Department of Anatomy & Cell Biology, University of Melbourne, Parkville 3010, Australia.
Neuropeptides. 2012 Feb;46(1):55-60. doi: 10.1016/j.npep.2011.09.002. Epub 2011 Oct 17.
The aims of the present study were to determine if there is neuronal Cocaine and amphetamine regulated transcripts (CART) peptide expression (CART+) in parasympathetic (sphenopalatine (SPG); otic (OG)) and sensory (trigeminal (TG)) ganglia of the head and to examine the neurochemical phenotype (calcitonin gene-related peptide (CGRP), neurofilament 200 (NF200), isolectin B4 (IB4) binding, vasoactive intestinal peptide (VIP), neuropeptide Y (NPY) and enkephalin (ENK) immunoreactivity) and projection targets (lacrimal gland (LG), parotid gland (PG), nasal mucosa (NM), temporomandibular joint (TMJ), middle cerebral artery (MCA) and middle meningeal artery (MMA)) of CART expressing neurons in these ganglia. We found CART+ neurons in both the SPG (5.25±0.07%) and OG (4.32±0.66). A significant proportion of these CART+ neurons contained VIP, NPY or ENK (34%, 26% and 11%, respectively). SPG neurons retrogradely labelled from the lacrimal gland (29%) were CART+, but we were unable to demonstrate CART+ labelling in any of the SPG or OG neurons labelled from other targets. This supports a role for CART peptides in lacrimation or regulation of vascular tone in the lacrimal gland, but not in salivation or nasal congestion. CART+ neurons were also present in the trigeminal ganglion (1.26±0.38%), where their size distribution was confined almost completely to neurons smaller than 800 μm2 (mean=410 μm2; 98%<800 μm2), and were almost always CGRP+, but did not bind IB4. This is consistent with a role for CART peptides in trigeminal pain. However, there were few CART+ neurons amongst any of the trigeminal neurons retrogradely labelled from the targets we investigated and thus we cannot comment on the tissue type where such pain may have originated. Our study shows that some specialization of CART peptide expression (based on neurochemical phenotype and target projection) is evident in sensory and parasympathetic ganglia of the head.
本研究的目的是确定头部分泌型（蝶腭神经节（SPG）；耳神经节（OG））和感觉型（三叉神经节（TG））神经节中是否存在可卡因和安非他命调节的转录物（CART）肽表达（CART+），并检查神经化学表型（降钙素基因相关肽（CGRP）、神经丝 200（NF200）、异硫氰酸荧光素 B4（IB4）结合、血管活性肠肽（VIP）、神经肽 Y（NPY）和脑啡肽（ENK）免疫反应性）和投射靶标（泪腺（LG）、腮腺（PG）、鼻粘膜（NM）、颞下颌关节（TMJ）、大脑中动脉（MCA）和脑膜中动脉（MMA））的 CART 表达神经元。我们发现 SPG（5.25±0.07%）和 OG（4.32±0.66）中均存在 CART+神经元。这些 CART+神经元中有相当一部分含有 VIP、NPY 或 ENK（分别为 34%、26%和 11%）。从泪腺逆行标记的 SPG 神经元（29%）为 CART+，但我们未能证明从其他靶标标记的任何 SPG 或 OG 神经元中存在 CART+标记。这支持 CART 肽在泪液分泌或调节泪腺血管张力中的作用，但不支持在唾液分泌或鼻塞中的作用。CART+神经元也存在于三叉神经节（1.26±0.38%）中，其大小分布几乎完全局限于小于 800μm2 的神经元（平均值=410μm2；98%<800μm2），并且几乎总是 CGRP+，但不结合 IB4。这与 CART 肽在三叉神经痛中的作用一致。然而，在我们研究的任何靶标逆行标记的三叉神经神经元中，CART+神经元的数量都很少，因此我们无法对可能起源于该组织类型的疼痛进行评论。我们的研究表明，一些 CART 肽表达的专业化（基于神经化学表型和靶标投射）在头部的感觉和副交感神经节中是明显的。
