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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 effects of 5-hydroxytryptamine (5-HT) on an inward current activated by extracellular ATP were investigated in rat pheochromocytoma PC12 cells. Under whole-cell voltage-clamp conditions 5-HT (10 microM) reversibly enhanced the amplitude of the current activated by 30 microM ATP. The enhancement may not be due to an increase in the number of functional channels because the current activated by 300 microM ATP was not remarkably augmented compared with the current activated by 30 microM ATP. The current enhancement by 100 microM 5-HT was less obvious than that by 10 microM 5-HT. When the current kinetics were compared, activation of the ATP-evoked current was accelerated to the same extent by either 10 or 100 microM 5-HT, whereas deactivation was largely more accelerated by 100 microM 5-HT. Propranolol (10 microM), a 5-HT1 receptor antagonist, or LY53857 (10 microM), a 5-HT2 receptor antagonist, exerted an agonistic effect: the ATP-activated current was facilitated by these compounds. Metoclopramide (10 microM), a 5-HT3 receptor antagonist, neither facilitated the ATP-activated current, nor blocked the current facilitation by 5-HT. Guanosine 5'-O-(2-thiodiphosphate) (GDP[beta S]) (2 mM), the non-hydrolysable analog of guanosine 5'-triphosphate (GTP), or K-252a (2 microM), a protein kinase inhibitor, did not affect the facilitation by 5-HT of the ATP-activated current when they were included in the intracellular solution. The ATP-activated current pre-facilitated by 10 microM dopamine was not enhanced by 10 microM 5-HT. Similarly, the pre-facilitation by 5-HT attenuated the current enhancement by dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Facilitation by 5-hydroxytryptamine of ATP-activated current in rat pheochromocytoma cells. 752 34

The extrinsic neural pathways and transmitter mechanisms involved in neural influences controlling lower oesophageal sphincter (LOS) pressure have been evaluated in three groups of experiments in urethane anaesthetized rats. A miniature perfused sleeve/sidehole catheter measured gastric, LOS and oesophageal pressures. Group 1: Vago-vagal and vago-spinal reflex pathways were activated simultaneously via the central nervous system by stimulation of the central cut end of the left vagus. This caused a prolonged drop in LOS pressure with a rapid onset and a slow return to baseline. Subsequent right (bilateral) vagotomy in these animals increased basal LOSP (P < 0.001). Central vagal stimulation-induced reduction of LOSP was not significantly changed in amplitude but was shorter in duration (P < 0.01) than before bilateral vagotomy. IV administration of the 5-HT3 receptor antagonist granisetron (50 micrograms/kg), after bilateral vagotomy had no effect on the response to central vagal stimulation. The nitric oxide (NO) synthase inhibitor L-nitroarginine methyl ester (L-NAME) (100 mg/kg) reduced the depth of relaxation (P < 0.01) and temporarily increased basal LOSP. Propranolol (1.5 mg/kg, i.v.) subsequently increased basal LOSP (P < 0.01), but had no further effect on the vagal stimulation-induced reduction in LOSP. Alpha adrenergic blockade with phentolamine (1 mg/kg, i.v.) decreased basal LOSP (P < 0.01), and nearly abolished the response to vagal stimulation (P < 0.01). Group 2: Both alpha 1- and alpha 2-adrenoceptors were shown to be involved by the combined use of the more selective antagonists yohimbine (1 mg/kg, i.v.) and prazosin (200 micrograms/kg) in place of phentolamine. Group 3: To observe neurotransmitter mechanisms in the vago-vagal pathway, central left vagal stimulation was performed after left vagotomy, and subsequently after blockade of sympathetic motor pathways with guanethidine (5 mg/kg), leaving intact efferent pathways in the right vagus. Guanethidine increased basal LOSP (P < 0.01), and reduced the duration of vagal-induced LOS relaxation (P < 0.05). Depth of relaxation was unchanged. Subsequently, granisetron and L-NAME had no significant effects. Finally, additional right vagotomy abolished the remaining response. Our data indicate the existence of vago-spinal and vago-vagal inhibitory reflex pathways to the rat LOS. The inhibitory vago-spinal pathway is mainly alpha-adrenergic, and has a minor NO-mediated component, but no 5-HT3 receptor-mediated mechanism. In the vago-vagal pathway, no significant involvement of NO-mediated or 5-HT3 receptor-mediated effects was observed. Other non-adrenergic inhibitory mechanisms were, however, apparent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Transmitter mechanisms in vagal afferent-induced reduction of lower oesophageal sphincter (LOS) pressure in the rat. 796 67

