Palmer G C
Neurosci Biobehav Rev. 1986 Summer;10(2):79-101. doi: 10.1016/0149-7634(86)90020-5.
The discovery that monoamine nerves end on the central microvessels of the choroid plexus, pia-arachnoid and parenchyma has prompted an intense investigation as to their physiological and neuropathological roles. The source of the monoamine fibers to the pial vessels and choroid plexus was shown to be the superior cervical ganglion. Ganglionic stimulation causes vasoconstriction or vasodilation of pial vessels, an event depending upon the functional ratio of alpha to beta adrenergic receptors. Moreover, stimulation of the superior cervical ganglion evokes an inhibition of cerebrospinal fluid formation in choroid plexus. The locus coeruleus is the site of adrenergic nerve supply to the parenchymal capillaries and stimulation of this nucleus increases capillary permeability to small molecules and water. Neurotransmitter receptors (adrenergic, histamine, adenosine, dopamine, prostacyclin, prostaglandins and specific amino acids or neuropeptides) have been identified on microvessels and in many instances these transmitter actions are coupled to cyclic AMP synthesis. Moreover, cyclic AMP has been shown to increase the rate of capillary endothelial pinocytosis and produce brain edema. In small vessels containing smooth muscle cells cyclic AMP production improves cerebral blood flow via an initiation of vasodilatory processes. The presence of receptors for serotonin and acetylcholine have likewise been demonstrated to occur on cerebral microvessels. Limited information is available as to the receptor coupled actions of these two transmitters, but cholinergic mechanisms may act to restrict catecholamine-induced formation of cyclic AMP. Altered sensitivity of microvessels to neurotransmitters has been demonstrated following conditions of stroke, hypertension, aging, diabetes and X-irradiation.
单胺神经末梢位于脉络丛、软脑膜 - 蛛网膜和实质的中央微血管这一发现，引发了对其生理和神经病理学作用的深入研究。已证明，支配软脑膜血管和脉络丛的单胺纤维来源是颈上神经节。刺激神经节会导致软脑膜血管收缩或舒张，这一现象取决于α和β肾上腺素能受体的功能比例。此外，刺激颈上神经节会抑制脉络丛中脑脊液的生成。蓝斑是向实质毛细血管提供肾上腺素能神经的部位，刺激该核会增加毛细血管对小分子和水的通透性。在微血管上已鉴定出神经递质受体（肾上腺素能、组胺、腺苷、多巴胺、前列环素、前列腺素以及特定氨基酸或神经肽），在许多情况下，这些递质作用与环磷酸腺苷（cAMP）的合成相关。此外，已表明cAMP可增加毛细血管内皮细胞的胞饮速率并导致脑水肿。在含有平滑肌细胞的小血管中，cAMP的产生通过启动血管舒张过程来改善脑血流量。同样已证明，5-羟色胺和乙酰胆碱的受体存在于脑微血管上。关于这两种递质的受体偶联作用的信息有限，但胆碱能机制可能起到限制儿茶酚胺诱导的cAMP形成的作用。在中风、高血压、衰老、糖尿病和X射线照射等情况下，已证明微血管对神经递质的敏感性会发生改变。
