Axo-axonal interaction in autonomic regulation of the cerebral circulation.

摘要: Noradrenaline (NE) and acetylcholine (ACh) released from the sympathetic parasympathetic neurones in cerebral blood vessels were suggested initially to be respective vasoconstricting dilating transmitters. Both substances, however, are extremely weak post-synaptic Compelling evidence indicates that nitric oxide (NO) which is co-released with ACh same nerves major transmitter for vasodilation, its release inhibited by ACh. NE nerve, acting on presynaptic β2-adrenoceptors located neighbouring nitrergic nerves, facilitates NO enhanced vasodilation. This axo-axonal interaction mediating transmission supported close apposition between nerve terminals, has been shown vivo at base of brain cortical circulation. result reveals physiological need increased regional flow ‘fight-or-flight response’ during acute stress. Furthermore, α7- α3β2-nicotinic receptors (nAChRs) terminals mediate NE, leading α7-nAChR-mediated but not α3β2-nAChR-mediated vasodilation blocked β-amyloid peptides (Aβs). may provide an explanation hypoperfusion seen patients Alzheimer’s disease. cholinesterase inhibitors (ChEIs) widely used treating disease, possible hypoperfusion. contribute limitation clinical use ChEIs. ChEI blockade nAChR-mediated dilation like Aβs prevented statins pretreatment, suggesting efficacy ChEIs improved concurrent statins.