Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P46098 (5-HT3 receptor)
 2,290 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three major areas of medicine are identified in which there is a need for new antiemetic drugs. These are the nausea and vomiting arising from gastrointestinal motility disturbances (functional dyspepsia, diabetic neuropathy, classical migraine), the sickness evoked by abnormal motion, and the severe emesis experienced by cancer patients as a result of certain cytotoxic therapies. For gastrointestinal-related nausea, selective stimulants of gut motility are suggested to form the basis for a new type of antiemetic therapy. In motion sickness, there has been progress in the understanding of the illness, but little advance in the development of new drugs that selectively prevent this type of sickness. In cancer chemo- and radio-therapy, the discovery that selective 5-HT3 (5-HT, 5-hydroxytryptamine) receptor antagonists can prevent severe cytotoxic-evoked emesis now promises to radically change the type of antiemetic therapy given to these patients. This type of antiemetic compound and the pharmacology of the new 5-HT3 receptor antagonists are, therefore, discussed in detail.
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PMID:New antiemetic drugs. 217 55

Diabetic neuropathy has a profound impact in the quality of life of patients who frequently complain of pain. The mechanisms underlying diabetic neuropathic pain (DNP) are no longer ascribed only to damage of peripheral nerves. The effects of diabetes at the central nervous system are currently considered causes of DPN. Management of DNP may be achieved by antidepressants that act on serotonin (5-HT) uptake, namely specific serotonin reuptake inhibitors. The rostroventromedial medulla (RVM) is a key pain control center involved in descending pain modulation at the spinal cord through local release of 5-HT and plays a peculiar role in the balance of bidirectional control (i.e. inhibitory and facilitatory) from the brain to the spinal cord. This review discusses recently uncovered neurobiological mechanisms that mediate nociceptive modulation from the RVM during diabetes installation. In early phases of the disease, facilitation of pain modulation from the RVM prevails through a triplet of mechanisms which include increase in serotonin expression at the RVM and consequent rise of serotonin levels at the spinal cord and upregulation of local facilitatory 5HT3 receptors, enhancement of spontaneous activity of facilitatory RVM neurons and up-regulation of the expression of transient receptor potential vanilloid type 1 (TRPV1) receptor. With the progression of diabetes the alterations in the RVM increase dramatically, with oxidative stress and neuronal death associated to microglia-mediated inflammation. In a manner similar to other central areas, like the thalamus, the RVM is likely to be a "pain generator/amplifier" during diabetes, accounting to increase DNP. Early interventions in DNP prevention using strategies that simultaneously tackle the exacerbation of 5-HT3 spinal receptors and of microglial RVM activity, namely those that increase the levels of anti-inflammatory cytokines, should be considered in the future of DNP treatment.
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PMID:Pain modulation from the brain during diabetic neuropathy: Uncovering the role of the rostroventromedial medulla. 2771 82