Shyu B C, Leung G M, Hu J W, Sessle B J
Faculty of Dentistry, University of Toronto, Ontario, Canada.
Exp Neurol. 1993 Oct;123(2):243-50. doi: 10.1006/exnr.1993.1157.
Previous studies have demonstrated that tooth pulp deafferentation is associated with statistically significant alterations in the low-threshold facial mechanoreceptive field properties of brain stem neurons in trigeminal (V) subnucleus oralis. A loss of spinal afferent-induced presynaptic inhibition as a consequence of a decrease in primary afferent depolarization (PAD) following spinal nerve deafferentation has been invoked as a mechanism underlying deafferentation-induced somatosensory neuroplasticity. Therefore, this study was initiated to determine if these pulp deafferentation-induced neuroplastic changes could be accounted for by an alteration in PAD of low-threshold facial afferent endings in subnucleus oralis of anesthetized rats. In control (unoperated) rats (n = 7) and rats (n = 7) that had undergone mandibular pulp deafferentation 6-10 days previously, antidromic compound action potentials evoked by test stimulation in V subnucleus oralis were recorded in branches of the infraorbital (IO) and supraorbital (SO) nerves, and conditioning stimuli were applied to some of the same nerves. PAD of the afferent endings in oralis of these nerve branches was documented in all animals, and there was no significant difference between the two groups in the incidence or any of the other features of PAD. The features of the PAD were consistent with those described in several previous studies of normal animals. These findings indicate that the reported deafferentation-induced loss of spinal presynaptic regulatory mechanisms cannot be entrapolated to all forms of deafferentation injury and that the mechanoreceptive field changes that can occur in central V somatosensory neurons as a result of tooth pulp deafferentation may not reflect an alteration in PAD.
以往研究表明，牙髓去传入与三叉神经（V）口侧亚核中脑干神经元低阈值面部机械感受野特性的统计学显著改变有关。脊髓去传入后，由于初级传入去极化（PAD）降低导致脊髓传入诱导的突触前抑制丧失，这被认为是去传入诱导的体感神经可塑性的一种机制。因此，本研究旨在确定麻醉大鼠口侧亚核中低阈值面部传入末梢的PAD改变是否可以解释这些牙髓去传入诱导的神经可塑性变化。在对照组（未手术）大鼠（n = 7）和6 - 10天前接受下颌牙髓去传入的大鼠（n = 7）中，在眶下（IO）神经和眶上（SO）神经分支中记录口侧亚核中测试刺激诱发的逆向复合动作电位，并对其中一些相同神经施加条件刺激。记录所有动物这些神经分支口侧传入末梢的PAD，两组在PAD的发生率或任何其他特征方面均无显著差异。PAD的特征与先前几项关于正常动物的研究中描述的一致。这些发现表明，所报道的去传入诱导的脊髓突触前调节机制丧失不能外推到所有形式的去传入损伤，并且牙髓去传入导致的中枢V体感神经元机械感受野变化可能不反映PAD的改变。
