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

The wildtype 5-HT3 receptor was expressed in Xenopus oocytes from a cloned cDNA. Two-electrode voltage-clamp and fura-2 techniques were used simultaneously to monitor the current induced by the activation of the 5-HT3 receptor and the cytoplasmic Ca2+ concentration ([Ca2+]i). The application of serotonin (5-HT; 50 microM) in a physiological bathing solution containing Ca2+ (1.8 mM) elicited inward currents of up to approximately 1.3 microA at a potential of -90 mV. There was little or no detectable change in [Ca2+]i. In experiments on oocytes bathing in a nominally Ca(2+)-free medium, the injection of (2,4,5)IP3, an analog of inositol 1,4,5-trisphosphate ((1,4,5)IP3), produced a large increase in [Ca2+]i levels due to the liberation of Ca2+ from intracellular stores. This response was followed by a sustained elevation of [Ca2+]i upon restoring extracellular Ca2+ (i.e. capacitative Ca2+ entry). Furthermore, when calcium-permeable heteromeric (NR1/NR2A) N-methyl-D-aspartate (NMDA) receptors were expressed in oocytes, the activation of these receptors led to a large increase in [Ca2+]i in a Ca(2+)-containing external medium. It is concluded that wildtype 5-HT3 receptors expressed in Xenopus oocytes and studied under conditions used here show little or no permeability for Ca2+.
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PMID:Activation of 5-HT3 receptors expressed in Xenopus oocytes does not increase cytoplasmic Ca2+ levels. 858 3

Ecstasy, 3,4-methylenedioxymetamphetamine (MDMA), is a recreational drug used among adolescents, including young pregnant women. MDMA passes the placental barrier and may therefore influence fetal development. The aim was to investigate the direct effect of MDMA on cortical cells using dissociated CNS cortex of rat embryos, E17. The primary culture was exposed to a single dose of MDMA and collected 5 days later. MDMA caused a dramatic, dose-dependent (100 and 400 microM) decrease in nestin-positive stem cell density, as well as a significant reduction (400 microM) in NeuN-positive cells. By qPCR, MDMA (200 microM) caused a significant decrease in mRNA expression of the 5HT3 receptor, dopamine D(1) receptor, and glutamate transporter EAAT2-1, as well as an increase in mRNA levels of the NMDA NR1 receptor subunit and the 5HT(1A) receptor. In conclusion, MDMA caused a marked reduction in stem cells and neurons in embryonic cortical primary cell cultures, which was accompanied by changes in mRNA expression of specific receptors and transporters for glutamatergic and monoaminergic neurotransmitters.
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PMID:MDMA (Ecstasy) decreases the number of neurons and stem cells in embryonic cortical cultures. 1954 26

Hyperalgesia in animal injury models is linked to activation of descending raphespinal modulatory circuits originating in the rostral ventromedial medulla (RVM). A neurokinin-1 (NK-1) receptor antagonist microinjected into the RVM before or after inflammation produced by complete Freund's adjuvant (CFA) resulted in an attenuation of thermal hyperalgesia. A transient (acute) or a continuous infusion of Substance P (SP) microinjected into the RVM of non-inflamed animals led to similar pain hypersensitivity. Intrathecal pretreatment or post-treatment of a 5-HT3 receptor antagonist (Y-25130 or ondansetron) blocked the SP-induced hyperalgesia. The SP-induced hyperalgesia was both GABA(A) and NMDA receptor-dependent after pre- and post-treatment with selective antagonists at the spinal level. A microinjection of SP into the RVM also led to increased NMDA NR1 receptor subunit phosphorylation in spinal cord tissue. The GABA(A) receptor-mediated hyperalgesia involved a shift in the anionic gradient in dorsal horn nociceptive neurons and an increase in phosphorylated NKCC1 protein (isoform of the Na-K-Cl cotransporter). Following a low dose of SP infused into the RVM, intrathecal muscimol (GABA(A) agonist) increased SP-induced thermal hyperalgesia, phosphorylated NKCC1 protein expression, and NMDA NR1 subunit phosphorylation in the spinal cord. The thermal hyperalgesia was blocked by intrathecal gabazine, the GABA(A) receptor antagonist, and MK-801, the NMDA receptor channel blocker. These findings indicate that NK-1 receptors in the RVM are involved in SP-induced thermal hyperalgesia, this hyperalgesia is 5-HT3-receptor dependent at the spinal level, and involves the functional interaction of spinal GABA(A) and NMDA receptors.
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PMID:Spinal cord mechanisms mediating behavioral hyperalgesia induced by neurokinin-1 tachykinin receptor activation in the rostral ventromedial medulla. 2088 91