Bronzetti Elena, Artico M, Kovacs I, Felici L M, Magliulo G, Vignone D, D'Ambrosio A, Forte F, Di Liddo R, Feher J
Department of Cardiovascular, Respiratory and Morphological Sciences, G Ferreri University of Rome La Sapienza, Via A. Borelli 50 - 00161 Rome Italy
Eur J Histochem. 2007 Oct-Dec;51(4):251-60.
Antidromic stimulation of the rat trigeminal ganglion triggers the release of substance P (SP) and calcitonin gene-related peptide (CGRP) from sensory nerve terminals of the capsaicin sensitive C-fibers. These pro-inflammatory neuropeptides produce a marked hyperemia in the anterior segment of the eye, accompanied by increased intraocular pressure, breakdown of the blood-aqueous barrier and myosis. To assess the effects of neurogenic inflammation on the retina, specifically on the immunostaining of neurotransmitters and neurotrophins, as well as on the expression of neurotrophin receptors in the retina. RT-PCR was also accomplished in control and stimulated animals to confirm the immunohistochemical results. In the electrically stimulated eyes, immunostaining for SP, CGRP, VIP and nNOS demonstrated a marked increase in the RPE/POS (Retinal Pigment Epithelium/Photoreceptor Outer Segments), in the inner and outer granular layers and in the ganglion cells in comparison to the control eyes. CGRP and SP were found increased in stimulated animals and this result has been confirmed by RT- PCR. Changes in neurotrophin immunostaining and in receptor expression were also observed after electric stimulation of trigeminal ganglia. Decrease of BDNF and NT4 in the outer and inner layers and in ganglion cells was particularly marked. In stimulated rat retinas immunostaining and RT-PCR showed a NGF expression increase. Neurotrophin receptors remained substantially unchanged. These studies demonstrated, for the first time, that antidromic stimulation of the trigeminal ganglion and subsequent neurogenic inflammation affect immunostaining of retinal cell neurotransmitter/neuropeptides and neurotrophins as well as the expression of neurotrophin receptors.
对大鼠三叉神经节进行逆向刺激,可触发辣椒素敏感的C纤维感觉神经末梢释放P物质(SP)和降钙素基因相关肽(CGRP)。这些促炎性神经肽可使眼前节出现明显的充血,同时伴有眼压升高、血-房水屏障破坏和瞳孔缩小。为了评估神经源性炎症对视网膜的影响,特别是对神经递质和神经营养因子免疫染色以及视网膜中神经营养因子受体表达的影响,我们还对对照动物和受刺激动物进行了逆转录聚合酶链反应(RT-PCR)以确认免疫组化结果。在电刺激的眼睛中,与对照眼相比,SP、CGRP、血管活性肠肽(VIP)和神经元型一氧化氮合酶(nNOS)的免疫染色显示视网膜色素上皮/光感受器外段(RPE/POS)、内颗粒层和外颗粒层以及神经节细胞中有明显增加。在受刺激的动物中发现CGRP和SP增加,这一结果已通过RT-PCR得到证实。对三叉神经节进行电刺激后,还观察到神经营养因子免疫染色和受体表达的变化。外层和内层以及神经节细胞中脑源性神经营养因子(BDNF)和神经营养因子4(NT4) 的减少尤为明显。在受刺激的大鼠视网膜中,免疫染色和RT-PCR显示神经生长因子(NGF)表达增加。神经营养因子受体基本保持不变。这些研究首次证明,对三叉神经节的逆向刺激及随后的神经源性炎症会影响视网膜细胞神经递质/神经肽和神经营养因子的免疫染色以及神经营养因子受体的表达。