Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Activation of serotonergic neurotransmission has been shown to increase plasma beta-endorphin-like immunoreactivity (beta-End-LI). To study the mechanism(s) of this action, we measured the effects of 3 potent serotonin (5-HT) agonists with different structures and 5-HT receptor binding profiles in conscious unrestrained Sprague-Dawley rats in vivo and in dispersed anterior pituicytes in vitro. The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), and the 5-HT2 agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), all markedly increased beta-End-LI in plasma in vivo. All 3 responses were blocked by dexamethasone pretreatment. Pituitary stalk transection (PST), as well as pretreatment with rabbit serum hyperimmune against rat corticotropin-releasing hormone (CRH, TS-6) completely abolished beta-End-LI response to 8-OH-DPAT and attenuated the responses by about 60% to DOI. Responses to m-CPP were markedly attenuated in PST rats, but pretreatment with TS-6 had no significant effect. To examine whether vasopressin (AVP) might be involved in the CRH neutralizing antibody-resistant beta-End-LI responses after m-CPP and DOI, we measured AVP concentrations after each agonist, m-CPP, but not DOI or 8-OH-DPAT, significantly elevated circulating AVP levels. As a proof of direct pituitary effect, DOI markedly stimulated beta-End-LI release from the anterior pituitary cell culture preparation in vitro. It was approximately as potent as CRH in the picomolar range, m-CPP was much less effective than DOI, while 8-OH-DPAT did not stimulate beta-End-LI release in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin responses to different serotonin agonists: involvement of corticotropin-releasing hormone, vasopressin and direct pituitary action. 215 Jul 76

The study examined the effect of both oxaprotiline (OXA) enantiomers on the serotonin system in rats and mice. (+)-OXA and (-)-OXA partly inhibit the behavioral syndrome induced by 8-OH-DPAT and 5-methoxy-dimethyltryptamine (5-MeODMT) in normal and reserpinized rats. Imipramine and desipramine produced a similar but less potent effect. (+)-OXA and, to a lesser extent, (-)-OXA antagonized the m-chlorophenylpiperazine (m-CPP)-induced hypothermia in mice. Imipramine and desipramine produced no such effect. (+)-OXA attenuated the head-twitch response to L-5-HTP in mice, but (-)-OXA has no such action. Neither enantiomer inhibited the fenfluramine-induced hyperthermia in rats nor antagonized m-CPP-induced stimulation of hind limb flexor reflex of spinal rat. The obtained results indicate that both enantiomers may have a 5-HT1B-antagonistic action and a less potent 5-HT1A-antagonistic one; on the other hand, they shown no 5-HT2-antagonistic activity.
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PMID:Pharmacological effects of oxaprotiline enantiomers on the central serotonin system. 253 22

The effects of three potent serotonin (5-HT) agonists with different structures and 5-HT receptor binding profiles on sympathoadrenomedullary and hypothalamo-pituitary-adrenocortical axis functions were assessed in conscious, freely moving male Sprague-Dawley rats. The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), and the 5-HT2/5-HT1C agonist, 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI), all produced marked dose-dependent increases in plasma epinephrine and ACTH concentrations. Both epinephrine and ACTH responses peaked at 10 min and showed strong positive correlations across all drugs and doses studied. Corticosterone increases showed a saturable response pattern and were close to the maximum level with a relatively small (approximately 2.5-fold) increase in plasma ACTH concentrations. Norepinephrine levels showed small dose-dependent increases after 8-OH-DPAT and m-CPP and decreases after DOI treatment. These results suggest that both the sympathoadrenomedullary system and the hypothalamo-pituitary-adrenocortical axis can be activated via 5-HT1 and 5-HT2 receptors and that these two systems may have common or similar regulatory mechanisms triggered by these stimuli.
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PMID:Serotonin agonists cause parallel activation of the sympathoadrenomedullary system and the hypothalamo-pituitary-adrenocortical axis in conscious rats. 255 61

