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首页> 外文期刊>The European Journal of Neuroscience >Modulation of ACh release by presynaptic muscarinic autoreceptors in the neuromuscular junction of the newborn and adult rat.
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Modulation of ACh release by presynaptic muscarinic autoreceptors in the neuromuscular junction of the newborn and adult rat.

机译：新生和成年大鼠神经肌肉接头中突触前毒蕈碱受体对ACh释放的调节。

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摘要

We studied the presynaptic muscarinic autoreceptor subtypes controlling ACh release and their relationship with voltage-dependent calcium channels in the neuromuscular synapses of the Levator auris longus muscle from adult (30-40 days) and newborn (3-6 and 15 days postnatal) rats. Using intracellular recording, we studied how several muscarinic antagonists affected the evoked endplate potentials. In some experiments we previously incubated the muscle with calcium channel blockers (nitrendipine, omega-conotoxin-GVIA and omega-Agatoxin-IVA) before determining the muscarinic response. In the adult, the M1 receptor-selective antagonist pirenzepine (10 micro m) reduced evoked neurotransmission ( approximately 47%). The M2 receptor-selective antagonist methoctramine (1 micro m) increased the evoked release ( approximately 67%). Both M1- and M2-mediated mechanisms depend on calcium influx via P/Q-type synaptic channels. We found nothing to indicate the presence of M3 (4-DAMP-sensitive) or M4 (tropicamide-sensitive) receptors in the muscles of adult or newborn rats. In the 3-6-day newborn rats, pirenzepine reduced the evoked release ( approximately 30%) by a mechanism independent of L-, N- and P/Q-type calcium channels, and the M2 antagonist methoctramine (1 micro m) unexpectedly decreased the evoked release ( approximately 40%). This methoctramine effect was a P/Q-type calcium-channel-dependent mechanism. However, upon maturation in the first two postnatal weeks, the M2 pathway shifted to perform the calcium-dependent release-inhibitory activity found in the adult. We show that the way in which M1 and M2 muscarinic receptors modulate neurotransmission can differ between the developing and adult rat neuromuscular synapse.
机译：我们研究了成人（30-40天）和新生儿（出生后3-6和15天）大鼠的Levator auris longus肌肉的神经肌肉突触中控制ACh释放的突触前毒蕈碱型自身受体亚型及其与电压依赖性钙通道的关系。使用细胞内记录，我们研究了几种毒蕈碱拮抗剂如何影响诱发的终板电位。在某些实验中，我们在确定毒蕈碱反应之前，先用钙通道阻滞剂（尼群地平，ω-芋螺毒素-GVIA和ω-Agatoxin-IVA）孵育肌肉。在成人中，M1受体选择性拮抗剂哌仑西平（10微米）减少了诱发的神经传递（约47％）。 M2受体选择性拮抗剂甲基辛特拉明（1微米）增加了诱发的释放（约67％）。 M1和M2介导的机制均依赖于经由P / Q型突触通道的钙流入。我们没有发现任何迹象表明成年或新生大鼠的肌肉中存在M3（对4-DAMP敏感）或M4（对托酰胺类敏感）受体。在3-6天的新生大鼠中，哌仑西平通过与L-，N-和P / Q型钙通道无关的机制和M2拮抗剂甲辛达明（1微米）意外降低了诱发的释放（约30％）降低了诱发的释放（约40％）。该甲基辛巴胺效应是P / Q型钙通道依赖性机制。但是，在出生后的前两周成熟时，M2途径转移，以执行成人中发现的钙依赖性释放抑制活性。我们显示，M1和M2毒蕈碱受体调节神经传递的方式在发育中和成年大鼠神经肌肉突触之间可能不同。

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