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Closed Access item A microdialysis study of the in vivo release of serotonin in the median raphe nucleus of the rat.
|Keywords:||5-Hydroxytryptamine, 5-HT1A receptors, reserpine, TTX, EEDQ, 8-OH-DPAT, BAY×3702, WAY-100635, median raphe nucleus, microdialysis|
|Publisher:||John Wiley & Sons|
|Citation:||British Journal of Pharmacology 125 (6) : 1361–1367 (1998)|
|Abstract:||The present study has examined several characteristics of the release of 5-HT in the median raphe nucleus in terms of its dependence of nerve impulse, provenance of a vesicular storage fraction as well as the regulatory role played by 5-HT1A receptors. Tetrodotoxin (1 microM) and reserpine (5 mg kg(-1), i.p.) virtually suppressed the output of 5-HT. The administration of EEDQ (10 mg kg(-1), i.p.) did not alter the basal release of 5-HT but abolished the reduction of 5-HT release induced by 8-OH-DPAT (0.1 mg kg(-1), s.c.). The perfusion of 1-100 microM of 8-OH-DPAT or the novel 5-HT1A agonist BAY x 3702 decreased the efflux of 5-HT, whereas the perfusion of the 5-HT1A antagonist WAY-100635 failed to alter 5-HT release. The decrease in dialysate 5-HT induced by 100 microM 8-OH-DPAT was reversed by the concurrent perfusion of 100 microM WAY-100635. Also, the perfusion of 100 microM WAY-100635 for 2 h inhibited partly the reduction of 5-HT release evoked by the systemic administration of 8-OH-DPAT (0.1 mg kg(-1)). These results indicate that extracellular 5-HT in the median raphe nucleus is stored in vesicles and released in an impulse-dependent manner. Also, the basal release of 5-HT in the median raphe nucleus does not appear to be under the tonic control of somatodendritic 5-HT1A receptors by endogenous 5-HT. Instead, this feedback mechanism seems to be triggered when an excess of the transmitter or a 5-HT1A agonist is present in the extracellular space of the median raphe nucleus.|
|Publisher version (URL):||http://onlinelibrary.wiley.com/doi/10.1038/sj.bjp.0702206/full|
|E-ISSNmetadata.dc.identifier.doi = DOI:||1476-5381|
|Appears in Collections:||(IIBB) Artículos|
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