Samsam M, Coveñas R, Ahangari R, Yajeya J, Narváez J A, Tramu G
Instituto de Neurociencias de Castilla y León, Facultad de Medicina, Dpto. de Biología Celular y Patología, Salamanca, Spain.
Neurosci Lett. 1999 Feb 19;261(3):179-82. doi: 10.1016/s0304-3940(98)00989-6.
We have carried out an immunohistochemical study on the presence of neurokinin A (NKA) and substance P (SP) in the rat caudal trigeminal nucleus (CTN) after electrical stimulation of the trigeminal ganglion (TG), used as an experimental model to induce alterations, some of which may occur during migraine attacks (release of vasoactive peptides from perivascular trigeminal axons and neurogenic inflammation). Both unilateral, 30 min electrical stimulation (5 Hz, 5 ms, 0.1-1 mA) of the TG and 5 min stimulation with a slight increase in the stimulating parameters (7.5 Hz, 5 ms, 1.4 mA) caused a significant depletion of the NKA and SP immunoreactivities (-IR) of the TG nerve central terminals in the ipsilateral CTN. Calcitonin gene-related peptide (CGRP)-IR of the ipsilateral CTN was also studied in the CTN using the increased stimulating parameters and a marked depletion of CGRP-IR was also observed following TG stimulation. Such depletion may be due to the release of neuropeptides from the trigeminal central terminals. These findings suggest that NKA, SP and CGRP could act as neurotransmitters at the first central synapses of the trigeminal nociceptive pathway to transmit the sensory stimuli to the higher brain centers.
我们对三叉神经节（TG）进行电刺激后，大鼠尾侧三叉神经核（CTN）中神经激肽A（NKA）和P物质（SP）的存在情况开展了一项免疫组织化学研究。TG电刺激被用作一种实验模型来诱发改变，其中一些改变可能在偏头痛发作期间出现（血管周围三叉神经轴突释放血管活性肽以及神经源性炎症）。对TG进行单侧30分钟的电刺激（5赫兹，5毫秒，0.1 - 1毫安）以及将刺激参数略微提高（7.5赫兹，5毫秒，1.4毫安）进行5分钟刺激，均导致同侧CTN中TG神经中枢终末的NKA和SP免疫反应性（-IR）显著减少。使用提高后的刺激参数，还对同侧CTN中的降钙素基因相关肽（CGRP）-IR进行了研究，并且在TG刺激后也观察到CGRP-IR显著减少。这种减少可能是由于三叉神经中枢终末释放神经肽所致。这些发现表明，NKA、SP和CGRP可能在三叉神经痛觉传导通路的首个中枢突触处作为神经递质，将感觉刺激传递至更高的脑中枢。
