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)

Administration of m-chlorophenylpiperazine [m-CPP, a serotonin (5-HT) agonist] to rats increases plasma concentrations of prolactin and corticosterone. Pretreatment with various doses of ritanserin (5-HT1C/5-HT2 antagonist), ICS 205-930 and MDL-72222 (5-HT3 antagonists), iodocyanopindolol or CG361A (beta adrenoceptor antagonists) and spiperone (5-HT1A/5-HT2 antagonist) did not attenuate m-CPP-induced increases in plasma concentrations of prolactin. In contrast, pretreatment with various doses of metergoline (5-HT1/5-HT2 antagonist), propranolol (beta adrenoceptor antagonist that also has binding affinity for 5-HT1A, 5-HT1B and 5-HT1C sites), mesulergine and mianserin (5-HT1C/5-HT2 antagonists) attenuated m-CPP-induced increases in plasma prolactin. On the other hand, m-CPP-induced increases in corticosterone concentrations were attenuated only by pretreatment with a low dose of mianserin and a high dose of spiperone. When administered without m-CPP, metergoline, mesulergine, ritanserin, ICS 205-930 and high doses of mianserin, spiperone and propranolol increased plasma corticosterone secretion. On the other hand, none of the antagonists used in the present study, except spiperone, had any significant effect on plasma prolactin secretion. These findings suggest that m-CPP-induced prolactin secretion is mediated by stimulation of 5-HT1C receptors while corticosterone secretion may be mediated either by an antagonistic effect at 5-HT3 receptor subtype or by nonserotonergic mechanisms. Alternatively, enhancement of corticosterone secretion by the 5-HT antagonists when administered alone may be responsible for their failure to block m-CPP-induced corticosterone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of various serotonin receptor subtype-selective antagonists alone and on m-chlorophenylpiperazine-induced neuroendocrine changes in rats. 143 90

The level of cyclic AMP in NCB-20 cells was increased by serotonin (5-HT), 5-methoxytryptamine and 2-methyl-5-HT with EC50 of 0.5 +/- 0.1, 1.0 +/- 0.1, 10 +/- 0.1 microM, respectively. The 5-HT-mediated increase of cyclic AMP content was completely blocked by metergoline but unaffected by 5-HT3 antagonists, ICS 205-930, MDL 72222, quipazine and 5-HT2 antagonist, ketanserin. Putative 5-HT1A agonists (8-OH-DPAT, ipsapirone, and buspirone) and 5-HT1B agonists (TFMPP and m-CPP) affected neither basal nor forskolin-dependent cyclic AMP accumulation. Receptor binding studies suggest that NCB-20 cells are devoid of 5-HT1A and 5-HT1B receptor sites. Application of 5-HT onto NCB-20 cells resulted in membrane depolarization by an evoked inward current which displayed rapid desensitization. 5-HT-mediated current had a reversal potential around 0 mV and was potently and reversibly inhibited by ICS 205-930. Our data suggest that in NCB-20 cells the 5-HT3 receptor is involved in the generation of inward currents, while the 5-HT receptor coupled to adenylate cyclase does not seem to correspond to any of the known receptor subtypes.
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PMID:Characterization of two distinct 5-HT receptors coupled to adenylate cyclase activation and ion current generation in NCB-20 cells. 168 72

The effects of serotonergic activation on cold-stimulated thyrotropin (TSH) and prolactin secretion were studied in male rats. Peripheral injections of both 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, and 1-(3-chlorophenyl)piperazine (m-CPP), a 5-HT1 agonist, decreased TSH levels. The action of 8-OH-DPAT was antagonized by (+/-)-pindolol, which is known to have 5-HT1 antagonist activity, but not by metergoline or ketanserin. The action of m-CPP was antagonized by ketanserin but not by metergoline. TSH levels were not affected by a 5-HT3 receptor agonist, 2-methyl-5-HT, or by a 5-HT3 antagonist, MDL 72222. Infusion of 8-OH-DPAT into the anterior third ventricle increased TSH levels; 5-HT tended to increase TSH levels, but the effect was not significant. Inversely, infusion of 5-HT, 8-OH-DPAT or m-CPP into the posterior third ventricle decreased TSH levels. The action of 5-HT was counteracted by metergoline, ketanserin and (+/-)-pindolol. Unexpectedly, m-CPP infusion into the anterior third ventricle also inhibited TSH secretion. The prolactin-elevating effects of 5-HT, 8-OH-DPAT and m-CPP were neither consistent nor site-specific. In conclusion, stimulation of both 5-HT1 and 5-HT2 receptors may inhibit TSH secretion, but the exact mechanism underlying the site-dependent action of 5-HT and 8-OH-DPAT on TSH secretion remains to be identified.
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PMID:Complex actions of serotonergic agonists on cold-stimulated TSH secretion in male rats. 214 94

