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Central clock excites vasopressin neurons by waking osmosensory afferents during late sleep.

机译:中央时钟通过在晚睡时唤醒渗透觉传入来刺激血管加压素神经元。

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摘要

Osmoregulated vasopressin release is facilitated during the late sleep period (LSP) to prevent dehydration and enuresis. Previous work has shown that clock neurons in the suprachiasmatic nucleus (SCN) have low firing rates during the LSP, but it is not known how this reduced activity enhances vasopressin release. We found that synaptic excitation of rat supraoptic nucleus neurons by osmosensory afferents is facilitated during the LSP. Stimulation of the SCN at this time inhibited excitatory synaptic currents induced in supraoptic neurons by activation of osmosensory afferents. This effect was associated with an increased rate of synaptic failures and occurred without changes in frequency facilitation, quantal size or in the ratio of postsynaptic responses mediated by AMPA and NMDA receptors. We conclude that clock neurons mediate an activity-dependent presynaptic silencing of osmosensory afferent synapses onto vasopressin neurons and that osmoregulatory gain is enhanced by removal of this effect during late sleep.
机译:睡眠后期(LSP)促进渗透压释放的加压素可防止脱水和遗尿。先前的工作表明,在LSP期间,视交叉上核(SCN)中的时钟神经元的放电率较低,但尚不清楚这种降低的活性如何增强血管加压素的释放。我们发现在LSP期间,渗透压传入大鼠的大鼠视上核神经元的突触兴奋。此时,SCN的刺激抑制了渗透压传入神经的激活,从而在视上神经元中诱导了兴奋性突触电流。这种作用与突触失败率的增加有关,并且在频率促进,数量大小或由AMPA和NMDA受体介导的突触后反应的比率没有改变的情况下发生。我们得出的结论是,时钟神经元介导渗透压传入神经突触对血管加压素神经元的活动依赖的突触前沉默,并通过在晚睡时消除此效应而增强了渗透调节性增益。

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