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)

Intrathecal administration (ith) of 5-hydroxytryptamine (5-HT, 1.56, 3.125, 6.25 and 12.5 micrograms/10 microliters) to conscious rats produced a marked dose-dependent hypertensive effect without significant change in heart rate (HR). Ith administration of fluoxetine (10 micrograms/microliters), one of the presynaptic reuptake inhibitors of 5-HT, produced a marked increase in the mean arterial blood pressure (mABP). This effect could be prevented by a pretreatment with cinanserin (25 micrograms ith) as a blocker of 5-HT receptor. It was further observed that ith of 8-OH-DAPT (2.5, 5, 10 micrograms/10 microliters), a 5-HT1A receptor agonist, produced a dose-dependent increase of mABP and lowering of HR. However, ith of 5-HT3 receptor agonist 2-Methylserotonin (25, 50, 100 micrograms/10 microliters), decreased mABP markedly without change in HR. The results indicate that 5-HT in the spinal cord may extra hypertensive effect via 5-HT1A receptor and a hypotensive effect via 5-HT3 receptor. This gives a possible explanation about the conflicting reports concerning the effect of 5-HT in the central nervous system on blood pressure.
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PMID:[Cardiovascular reactions mediated by 5-HT1A and 5-HT3 receptors in the spinal cord of conscious rats]. 179 18

The actions of 5-hydroxytryptamine (5-HT) on the electrically induced twitch responses of mouse vas deferens were studied. 5-HT at the concentration range of 10(-8) to 10(-4) M produced a "bell-shaped" concentration-response curve on the field-stimulated twitch contractions; the enhancement of the contractions was maximum at 10(-5) M and progressively reduced at the concentrations of more than 10(-5) M. In the presence of ketanserin, whereas the stimulatory response to low concentrations of 5-HT (less than or equal to 10(-6) M) was not changed, that to high concentrations was reversed. The stimulation by 5-HT (less than or equal to 10(-5) M) was principally antagonized by MDL 72222. In the presence of both MDL 72222 and ketanserin, 5-HT inhibited the twitch contractions in a dose-dependent manner. 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and BP-554 (1-[3-(3,4-methylenedioxyphenoxy)propyl]-4-phenyl piperazine), selective 5-HT1A agonists, only inhibited the twitch contractions. Downward slope of the contraction-response curve of 5-HT (greater than or equal to 10(-5) 5 M) was shifted to right in the presence of 8-OH-DPAT. 5-HT and 8-OH-DPAT had no effect on the tension of unstimulated organs. Contractions elicited by ATP were potentiated by 5-HT, which was antagonized by ketanserin. 8-OH-DAPT did not affect ATP-elicited contractions. These results suggest the presence of presynaptic 5-HT1, maybe 5-HT1A and 5-HT3 receptors mediating inhibition and potentiation, respectively, of neurotransmitter release and of postsynaptic responsible for enhancing neurogenic contractions in mouse vas deferens.
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PMID:5-Hydroxytryptamine modulation of electrically induced twitch responses of mouse vas deferens: involvement of multiple 5-hydroxytryptamine receptors. 239 4

Multiple extracellular recording electrodes were used to study the intra- and interhemispheric spread of stimulus-evoked epileptiform responses in adult mouse neocortical slices. Bath application of 20 microM bicuculline methiodide induced epileptiform activity that propagated at approximately 0.08 m/s over several millimeters in rostro-caudal and medio-lateral direction within the ipsilateral hemisphere and across the corpus callosum to the contralateral hemisphere. A vertical incision from layer II to subcortical regions did not prevent the spread to remote cortical regions, indicating that layer I plays a major role in the lateral propagation of epileptiform activity. The intra- and interhemispheric spread was not influenced by application of an N-methyl-d-aspartate (NMDA) receptor antagonist, but blocked by an antagonist acting at the (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-type glutamate receptor. The potential role of potassium channel activation in controlling the generation or spread of epileptiform activity was tested by applying the potassium channel opener cromakalim and the serotonin type 1A (5-HT1A) receptor agonist (+/-)-8-hydroxydipropylaminotetralin (8-OH-DPAT) to the disinhibited slices. Whereas cromakalim reduced the neuronal excitability and blocked all epileptiform responses, 8-OH-DAPT did not affect the activity pattern. Our results suggest that propagating epileptiform activity in disinhibited neocortical structures is predominantly mediated by activation of AMPA receptors and controllable by activation of a voltage-dependent potassium current.
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PMID:Pattern and pharmacology of propagating epileptiform activity in mouse cerebral cortex. 974 72

This study examined the influence of pretreatment with N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclohexane carboxamide maleate (WAY100635, full 5-HT1A receptor antagonist, 37 nmol) on feeding effects evoked by local injections of 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT, 5-HT(1A) and 5-HT(7) receptor agonist, 6 nmol) into the LH and into the ARC of female rats adapted to a wet mash diet (enriched with 10% sucrose), during diestrus or estrus. The results showed that the LH-pretreatment with WAY100635 suppressed the hypophagic effects evoked by 8-OH-DPAT during estrus as well as diestrus. The ARC pretreatment with WAY100635 blockaded the hypophagia evoked by 8-OH-DPAT in estrus rats. The previous treatment with WAY100635 in the ARC also suppressed the feeding duration decrease evoked by 8-OH-DPAT in estrus. The latency to start feeding, the drinking behavior and the durations of other non-ingestive behaviors were not affected by the different treatments, hypothalamic regions (LH or ARC), and/or estrous cycle stages (diestrus and estrus), except for the locomotion duration increase after 8-OH-DAPT in LH-pretreated rats in diestrus. The present findings confirm our previous suggestion that ARC- and the LH-5-HT(1A) receptors participate in the serotonergic control of feeding and that these feeding-related serotonergic circuits in LH are affected by ovarian hormones, since the treatment with WAY100635 evoked a hypophagia response during the diestrus phases.
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PMID:WAY100635 blocks the hypophagia induced by 8-OH-DPAT in the hypothalamic nuclei. 2013 4