Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors.
Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors.
复制标题
葡萄糖通过调节 5-HT3 受体来增加迷走神经传入中枢神经末梢的突触传递。
DOI:
10.1152/ajpgi.90288.2008
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发表时间:
2008
期刊:
影响因子:
--
通讯作者:
Browning,KirsteenN
中科院分区:
文献类型:
--
作者:
Wan,Shuxia;Browning,KirsteenN
Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT3receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT3receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT3receptors, and the number of 5-HT3receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT3receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.
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期刊:
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