Cowen T, Thrasivoulou C, Shaw S A, Abdel-Rahman T A
Department of Anatomy and Developmental Biology, Royal Free Hospital School of Medicine, London, UK.
J Auton Nerv Syst. 1996 May 6;58(3):153-62. doi: 10.1016/0165-1838(95)00127-1.
Contact with sweat gland acini causes sympathetic neurons to switch from a catecholaminergic to a cholinergic phenotype during development and following experimental manipulations. Substantial reductions of cholinergic innervation have been shown in the sweat glands of ageing rats and humans. Using in oculo transplantation, we have now studied whether sweat gland target tissues retain the capacity to regulate changes in the phenotype of sympathetic neurons observed in maturity and old age, including a switch from catecholaminergic to cholinergic characters. Markers have been used which indicate changes in nerve fibre morphology (the pan-neuronal marker, PGP9.5) as well as neurotransmitter expression (acetylcholinesterase (AChE), vasocative intestinal polypeptide (VIP) and tyrosine hydroxylase (TH)). Sweat glands from young and old donor rats became reinnervated by an organotypic pattern of cholinergic host nerves. Surgical sympathectomy demonstrated that these cholinergic nerve fibres originate from sympathetic neurons of the host superior cervical ganglion (SCG). Retrograde tracing combined with staining for VIP (a marker associated with cholinergic phenotype in neurons supplying sweat glands) showed that SCG neurons projecting to irises with sweat gland implants may be induced to express VIP. We hypothesise that these neurons have been switched from their normal catecholaminergic phenotype to a cholinergic one by contact with the sweat gland implants. Transplants from old donors attracted a density of reinnervation by young host nerves which was appropriate to the age of the donor, thus old sweat glands received a significantly reduced density of innervation compared to young glands. Despite the reduced density of innervation, there was no obvious difference in the ability of young and old implants to induce the switch to a cholinergic phenotype, suggesting that different mechanisms regulate nerve growth and neurotransmitter phenotype.
在发育过程中以及经过实验操作后，与汗腺腺泡接触会使交感神经元从儿茶酚胺能表型转变为胆碱能表型。在衰老大鼠和人类的汗腺中，已显示胆碱能神经支配显著减少。我们通过眼内移植，研究了汗腺靶组织是否保留调节在成熟和老年期观察到的交感神经元表型变化的能力，包括从儿茶酚胺能特征向胆碱能特征的转变。使用了一些标志物来指示神经纤维形态的变化（泛神经元标志物PGP9.5）以及神经递质表达（乙酰胆碱酯酶（AChE）、血管活性肠肽（VIP）和酪氨酸羟化酶（TH））。来自年轻和年老供体大鼠的汗腺通过胆碱能宿主神经的器官型模式实现了重新神经支配。手术去交感神经表明，这些胆碱能神经纤维起源于宿主颈上神经节（SCG）的交感神经元。逆行追踪结合VIP染色（一种与供应汗腺的神经元中的胆碱能表型相关的标志物）表明，投射到带有汗腺植入物的虹膜的SCG神经元可能被诱导表达VIP。我们假设这些神经元通过与汗腺植入物接触已从其正常的儿茶酚胺能表型转变为胆碱能表型。来自老年供体的移植物吸引了年轻宿主神经的重新神经支配密度，该密度与供体年龄相适应，因此与年轻腺体相比，老年汗腺接受的神经支配密度显著降低。尽管神经支配密度降低，但年轻和老年植入物诱导向胆碱能表型转变的能力没有明显差异，这表明不同的机制调节神经生长和神经递质表型。
