Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo, 102-8159, Japan.
Mol Pain. 2010 May 26;6:30. doi: 10.1186/1744-8069-6-30.
Although it has been widely accepted that the primary somatosensory (SI) cortex plays an important role in pain perception, it still remains unclear how the nociceptive mechanisms of synaptic transmission occur at the single neuron level. The aim of the present study was to examine whether noxious stimulation applied to the orofacial area evokes the synaptic response of SI neurons in urethane-anesthetized rats using an in vivo patch-clamp technique.
In vivo whole-cell current-clamp recordings were performed in rat SI neurons (layers III-IV). Twenty-seven out of 63 neurons were identified in the mechanical receptive field of the orofacial area (36 neurons showed no receptive field) and they were classified as non-nociceptive (low-threshold mechanoreceptive; 6/27, 22%) and nociceptive neurons. Nociceptive neurons were further divided into wide-dynamic range neurons (3/27, 11%) and nociceptive-specific neurons (18/27, 67%). In the majority of these neurons, a proportion of the excitatory postsynaptic potentials (EPSPs) reached the threshold, and then generated random discharges of action potentials. Noxious mechanical stimuli applied to the receptive field elicited a discharge of action potentials on the barrage of EPSPs. In the case of noxious chemical stimulation applied as mustard oil to the orofacial area, the membrane potential shifted depolarization and the rate of spontaneous discharges gradually increased as did the noxious pinch-evoked discharge rates, which were usually associated with potentiated EPSP amplitudes.
The present study provides evidence that SI neurons in deep layers III-V respond to the temporal summation of EPSPs due to noxious mechanical and chemical stimulation applied to the orofacial area and that these neurons may contribute to the processing of nociceptive information, including hyperalgesia.
尽管人们普遍认为初级躯体感觉(SI)皮层在疼痛感知中起着重要作用,但突触传递的伤害性机制如何在单个神经元水平上发生仍不清楚。本研究旨在使用体内膜片钳技术检查在乌拉坦麻醉大鼠中,面部区域的伤害性刺激是否会引起 SI 神经元的突触反应。
在大鼠 SI 神经元(III-IV 层)中进行了体内全细胞电流钳记录。在口腔区域机械感受野中鉴定出 63 个神经元中的 27 个(36 个神经元没有感受野),并将它们分为非伤害性(低阈值机械感受;6/27,22%)和伤害性神经元。伤害性神经元进一步分为宽动态范围神经元(3/27,11%)和伤害性特异性神经元(18/27,67%)。在这些神经元中的大多数中,一部分兴奋性突触后电位(EPSP)达到阈值,然后产生随机的动作电位放电。在感受野中施加的伤害性机械刺激会在 EPSP 的爆发中引发动作电位的放电。在将芥末油应用于口腔区域的伤害性化学刺激的情况下,细胞膜电位向去极化转移,自发放电率逐渐增加,伤害性捏合诱发的放电率也逐渐增加,这通常与增强的 EPSP 幅度相关。
本研究提供的证据表明,深层 III-V 层的 SI 神经元对口腔区域施加的伤害性机械和化学刺激引起的 EPSP 的时间总和作出反应,这些神经元可能有助于伤害性信息的处理,包括痛觉过敏。