The effects of chronic cortisol treatment on neuroendocrine and behavioral responses to serotonin1 (5-HT1) receptor agonists were studied in conscious, freely moving rats. Seven-day cortisol treatment (25 mg/kg/day with osmotic minipumps) markedly suppressed basal plasma corticotropin (ACTH) and corticosterone concentrations, indicating a suppression of the hypothalamo-pituitary-adrenocortical axis. Cortisol also decreased body weight, food intake, plasma norepinephrine (NE), and epinephrine (E) levels. In the drug challenge studies, we used two 5-HT1 agonists, the 5-HT1B and 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), and the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OHDPAT), to examine the effect of cortisol on their behavioral and neuroendocrine effects. After 7-day cortisol treatment, plasma prolactin responses to both m-CPP and 8-OHDPAT were significantly decreased. While the plasma NE, E, and food intake responses to m-CPP were also significantly reduced by cortisol treatment, these same responses to 8-OHDPAT were unchanged. The effect of m-CPP on locomotor activity was also decreased. Since only the responses to m-CPP and 8-OHDPAT previously shown to be antagonized by pretreatment with the 5-HT1/5-HT2 antagonist, metergoline, were significantly attenuated after cortisol treatment, these changes may be specific to 5-HT receptors. These data indicate that chronic exposure to high glucocorticoid levels alters 5-HT1 receptor-mediated functions and provides additional evidence relevant to the contribution of glucocorticoid elevation to the symptoms of depression.
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PMID:Long-term cortisol treatment impairs behavioral and neuroendocrine responses to 5-HT1 agonists in the rat. 255 39

The effects of several 5-HT1A agonists and excitatory amino acid antagonists were compared to the standard benzodiazepines, diazepam and chlordiazepoxide (CDP) in two assays predictive of anxiolytic activity, the social interaction and elevated plus maze procedures. Indicative of anxiolytic effects the 5-HT1A agonists, buspirone, gepirone and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) all significantly increased social interaction time and open arm exploration time in the social interaction and elevated plus maze procedures, respectively. Likewise, anxiolytic activity in these assays were also produced by the competitive N-methyl-D-aspartate (NMDA) antagonists, 2-amino-5-phosphonovaleric acid (AP-5), 2-amino-7-phosphonoheptanoic acid (AP-7), 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and the non-competitive NMDA antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) while NMDA produced anxiogenic effects. Furthermore, the anxiolytic effects of these agents were of equal magnitude to the benzodiazepines. These two classes of compounds were differentiated in the yohimbine-induced seizure assay, with the NMDA antagonists dose dependently antagonizing seizures similar to the benzodiazepines while the 5-HT1A agonists were inactive. These results suggest that the 5-HT1A agonists and the NMDA antagonists may be potential non-classical anxiolytic agents with different mechanisms of action.
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PMID:Effects of 5-HT1A receptor agonists and NMDA receptor antagonists in the social interaction test and the elevated plus maze. 257 84

Using standard operant procedures, rats were trained to discriminate the 5-HT agonist RU24969 (0.5 mg/kg IP) from saline. Stable responding was established and tests of stimulus generalisation and stimulus antagonism were performed with a range of 5-HT receptor ligands. The RU24969 cue was selective as neither 5-HT receptor ligands MK212, DPAT, ipsapirone, GR38032F or the 5-HT releasing agent, fenfluramine nor yohimbine were able to substitute for RU24969 in tests of generalisation. However, TFMPP, CPP and, of particular interest, propranolol substituted for the RU24969 stimulus, although full substitution only occurred with doses that disrupted responding. The RU24969 stimulus was not antagonised by propranolol, metergoline, ritanserin or GR38032F. This pharmacological profile suggests that the RU24969 stimulus is mediated via a subtype of 5-HT1 sites different from 5-HT1A and that propranolol may be an agonist at this site.
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PMID:The discriminative stimulus properties of the 5HT1 agonist RU24969. 261 95

