Vaucher E, Linville D, Hamel E
Neurobiology Unit, Montreal Neurological Institute, McGill University, Québec, Canada.
Neuroscience. 1997 Aug;79(3):827-36. doi: 10.1016/s0306-4522(97)00033-x.
Stimulation of basal forebrain neurons elicits regional cerebral blood flow increases which are reportedly mediated by acetylcholine and nitric oxide. However, the modality of interaction between these two mediators remains unclear. Particularly, little is known about the source, i.e. endothelial, glial and/or neuronal, of the potent gaseous vasodilator nitric oxide. In the present study, we examined, by double immunocytochemical labelling of nitric oxide synthase and choline acteyltransferase at the light and electron microscopic level, the existence of morphological relationships between cortical nitric oxide synthase-containing neurons and cholinergic cells or nerve fibres. Using anterograde tract tracing and selective basal forebrain lesions, we further investigated the origin of the cholinergic input to cortical nitric oxide synthase neurons. The results confirm that cortical nitric oxide synthase-immunoreactive neurons are often associated with the local microvascular bed, show that intracortical neurons immunostained for nitric oxide synthase and choline acetyltransferase belong to two distinct neuronal populations and, further, that a subset of nitric oxide synthase-containing cell bodies and their proximal dendrites receive a cholinergic input which originates primarily from basalocortical projections. Altogether, these findings suggest that cholinergic basal forebrain neurons could increase cortical blood flow partly via a local nitric oxide relay neuron whereby the freely diffusing gas would be the direct smooth muscle vasodilator agent. It is concluded that this interaction might contribute to the complex relationships between the basal forebrain and the cortical microcirculation, interactions which result in fine regulation of cortical perfusion.
刺激基底前脑神经元可引起局部脑血流增加，据报道这是由乙酰胆碱和一氧化氮介导的。然而，这两种介质之间的相互作用方式仍不清楚。特别是，对于强效气态血管扩张剂一氧化氮的来源，即内皮细胞、神经胶质细胞和/或神经元，人们了解甚少。在本研究中，我们通过在光镜和电镜水平对一氧化氮合酶和胆碱乙酰转移酶进行双重免疫细胞化学标记，检查了含皮质一氧化氮合酶的神经元与胆碱能细胞或神经纤维之间形态学关系的存在情况。利用顺行束路追踪和选择性基底前脑损伤，我们进一步研究了皮质一氧化氮合酶神经元胆碱能输入的起源。结果证实，皮质一氧化氮合酶免疫反应性神经元常与局部微血管床相关，表明对一氧化氮合酶和胆碱乙酰转移酶进行免疫染色的皮质内神经元属于两个不同的神经元群体，此外，含一氧化氮合酶的细胞体及其近端树突中的一部分接受主要源自基底皮质投射的胆碱能输入。总之，这些发现表明，胆碱能基底前脑神经元可能部分通过局部一氧化氮中继神经元增加皮质血流，由此自由扩散的气体将成为直接的平滑肌血管扩张剂。得出的结论是，这种相互作用可能有助于基底前脑与皮质微循环之间的复杂关系，这些相互作用导致对皮质灌注的精细调节。
