule based drug screening? Behavioral assays are often more complex than cell based assays and subject to more variability from both genetic and environmental influences. A recent review by Kokel and Peterson argues that these problems can be overcome, and such screening represents a necessity for systematic drug discovery The zebrafish nervous system is similar to that of mammals, and is accessible to small molecule drugs.

These features make zebrafish a potentially suitable organism to evaluate the impact of drugs on neuronal development and function. However, before such potential can be fully realized, a better understanding of its nervous system and further establishment of appropriate models for human conditions are needed. For the purpose of drug discovery, the small size and relative abundance of zebrafish embryos allow for well format chemical screening.

However, such phenotype-based screens still provide much lower throughput than in vitro assay-based screening. Thus, additional technological breakthroughs in animal handling, imaging, and quantification are necessary to help further automate the screening process as much as possible. At present, the drug discovery process is either largely serendipitous or based on in vitro screens. Serendipity is not a reliable and rational approach, whereas in vitro assay-based screening often leads to compounds that have limited in vivo efficacy or unforeseeable toxicity. The pre-clinical drug testing process almost exclusively uses mammalian animal models, with a low throughput and high cost.

The use of zebrafish could potentially facilitate both drug screening and the processes of evaluating candidate drugs. Investment into this organism, to further understand its biology and disease modeling capability, and to facilitate technological build-ups, has the possibility of revolutionizing drug discovery for CNS disorders.

I apologize to authors whose work cannot be cited in this review due to space limitations. Sun for helpful comments on the review. National Center for Biotechnology Information , U. Expert Opin Drug Discov. Author manuscript; available in PMC Jul 1. The publisher's final edited version of this article is available at Expert Opin Drug Discov.

See other articles in PMC that cite the published article. Conclusion These studies hold promise to reveal fundamental mechanisms governing nervous system development and function, and to facilitate small molecule drug discovery for the many types of neurological disorders. Introduction Structural similarity of the nervous system emerges at the level of vertebrates, with the central nervous system CNS derived from a sheet of dorsally located neuroectoderm that is regionally patterned into the forebrain, midbrain, hindbrain, and spinal cord, while the peripheral nervous system PNS is derived from the migratory neural crest cells.

The zebrafish nervous system: Open in a separate window. Connectivity and circuitry in the adult nervous system Because of the scarcity of connectivity information in zebrafish, data from the closely related goldfish is used as a reference Molecular architecture of the zebrafish nervous system In addition to neuroanatomical similarities, the zebrafish nervous system also expresses many signaling molecules that show similarities to that of mammals.

Effects of known drugs on neural development and function in zebrafish Zebrafish, particularly larval zebrafish, have been used in toxicological studies to analyze the effects of neurotoxins and neuroprotectants on the developing nervous system 43 — Table 1 Agonists and antagonists of various neurotransmitter- or neuropeptide-systems that have predicted effects in zebrafish. Strategies for modeling human neurological disorders and identifying neuro-active compounds in zebrafish In general, several alternative strategies can be employed in animal systems to model human diseases: Conclusions The zebrafish nervous system is similar to that of mammals, and is accessible to small molecule drugs.

Expert opinion At present, the drug discovery process is either largely serendipitous or based on in vitro screens. Acknowledgments I apologize to authors whose work cannot be cited in this review due to space limitations.

Using zebrafish to assess the impact of drugs on neural development and function

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Using zebrafish to assess the impact of drugs on neural development and function

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Questions & Answers on Nervous System Related Disorders: Seventy-Seven Thought-Provoking Q & As!

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