Department of Neurology, Charité - Universitätsmedizin Berlin, Germany.
Cephalalgia. 2012 Jul;32(9):659-67. doi: 10.1177/0333102412447701. Epub 2012 May 30.
Administration of inflammatory soup (IS) leads to a significant release of calcitonin gene-related peptide (CGRP). Whether IS-induced CGRP release originates in primary or secondary neurons of the trigeminovascular system has not been clarified.
We determined CGRP release into the external jugular vein and in cerebrospinal fluid (CSF) following intracisternal IS administration using an in vivo rat model. We further performed polymerase chain reaction (PCR) and immunohistochemistry of the trigeminal ganglion and brainstem (trigeminal nucleus caudalis). To further elucidate a primary vs. secondary origin, experiments were repeated after neonatal capsaicin treatment (NCT) as this treatment destroys primary trigeminal afferents.
IS-induced CGRP release into the external jugular vein and CSF were significantly reduced after NCT in both compartments but inhibition was more pronounced in jugular vein blood than in CSF. Baseline CGRP levels were not affected by NCT. PCR results show that following NCT, CGRP mRNA was significantly reduced in the trigeminal ganglion but not in the brainstem. Immunohistochemistry of the TG and brainstem support these results.
We conclude that resting state CGRP levels can be maintained after trigeminal denervation of the meninges. However, for functional purposes primary trigeminal afferents are mandatory as they are the major source for stimulus-induced CGRP release.
给予炎症汤（IS）会导致降钙素基因相关肽（CGRP）的大量释放。IS 诱导的 CGRP 释放是否起源于三叉血管系统的初级或次级神经元尚未阐明。
我们使用体内大鼠模型确定了 IS 经蛛网膜下腔给药后颈外静脉和脑脊液（CSF）中 CGRP 的释放情况。我们进一步对三叉神经节和脑干（尾状核三叉神经核）进行了聚合酶链反应（PCR）和免疫组织化学分析。为了进一步阐明原发性与继发性起源，我们在新生辣椒素处理（NCT）后重复了实验，因为这种处理会破坏初级三叉神经传入纤维。
NCT 后，IS 诱导的颈外静脉和 CSF 中 CGRP 的释放均明显减少，但颈外静脉血中的抑制作用比 CSF 中更为明显。NCT 并未影响基础 CGRP 水平。PCR 结果显示，NCT 后，三叉神经节中的 CGRP mRNA 明显减少，但脑干中没有。TG 和脑干的免疫组织化学支持这些结果。
我们得出结论，脑膜三叉神经切断后，静息状态下的 CGRP 水平可以维持。然而，对于功能目的来说，初级三叉神经传入纤维是必需的，因为它们是刺激诱导的 CGRP 释放的主要来源。
