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 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

1. The effects of 1-(3-chlorophenyl)piperazine (mCPP) and 1-[3-(trifluoromethyl)phenyl] piperazine (TFMPP) on activity of rats in a novel cage, and on the rotorod and elevated bar co-ordination tests was examined. 2. Peripherally administered mCPP and TFMPP dose-dependently reduced locomotion, rearing, and feeding scores but not grooming of freely fed rats placed in a novel observation cage. Yawning behaviour was increased. Similar effects were also observed after injection of mCPP into the 3rd ventricle. 3. Co-ordination on a rotating drum of both untrained and trained rats was impaired following mCPP but co-ordination on an elevated bar was not. 4. The hypoactivity induced by mCPP was opposed by three antagonists with high affinity for the 5-hydroxytryptamine (5-HT1C) site; metergoline, mianserin, cyproheptadine and possibly also by a fourth antagonist mesulergine. Metergoline, mianserin and cyproheptadine also opposed the reduction in feeding scores. However, neither effect of mCPP was antagonized by the 5-HT2-receptor antagonists ketanserin or ritanserin, the 5-HT3-receptor antagonist ICS 205-930, the 5-HT1A and 5-HT1B-receptor antagonists (-)-pindolol, (-)-propranolol and (+/-)-cyanopindolol or the 5-HT1A-, 5-HT2- and dopamine receptor antagonist spiperone. The specific alpha 2-adrenoceptor antagonist idazoxan was also without effect. 5. Hypoactivity induced by TFMPP was similarly antagonized by mianserin but unaffected by (+/-)-cyanopindolol. 6. These results suggest that the hypoactivity is mediated by central 5-HT1C-receptors and that mCPP and possibly TFMPP may be 5-HT1C-receptor agonists. 7. As mianserin, cyproheptadine and mesulergine in the absence of mCPP did not increase locomotion but increased the number of feeding scores, the activation of 5-HT1C-receptors may be of physiological importance in the control of appetite. The possible relevance of these results to the therapeutic and side-effects of clinically used antidepressants (particularly trazodone and mianserin) and anorexigenic drugs is discussed.
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PMID:Evidence that mCPP may have behavioural effects mediated by central 5-HT1C receptors. 340 32

Decreased activity of the medial prefrontal cortex (mPFC) has been considered a basis for core symptoms of schizophrenia, an illness associated with a neurodevelopmental origin. Evidence from preclinical and clinical studies indicates that serotonin (5-HT)1A receptors play a crucial role in the energy metabolism of the mPFC. This study was undertaken to determine (1) if transient blockade of N-methyl-D-aspartate receptors during the neonatal stage inhibit energy demands in response to stress, as measured by extracellular lactate concentrations, in the mPFC at the young adult stage, and (2) if tandospirone, a 5-HT1A partial agonist, reverses the effect of the neonatal insult on energy metabolism. Male pups received MK-801 (0.20 mg/kg) on postnatal days (PDs) 7-10. On PD 63, footshock stress-induced lactate levels were measured using in vivo microdialysis technique. Tandospirone (0.1, 1.0, and 5.0 mg/kg) was administered once daily for 14 days before the measurement of lactate levels. Neonatal MK-801 treatment suppressed footshock stress-induced lactate production in the mPFC, but not caudate-putamen, whereas basal lactate levels were not significantly changed in either brain region. The MK-801-induced suppression of footshock stress-induced lactate production in the mPFC was attenuated by tandospirone at 1.0mg/kg/day, but not 0.1 or 5.0 mg/kg/day, which is an effect antagonized by coadministration of WAY-100635, a selective 5-HT1A antagonist. These results suggest a role for impaired lactate metabolism in some of the core symptoms of schizophrenia, for example, negative symptoms and cognitive deficits. The implications for the ability of 5-HT1A agonism to ameliorate impaired lactate production in the mPFC of this animal model are discussed.
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PMID:Effect of transient blockade of N-methyl-D-aspartate receptors at neonatal stage on stress-induced lactate metabolism in the medial prefrontal cortex of adult rats: role of 5-HT1A receptor agonism. 2221 69