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Capsaicin-evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation

机译：辣椒素引起的大鼠颊粘膜释放的CGRP：研究神经源性炎症的三叉神经机制的模型系统的开发

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Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 μM), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mM) or by the calcium ionophore A23187 (1 μM). The specific, capsaicin receptor antagonist, capsazepine (300 μM), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.
机译：与皮肤组织中的神经源性炎症过程相关的许多生理特征类似地存在于口面结构内。这样的属性包括对辣椒素敏感的感觉神经元的依赖性和其中衍生的某些炎性介质的参与，包括降钙素基因相关肽（CGRP）。但是，三叉神经系统和脊柱神经系统之间也存在重要差异，并且尚未充分阐明神经源性过程对三叉神经系统内炎症性疾病的潜在贡献。我们在这里提出了一个模型系统，该模型系统能够研究调节可能在口腔内引起神经源性炎症的肽能性末端的传出功能的机制。将成年雄性Sprague-Dawley大鼠的新鲜切开的颊粘膜组织放入小室中，并与含氧的Krebs缓冲液融合。采集流出的超融合液的系列等分试样，并通过放射免疫分析法分析免疫反应性CGRP（iCGRP）。在超融合缓冲液中添加选择性兴奋性毒素辣椒素（10–300μM）导致iCGRP超融合水平显着，浓度依赖性地增加。同样，也可以通过去极化浓度的氯化钾（50 mM）或钙离子载体A23187（1μM）引起iCGRP从颊粘膜释放。辣椒素受体特异性拮抗剂辣椒素（300μM）完全消除了辣椒素引起的iCGRP释放，但对钾引起的释放没有任何影响。此外，辣椒素引起的释放取决于细胞外钙离子的存在，尽管不完全，但辣椒素引起的神经支配作用明显减弱了辣椒素的释放。总的来说，这些数据表明，响应辣椒素的iCGRP的神经分泌是通过类香草醇受体介导的胞吐机制发生的。此处描述的模型系统应极大地促进将来的研究，这些研究旨在识别和表征调节CGRP或其他神经分泌物质在分离组织中释放的刺激。该系统还可以用于阐明这些介质在三叉神经支配领域内炎症过程的病因学中的作用。

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