1. Mice were isolated for 7-9 days. An isolated mouse and a mouse reared in group showed a difference in their behaviour when observed together under an inverted beaker. The isolated mouse makes one half escape attempts in regard to the grouped mouse. This is considered as a social behavioural deficit. 2. 1- 3-(trifluoromethyl)phenyl piperazine (TFMPP), 1-(3-chlorophenyl)piperazine (m-CPP) and 5-methoxy-3 (1,2,3,6-tetrahydropyridin-4-yl) 1-H indole (RU-24969) activating preferentially the 5-HT1B receptors increased the number of escape attempts of the isolated mice up to the level of grouped mice. 3. Penbutolol, a beta-blocking drug acting also at 5-HT1 receptors, devoid of effect when given alone, antagonized significantly and dose-dependently the effects of TFMPP, m-CPP and RU-24969. 4. The interaction between TFMPP and five various serotonin antagonists was examined. Neither the 5-HT2 receptor antagonist ritanserine, the 5-HT3 receptor antagonist ICS 205-930, the 5-HT1C receptor antagonists mianserin and cyproheptadine antagonized the effect of TFMPP. The neuroleptic spiperone decreased by itself the number of escape attempts and opposed the TFMPP effect. 5. Taken together, these results suggest that the isolation-induced social behavioural deficit may be considered as a behavioural model responsive to 5-HT1B agonists.
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PMID:Improvement of the isolation-induced social behavioural deficit involves activation of the 5-HT1B receptors. 230 Jun 82

1. A study was made of the effects of 5-hydroxytryptamine (5-HT) on pressor response induced in vivo by electrical stimulation of the sympathetic outflow from the spinal cord of pithed rats. All animals had been pretreated with atropine. Intravenous infusion of 5-hydroxytryptamine at doses of 10 and 20 micrograms kg-1 min-1 reduced the pressor effects obtained by electrical stimulation at intervals of 10 min over the 1 h of infusion. 2. This inhibitory action of 5-HT was depressed by cyproheptadine and methiothepin but was not modified by ketanserin or MDL-72222. By contrast, the inhibitory action of 5-HT was lost in pithed rats that had been pretreated with exogenous noradrenaline. 3. The 5-HT1 receptor agonist 5-carboxamidotryptamine (5-CT) caused an inhibition of the pressor response, whereas the 5-HT3 receptor agonist, 1-phenylbiguanide, produced a variable but significant increase in the pressor response. The 5-HT2 receptor agonist, m-CPP, did not modify the pressor sympathetic response. 4. Our results suggest that 5-hydroxytryptamine interferes with sympathetic neurotransmission by inhibiting pressor effects as a result of stimulation of the complete sympathetic outflow, and that this inhibition is mainly through a presynaptic 5-HT1 mechanism.
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PMID:Inhibitory 5-hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats. 788 92

Effects of the non-selective 5-hydroxytryptamine (5-HT) receptor agonist m-chlorophenylpiperazine (m-CPP) on the nociceptive responsiveness in a hot plate and tail flick tests were examined in mice. Intraperitoneal administration of m-CPP (1-10 mg/kg) produced a dose-dependent antinociception in both those tests; the effect of m-CPP in the hot plate test was stronger. The antinociceptive effect of m-CPP in either test was abolished by pretreatment with mesulergine (2 mg/kg), ritanserin (1-2 mg/kg), 5-HT2A/5-HT2C receptor antagonists, and metergoline (0.5-2 mg/kg), a non-selective 5-HT receptor antagonist. On the other hand, spiperone (0.25-0.5 mg/kg), a dopamine, 5-HT1A and 5-HT2A receptor antagonist; pindolol (4-8 mg/kg), a beta-adrenoceptor, 5-HT1A and 5-HT1B receptor antagonist and zacopride (0.1-1 mg/kg) a 5-HT3 receptor antagonist, did not affect the analgesia induced by m-CPP. Neither of the drugs used as putative receptor antagonists changed the nociceptive responsiveness in mice. The obtained results suggest that the analgesia induced by m-CPP is mediated by 5-HT2C receptors.
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PMID:Involvement of 5-HT2C receptors in the m-CPP-induced antinociception in mice. 789 29

A study was made of the effects of 5-hydroxytryptamine (5-HT) on bradycardia induced in vivo by electrical stimulation of the vagus nerves in pithed rats pretreated with atenolol. 5-HT significantly decreased vagally induced, but not acetylcholine-induced, bradycardia. The first effect was blocked by methiothepin, ketanserin or methiothepin with ketanserin. When 5-HT1 and 5-HT2 receptors were blocked, 5-HT produced an increase in vagally induced bradycardia. Both the inhibition and the potentiation were blocked by simultaneous pretreatment with methiothepin, ketanserin and MDL-72222. The 5-HT2 receptor agonist m-CPP (1-(3-chlorophenyl) piperazine dihydrochloride) caused an inhibition of vagally induced bradycardia whereas the 5-HT3 receptor agonist m-CPBG (1-(m-chlorophenyl)biguanide hydrochloride) produced a significant increase. The data suggest the presence of presynaptic and/or ganglionic 5-HT2 receptors in parasympathetic innervation of the rat heart, stimulation of which inhibits the release of acetylcholine. The presence of 5-HT3 receptors is also suggested, stimulation of which induces the release of acetylcholine.
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PMID:Pharmacological characterization of 5-HT receptors in parasympathetic innervation of rat heart. 815 57