5-Hydroxytryptamine (5-HT) potentiated contractions of isolated rat bronchi evoked by electrical field stimulation (EFS). The degree of potentiation caused by 5-HT was dependent upon concentration of the amine present in the tissue bath. The effects of antagonists selective for different subtypes of the 5-HT receptor on potentiation of EFS-induced contractions by 5-HT were examined. Propranolol, a nonselective beta-adrenoceptor antagonist which can act as a 5-HT1 receptor antagonist, did not inhibit the effect of 5-HT on EFS-induced contractile responses. Similarly, 5-HT3 receptor antagonism with MDL 72222 or ICS 205-930, did not inhibit the facilitatory effects of 5-HT. However, ketanserin, mianserin and spiperone, 5-HT2 receptor antagonists, abolished the effects of 5-HT on EFS-induced responses. These latter results suggested that the potentiation was dependent upon activation of 5-HT2 receptors thus additional experiments were conducted using the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT). alpha-Me-5-HT caused a concentration-dependent potentiation of EFS-induced contractile responses comparable to that observed with 5-HT. Concentrations of alpha-Me-5-HT that significantly potentiated EFS-induced contraction were essentially without effect on airway smooth muscle contraction elicited by exogenous acetylcholine. These results are consistent with a role for 5-HT2 receptor activation in mediating the facilitatory effects of 5-HT on cholinergic nerve-mediated responses in airways.
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PMID:5-HT2 receptors augment cholinergic nerve-mediated contraction of rat bronchi. 844 26

Serotonin (5-HT) receptors can be classified into at least three, possibly up to seven, classes of receptors. They comprise the 5-HT1, 5-HT2, and 5-HT3 classes, the "uncloned' 5-HT4 receptor and the recombinant receptors 5-ht5, 5-ht6 and 5-ht7. We investigated the role of different serotonin receptor types in a neuroendocrine response to the activation of the serotonergic system. Female immature rats were chosen as an experimental model as it has been shown that during the 3rd week of life, and not at later developmental stages, 5-hydroxytryptophan (5-HTP, a serotonin precursor) induces gonadotropin release in females and not in males. Besides, at this age, serotonin releases prolactin in both sexes. 5-HTP (50 mg/kg) released prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as expected. Ketanserin (5-HT2A antagonist) and methysergide (5-HT2C antagonist) blocked 5-HTP-induced prolactin release, but did not block the LH or FSH responses. Ondansetron (5-HT3 receptor antagonist) did not modify prolactin response to 5-HTP, whereas it blocked 5-HTP-induced LH and FSH release. Propranolol (5-HT1 and beta-adrenergic antagonist) blocked prolactin, LH and FSH release induced by 5-HTP. The 5-HT2C agonist 1-(3-chlorophenyl)piperazine dihydrochloride released prolactin, without modifying LH or FSH release. Methyl-quipazine and phenylbiguanide (5-HT3 agonists) increased both LH and FSH levels, without altering prolactin secretion. The present experiments indicate that serotonin acting at the 5-HT3 receptor mediates LH and FSH release in infantile female rats, whereas 5-HT2C or 2A receptor types participate in the release of prolactin at this age. 5-HT1 receptor type may be involved in the release of the three hormones, though a beta-adrenergic component of the response cannot be discarded.
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PMID:Different serotonin receptor types participate in 5-hydroxytryptophan-induced gonadotropins and prolactin release in the female infantile rat. 873 78