Presynaptic noradrenergic regulation of glutamate inputs to hypothalamic magnocellular neurones

Presynaptic noradrenergic regulation of glutamate inputs to hypothalamic magnocellular neurones
复制标题

DOI:
10.1046/j.1365-2826.2003.01063.x
复制
发表时间:
2003-08-01
影响因子:
3.2
通讯作者:
Tasker, JG
Tasker, JG
中科院分区:
医学3区
文献类型:
--
作者:
Boudaba, C;Di, S;Tasker, JG

文献摘要

被引文献

相似文献

谷氨酸和去甲肾上腺素递质系统在下丘脑大细胞神经元的突触控制中起关键作用。我们最近报道了一个去甲肾上腺素敏感的谷氨酸电路在室旁核(PVN)的项目,以大细胞神经元。在这里,我们提出的证据去甲肾上腺素调节谷氨酸释放的PVN和视上核(SON)通过对突触前末梢的行动。记录全细胞突触电流在大细胞神经元的SON和PVN在急性切片制备。浴应用去甲肾上腺素(100 μ m)引起了一个强大的,可逆的增加,在100%的SON神经元(246%)和88%的PVN大细胞神经元(259%)的自发性突触后兴奋性电流的频率。去甲肾上腺素诱导的谷氨酸释放增加是通过激活突触前α(1)受体和α(2)受体介导的,但α(1)受体成分是反应的主要成分。去甲肾上腺素的突触前作用主要是,虽然不是完全,耐钠依赖性尖峰的封锁,涉及突触前终端位点的行动。有趣的是,尖峰依赖的组件的响应是更大的PVN比SON大细胞神经元。去甲肾上腺素对谷氨酸释放的这种强突触前促进作用,结合去甲肾上腺素已知的兴奋性突触后作用、对局部谷氨酸回路的激活作用和对γ-氨基丁酸释放的抑制作用,表明去甲肾上腺素在生理刺激期间对催产素和加压素释放的调节中具有强兴奋性作用。
Glutamate and norepinephrine transmitter systems play critical roles in the synaptic control of hypothalamic magnocellular neurones. We recently reported on a norepinephrine-sensitive glutamate circuit within the paraventricular nucleus (PVN) that projects to magnocellular neurones. Here, we present evidence for norepinephrine regulation of glutamate release in the PVN and supraoptic nucleus (SON) via actions on presynaptic terminals. Whole-cell synaptic currents were recorded in magnocellular neurones of the SON and PVN in an acute slice preparation. Bath application of norepinephrine (100 mum) caused a robust, reversible increase in the frequency of spontaneous glutamatergic excitatory postsynaptic currents in 100% of SON neurones (246%) and in 88% of PVN magnocellular neurones (259%). The norepinephrine-induced increase in glutamate release was mediated by activation of both presynaptic alpha(1) receptors and alpha(2) receptors, but the alpha(1) -receptor component was the predominant component of the response. The presynaptic actions of norepinephrine were predominantly, although not completely, resistant to blockade of Na-dependent spikes, implicating a presynaptic terminal locus of action. Interestingly, the spike-dependent component of the response was greater in PVN than in SON magnocellular neurones. This robust presynaptic facilitation of glutamate release by norepinephrine, combined with the known excitatory postsynaptic actions of norepinephrine, activational effects on local glutamate circuits, and inhibitory effects on gamma-aminobutyric acid release, indicate a strong excitatory role of norepinephrine in the regulation of oxytocin and vasopressin release during physiological stimulation.