Cholinergic neurotransmission is thought to be modulated by serotonin as documented in animal and human studies. We examined the effects of the muscarinic antagonist scopolamine (0.4 mg IV) given alone or together with the serotonin mixed agonist/antagonist m-chlorophenylpiperazine (m-CPP, 0.08 mg/kg IV), and the selective 5-HT3 receptor antagonist ondansetron (0.15 mg/kg IV). Ten normal elderly volunteers each received five separate pharmacologic challenges (placebo, ondansetron, scopolamine, scopolamine+ondansetron, and scopolamine+m-CPP). Cognitive, behavioral, and physiologic variables were analyzed using repeated measures analysis of variance. The acute effects of scopolamine in certain cognitive, behavioral, and physiological measures were significantly exaggerated by the addition of m-CPP. Scopolamine's cognitive effects were unaffected by ondansetron at the dose tested, nor did ondansetron given alone affect basal cognitive performance. This pilot study suggests that the serotonin mixed agonist/antagonist m-CPP may influence cholinergic neurotransmission. The changes associated with the combination of scopolamine and m-CPP do not appear to be secondary to simple pharmacokinetic alterations and suggest a complex interaction between the cholinergic and serotonergic systems centrally.
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PMID:Serotonergic modulation of anticholinergic effects on cognition and behavior in elderly humans. 852 75

1. This study was designed to investigate the effect of meta-chlorophenylpiperazine (m-CPP; a 5-hydroxytryptamine (5-HT) receptor agonist) on the formalin-induced nociceptive responses in normal, insulin-dependent streptozotocin (STZ) diabetic and non-insulin dependent genetically diabetic (db/db) mice. 2. A subcutaneous injection of diluted formalin (1% formaldehyde in 0.9% saline, 10 microliters) under the plantar surface of the left hindpaw induced biphasic nociceptive responses, the first and second phases considered to represent acute and chronic pain, respectively. The former response in db/db mice was significantly lower than those in normal mice, and the latter responses in STZ and db/db mice were significantly lower than those in normal mice. 3. In normal mice, m-CPP (0.32-3.2 mg ml-1, p.o.) exhibited potent antinociceptive activity, dose-dependently attenuating the first and second phase; the ID50 value of the second phase was 0.4 mg kg-1. m-CPP (0.32-3.2 mg kg-1, p.o.) also dose-dependently attenuated the formalin-induced nociceptive responses in STZ-induced diabetic mice and genetically diabetic db/db mice, and the activities were comparable to those in normal mice. 4. The antinociceptive activities of m-CPP (1 mg kg-1, p.o.) were significantly inhibited by pretreatment with pindolol (a 5-HT1-receptor antagonist, 1 mg kg-1, i.p.) or ketanserin (a 5-HT2 receptor antagonist, 1 mg kg-1, i.p.) but were hardly affected by ICS205-930 (a 5-HT3 receptor antagonist, 1 mg kg-1, i.p.). 5. These results suggest that m-CPP inhibits not only acute but also chronic pain transmission through 5-HT1 and 5-HT2 receptors, and that the 5-hydroxytryptaminergic antinociceptive pathways are little affected by diabetes.
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PMID:Meta-chlorophenylpiperazine attenuates formalin-induced nociceptive responses through 5-HT1/2 receptors in both normal and diabetic mice. 871 87

Several serotonin3 (5-HT3) antagonists have been shown to attenuate the anxiogenic effects of the serotonergic agent, m-chlorophenylpiperazine (m-CPP), in animal models, but little data regarding possible effects of 5-HT3 antagonists on responses to m-CPP are available from studies in humans. Therefore, we studied the behavioral, physiological and neuroendocrine responses of 12 healthy volunteers to i.v. administered placebo and m-CPP (0.08 mg/kg), with and without i.v. pretreatment with the selective 5-HT3 antagonist, ondansetron (0.15 mg/kg). Compared to placebo, m-CPP given alone significantly increased ratings of anxiety and several other behavioral measures. m-CPP also produced statistically significant increases in temperature, systolic and diastolic blood pressure, heart rate, and in plasma concentrations of adrenocorticotropic hormone, cortisol, prolactin and norepinephrine. Responses to ondansetron given alone were no different from those of placebo. Pretreatment with ondansetron did not affect peak behavioral responses to m-CPP, but was associated with a significantly earlier return to baseline levels of ratings of anxiety and functional deficit as well as a summary measure of overall behavioral effects. Following ondansetron pretreatment, the increases produced by m-CPP in systolic and diastolic blood pressure and heart rate were no longer significantly different from placebo. Ondansetron pretreatment significantly reduced their plasma cortisol response to m-CPP without affecting the other plasma hormone responses. Plasma concentrations of m-CPP were unaffected by ondansetron pretreatment. These findings suggest that in normal human subjects some behavioral, cardiovascular and neuroendocrine effects of m-CPP may be partially modulated by 5-HT3 receptor-mediated mechanisms.
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PMID:Behavioral, physiological and neuroendocrine responses in healthy volunteers to m-chlorophenylpiperazine (m-CPP) with and without ondansetron pretreatment. 910 5


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