Benarroch E E
Department of Neurology, Mayo Clinic, Rochester, MN 55905.
Ann Neurol. 1994 Jul;36(1):6-13. doi: 10.1002/ana.410360105.
Neuropeptides are ubiquitous in the sympathetic system and modulate transmission at the levels of the intermediolateral cell column, sympathetic ganglia, and neuroeffector junctions. Several neuropeptide-containing pathways from the hypothalamus and medulla modulate excitability of preganglionic neurons. Neuropeptides coexist with norepinephrine or acetylcholine in subpopulations of chemically coded, target-specific sympathetic ganglion neurons. Neuropeptide Y is colocalized in adrenergic vasoconstrictor neurons, whereas vasoactive intestinal polypeptide is colocalized in cholinergic sudomotor neurons. Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. Sympathetic denervation produces sprouting of sensory fibers containing substance P and calcitonin gene-related peptide in target tissues. Neuropeptides from preganglionic fibers (e.g., enkephalin) and primary afferents (e.g., substance P, vasoactive intestinal polypeptide) modulate transmission in sympathetic ganglia. Neuropeptide Y produces vasoconstriction, prejunctional inhibition of norepinephrine release, and postjunctional potentiation of norepinephrine effects. Plasma neuropeptide Y increases during intense sympathoexcitation, hypertension, and pheochromocytoma. Dystrophic neurites containing neuropeptide Y occur in human sympathetic ganglia during aging, diabetes, and dysautonomia. Sympathetic neuropeptides may thus have important clinical implications.
神经肽在交感神经系统中广泛存在，并在中间外侧细胞柱、交感神经节和神经效应器接头水平调节神经传递。来自下丘脑和延髓的几条含神经肽通路调节节前神经元的兴奋性。神经肽与去甲肾上腺素或乙酰胆碱共存于化学编码的、靶标特异性交感神经节神经元亚群中。神经肽Y与肾上腺素能血管收缩神经元共定位，而血管活性肠肽与胆碱能汗腺运动神经元共定位。神经肽表达具有可塑性；在发育过程中，从去甲肾上腺素能表型转变为胆碱能表型的神经元会增加血管活性肠肽、生长抑素和P物质的表达。节前输入会增加神经肽Y并抑制P物质的表达。交感神经去神经支配会导致靶组织中含有P物质和降钙素基因相关肽的感觉纤维发芽。来自节前纤维（如脑啡肽）和初级传入神经（如P物质、血管活性肠肽）的神经肽调节交感神经节中的神经传递。神经肽Y会引起血管收缩、去甲肾上腺素释放的节前抑制以及去甲肾上腺素效应的节后增强。在强烈的交感神经兴奋、高血压和嗜铬细胞瘤期间，血浆神经肽Y会增加。在衰老、糖尿病和自主神经功能障碍期间，人类交感神经节中会出现含有神经肽Y的营养不良性神经突。因此，交感神经肽可能具有重要的临床意义。
