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首页> 外文期刊>The European Journal of Neuroscience >Morphine withdrawal increases intrinsic excitability of oxytocin neurons in morphine-dependent rats.
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Morphine withdrawal increases intrinsic excitability of oxytocin neurons in morphine-dependent rats.

机译：吗啡戒断可增加吗啡依赖性大鼠中催产素神经元的内在兴奋性。

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摘要

To determine whether intrinsic mechanisms drive supraoptic nucleus oxytocin neuron excitation during morphine withdrawal, we calculated the probability of action potential (spike) firing with time after each spike for oxytocin neurons in morphine-naive and morphine-dependent rats in vivo and measured changes in intrinsic membrane properties in vitro. The opioid receptor antagonist, naloxone, increased oxytocin neuron post-spike excitability in morphine-dependent rats; this increase was greater for short interspike intervals (<0.1 s). Naloxone had similar, but smaller (P=0.04), effects in oxytocin neurons in morphine-naive rats. The increased post-spike excitability for short interspike intervals was specific to naloxone, because osmotic stimulation increased excitability without potentiating excitability at short interspike intervals. By contrast to oxytocin neurons, neither morphine dependence nor morphine withdrawal increased post-spike excitability in neighbouring vasopressin neurons. To determine whether increased post-spike excitability in oxytocin neurons during morphine withdrawal reflected altered intrinsic membrane properties, we measured the in vitro effects of naloxone on transient outward rectification (TOR) and after-hyperpolarization (AHP), properties mediated by K+ channels and that affect supraoptic nucleus neuron post-spike excitability. Naloxone reduced the TOR and AHP (by 20% and 60%, respectively) in supraoptic nucleus neurons from morphine-dependent, but not morphine-naive, rats. In vivo, spike frequency adaptation (caused by activity-dependent AHP activation) was reduced by naloxone (from 27% to 3%) in vasopressin neurons in morphine-dependent, but not morphine-naive, rats. Thus, multiple K+ channel inhibition increases post-spike excitability for short interspike intervals, contributing to the increased firing of oxytocin neurons during morphine withdrawal.
机译：为确定内源性机制是否在吗啡戒断期间驱动视光上核催产素神经元兴奋，我们计算了初生吗啡和吗啡依赖性大鼠体内催产素神经元每次加标后随时间激发动作电位（穗）的概率，并测量了内源性变化体外膜特性。阿片受体拮抗剂纳洛酮在吗啡依赖性大鼠中增加了突触后催产素神经元的兴奋性;对于短的尖峰间隔（<0.1 s），此增加更大。纳洛酮对未使用吗啡的大鼠催产素神经元具有相似但较小的影响（P = 0.04）。短间隔时间间隔增加的峰后兴奋性是纳洛酮所特有的，因为渗透刺激增加了兴奋性，而短间隔时间间隔却没有增强兴奋性。与催产素神经元相反，吗啡依赖性或吗啡戒断都不会增加邻近血管加压素神经元的峰后兴奋性。为了确定吗啡戒断期间催产素神经元的穗后兴奋性增加是否反映了固有的膜特性发生了变化，我们测量了纳洛酮对瞬时向外整流（TOR）和超极化后（AHP）的体外影响，以及K +通道介导的特性。影响穗后视上核神经元兴奋性。纳洛酮可降低吗啡依赖性但非吗啡依赖性大鼠的视上核神经元的TOR和AHP（分别降低20％和60％）。在体内，吗啡依赖性但非吗啡依赖性大鼠的加压素神经元中纳洛酮可将峰频率适应（由活动依赖性AHP激活引起）降低（从27％降至3％）。因此，多个K +通道抑制作用在短峰间时间间隔内增加了峰后兴奋性，从而促进了吗啡戒断期间催产素神经元的放电。

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