The serotonin (5-HT) agonist, m-chlorophenylpiperazine (m-CPP), has been shown to increase blood pressure (BP), heart rate (HR), plasma catecholamine and prolactin (PRL) concentrations and to cause hypoactivity in rodents. In the present study, we used selective 5-HT and adrenergic antagonists to study the involvement of different receptor subtypes on the effects of m-CPP in conscious, freely moving rats. Hypoactivity and PRL responses were blocked by pretreatment with metergoline but not by pretreatment with other antagonists. BP increases were antagonized by ritanserin (0.1, 0.63 and 2.0 mg/kg) and ketanserin; metergoline, xylamidine or prazosin pretreatment had only partial effects on BP responses. HR increases were antagonized by yohimbine, pindolol, ketanserin and by the two higher doses of ritanserin. After pretreatment with the two higher doses of ritanserin, m-CPP decreased markedly BP and HR. These decreases were prevented by metergoline pretreatment. Norepinephrine and epinephrine responses were dose-dependently attenuated by ritanserin; naloxone pretreatment attenuated epinephrine but not norepinephrine responses. These data suggest that hypoactivity, PRL responses, and cardiodepressive effects of m-CPP are mediated by 5-HT1 receptors. It is likely that the hypoactivity and PRL responses of m-CPP are mediated by 5-HT1B receptors, and the cardiodepressive effects by 5-HT1A receptors. Increases in BP appear to be primarily mediated by stimulation of 5-HT2 receptors. Both adrenergic and serotonergic mechanisms are involved in HR responses. The catecholamine responses to m-CPP appear to be partially mediated by 5-HT1C receptors and also by nonserotonergic mechanisms.
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PMID:Different serotonin receptors mediate blood pressure, heart rate, plasma catecholamine and prolactin responses to m-chlorophenylpiperazine in conscious rats. 274 12

The food intake suppressant effects of three serotonin agonists, m-CPP (a selective 5-HT1B agonist), 8-OHDPAT (a selective 5-HT1A agonist) and fenfluramine (a 5-HT releasing agent) were compared in three different rat strains: Wistar, Sprague-Dawley (SD) and Fawn-Hooded (FH) rats. Administration of all three serotonin agonists produced dose-dependent decreases in 1 h food intake in all three strains. FH animals were significantly less sensitive to the food intake suppressant effects of all three serotonin agonists than either Wistar or SD rats. Body weight gain over the 9-week course of the study was also significantly less in FH animals than either Wistar or SD animals. These findings support some other data that Fawn Hooded rats, a strain with a peripheral platelet serotonin storage disorder, also possess altered central nervous system serotonergic function.
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PMID:Fawn hooded rats are subsensitive to the food intake suppressant effects of 5-HT agonists. 296 18

In the present study we examined the effect of different drugs on the m-trifluoromethylphenylpiperazine (TFMPP)- and m-chlorophenylpiperazine (m-CPP)-induced hypothermia in mice. Both the hypothermias studied are blocked or reversed by pindolol, cyanopindolol and compound 21-009, but not by atenolol. Neither hypothermia is antagonized by 5-HT1A antagonists (ipsapirone, spiperone), a 5-HT1C antagonist (mesulergine), 5-HT2 antagonists (cyproheptadine, mianserin, methysergide), 5-HT3 antagonists (ICS 205930, metoclopramide). The examined hypothermias are not antagonized by other antihypothermic agents (pimozide, idazoxan, atropine). The 8-OH-DPAT-induced hypothermia is not affected by cyanopindolol or compound 21009. The obtained results indicate that the TFMPP- and m-CPP-induced hypothermias in mice are mediated by 5-HT1B. These hypothermias may be a good screening test for evaluation of the 5-HT1B-agonistic and 5-HT1B-antagonistic activity.
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PMID:Hypothermia induced by m-trifluoromethylphenylpiperazine or m-chlorophenylpiperazine: an effect mediated by 5-HT1B receptors? 296 49


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