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Query: UNIPROT:P46098 (
5-HT3 receptor
)
2,290
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effect of
5-HT3 receptor
agonists and antagonists on the hypoxia/
hypoglycemia
(ischemia)-induced decrease in CA1 field potential elicited by stimulation of Schaffer collaterals was investigated using rat hippocampal slices. Treatment with the
5-HT3 receptor
agonist, 2-methyl-5-HT (1-10 microM), exacerbated the ischemia-induced decreased in CA1 field potential, whereas treatment with the
5-HT3 receptor
antagonist, Y-25130 (0.1-100 microM), or the 5-HT2 receptor antagonist, ketanserin (10, 100 microM), produced dose-dependent neuroprotection against the ischemia-induced decrease. However, in normal non-ischemic solution these treatments did not significantly change the CA1 field potential. The protective action of Y-25130 was blocked by co-treatment with 2-methyl-5-HT. The magnitude of protection in the Y-25130-treated group (EC50, 1.8 microM) was about 20 times greater than that in the ketanserin-treated group (EC50, 33 microM). The present study demonstrated that stimulation of 5-HT3 receptors plays a detrimental role in the development of ischemic damage, whereas blockade of the
5-HT3 receptor
plays a neuroprotective role in ischemic damage, suggesting a facilitatory role of 5-HT neurons in ischemia-induced neuronal deficits.
...
PMID:Neuroprotective effect of 5-HT3 receptor antagonist on ischemia-induced decrease in CA1 field potential in rat hippocampal slices. 145 43
Effects of tryptamine on tolbutamide-induced
hypoglycemia
were investigated in mice. Tryptamine significantly inhibited
hypoglycemia
elicited by tolbutamide. The inhibitory effects of tryptamine were strongly blocked by the 5-HT1 and 5-HT2 receptor antagonist methysergide and the 5-HT2 receptor antagonist ketanserin, while the
5-HT3 receptor
antagonist ICS 205-930 was without effect. Tryptamine induced hyperglucagonemia in tolbutamide-treated mice, and this effect elicited by tryptamine was strongly inhibited by the 5-HT2 receptor antagonist ketanserin. These results suggest that the inhibitory effects of tryptamine on tolbutamide-induced
hypoglycemia
are mediated by 5-HT2 receptors and that tryptamine is involved in glucagon release.
...
PMID:Inhibitory effects of tryptamine on tolbutamide-induced hypoglycemia in mice: mediation by 5-HT receptors. 813 57
The present study was undertaken in order to establish the possible involvement of 5-HT3 serotonergic receptors in the control of basal and/or
hypoglycemia
-stimulated arginine vasopressin (AVP) and/or oxytocin (OT) secretion. For this purpose, 12 normal men were injected intravenously with a bolus of 4 mg ondansetron, a specific
5-HT3 receptor
antagonist, under basal conditions (n = 6) or 30 min before insulin (0.15 IU/kg body weight) administration (n = 6) (insulin tolerance test (ITT)). Control experiments with normal saline instead of ondansetron treatment were performed. Furthermore, on a different occasion, the same subjects were tested in identical experimental conditions with 8 mg ondansetron. Our results showed that the hypoglycemic response to insulin was similar during the ITT and ondansetron plus ITT. Inhibition of 5-HT3 serotonergic receptors with ondansetron (4 or 8 mg) did not modify the basal secretion of AVP and OT and the OT response to insulin-induced
hypoglycemia
. In contrast, the administration of 4 or 8 mg ondansetron significantly reduced in a similar manner
hypoglycemia
-induced AVP rise. Mean peak level at 45 min after insulin injection was 2.25 times higher than baseline in the control ITT and 1.5 times higher than basal value in the ondansetron (4 or 8 mg) plus ITT. These data demonstrate that 5-HT3 serotonergic receptors at least partially mediate the AVP response to
hypoglycemia
, without modifying the simultaneous OT response. On the other hand, 5-HT3 receptors do not appear to be involved in the control of basal posterior pituitary hormone secretions.
...
PMID:5-HT3 serotonergic receptor mediation of hypoglycemia-induced arginine-vasopressin but not oxytocin secretion in normal men. 963 16