Suppr超能文献

神经垂体神经元和肽的电生理研究。

Electrophysiological studies of neurohypophysial neurons and peptides.

作者信息

Pittman Q J, Kombian S B, Mouginot D, Chen X, van Eerdenberg F J

机构信息

Neuroscience Research Group, University of Calgary, Alberta, Canada.

出版信息

Prog Brain Res. 1998;119:311-20. doi: 10.1016/s0079-6123(08)61577-0.

Abstract

We have used hypothalamic slices of the supraoptic nucleus (SON) to investigate synaptic control of magnocellular vasopressinergic and oxytocinergic neurons. With the use of perforated patch recording techniques we identified and isolated excitatory or inhibitory postsynaptic currents elicited by electrical stimulation of afferent fibers. Both inhibitory and excitatory afferent fibers displayed presynaptic GABAB receptors; the GABAB agonist, baclofen caused a dose-dependent suppression of the evoked potentials in the absence of any effects on postsynaptic input resistance. Further evidence for a presynaptic locus included an increase in paired pulse ratio and a lack of effect on currents elicited by exogenously applied muscimol (a GABAA receptor agonist) or AMPA (a glutamate agonist). With the use of an GABAB receptor antagonist we demonstrated an action of endogenously released GABA, acting at GABAB receptors on excitatory terminals, to reduce excitatory transmission. In addition to presynaptic modulation by GABA of afferent inputs, we also observed actions of vasopressin and oxytocin, released from dendrites of magnocellular SON neurons, to gate afferent, excitatory transmission in the SON. Exogenously applied vasopressin and oxytocin, or these peptides when released by depolarizing stimuli of magnocellular neurons, reduced the size of evoked excitatory postsynaptic potentials at a presynaptic locus. We have also observed actions of arginine vasopressin to modulate the action of glutamate in slices of the ventral septal area and to attenuate a glutamate-mediated excitatory postsynaptic current in slices of the parabrachial nucleus.

摘要

我们利用视上核(SON)的下丘脑切片来研究大细胞血管加压素能神经元和催产素能神经元的突触控制。通过使用穿孔膜片钳记录技术,我们识别并分离了由传入纤维电刺激引发的兴奋性或抑制性突触后电流。抑制性和兴奋性传入纤维均显示有突触前GABAB受体;GABAB激动剂巴氯芬在对突触后输入电阻无任何影响的情况下,引起诱发电位的剂量依赖性抑制。突触前位点的进一步证据包括配对脉冲比率增加,以及对外源性应用的蝇蕈醇(一种GABAA受体激动剂)或AMPA(一种谷氨酸激动剂)引发的电流无影响。通过使用GABAB受体拮抗剂,我们证明了内源性释放的GABA作用于兴奋性终末上的GABAB受体,以减少兴奋性传递。除了GABA对传入输入的突触前调制外,我们还观察到从大细胞SON神经元树突释放的血管加压素和催产素对SON中传入兴奋性传递的门控作用。外源性应用的血管加压素和催产素,或这些肽在大细胞神经元去极化刺激下释放时,在突触前位点降低了诱发的兴奋性突触后电位的大小。我们还观察到精氨酸血管加压素对腹侧隔区切片中谷氨酸作用的调制,以及对臂旁核切片中谷氨酸介导的兴奋性突触后电流的减弱作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验