Ludwig M, Leng G
Department of Physiology, Medical School, University of Edinburgh, United Kingdom.
Adv Exp Med Biol. 1998;449:163-73.
Vasopressin and oxytocin are released into the extracellular space of the supraoptic (SON) and paraventricular nuclei (PVN). The dendrites of these neurones contain a high density of neurosecretory granules, and exocytotic profiles have been visualised by electron microscopy. Release within the SON has been measured using microperfusion techniques; release is tetrodotoxin-independent, calcium-dependent, and is activated by a range of physiological stimuli, including suckling, dehydration, haemorrhage and stress. Release of vasopressin into the SON is regulated by a number of forebrain and brainstem areas. Dendritic release does not necessarily parallel neurohypophyseal release, and may occur semi-independently of spike activity in the soma and axons. The physiological consequences of dendritic vasopressin release are not clear, vasopressin and oxytocin appear to induce further vasopressin and oxytocin release from the dendrites. In contrast, by combining retrodialysis and electrophysiology we have shown that, unlike oxytocin which excites oxytocin neurones, vasopressin inhibits the electrical activity of vasopressin neurones, and hence suppresses vasopressin release from the pituitary. Thus, vasopressin released from dendrites may act on vasopressin neurones to regulate their phasic activity by an auto-inhibitory action within the SON. Since dendritic vasopressin release is increased and prolonged after various stimuli, this mechanism may act to restrain excitation of vasopressin neurones (and hence vasopressin secretion from the neurohypophysis) during continuing stimulation.
血管升压素和催产素释放入视上核(SON)和室旁核(PVN)的细胞外间隙。这些神经元的树突含有高密度的神经分泌颗粒,通过电子显微镜已观察到胞吐现象。已使用微量灌注技术测量了SON内的释放;释放不依赖河豚毒素,依赖钙,并且可由一系列生理刺激激活,包括哺乳、脱水、出血和应激。血管升压素向SON内的释放受许多前脑和脑干区域调节。树突释放不一定与神经垂体释放平行,并且可能半独立于胞体和轴突中的动作电位活动而发生。树突释放血管升压素的生理后果尚不清楚,血管升压素和催产素似乎会诱导树突进一步释放血管升压素和催产素。相比之下,通过结合逆向透析和电生理学,我们已经表明,与刺激催产素神经元的催产素不同,血管升压素会抑制血管升压素神经元的电活动,从而抑制垂体释放血管升压素。因此,从树突释放出的血管升压素可能作用于血管升压素神经元,通过SON内的自抑制作用来调节它们的相位活动。由于在各种刺激后树突释放血管升压素会增加并延长,这种机制可能在持续刺激期间抑制血管升压素神经元的兴奋(从而抑制神经垂体分泌血管升压素)。