Nitric oxide and target-organ control in the autonomic nervous system: Anatomical distribution, spatiotemporal signaling, and neuroeffector maintenance

Authors
Citation
D. Blottner, Nitric oxide and target-organ control in the autonomic nervous system: Anatomical distribution, spatiotemporal signaling, and neuroeffector maintenance, J NEUROSC R, 58(1), 1999, pp. 139-151
Citations number
173
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE RESEARCH
ISSN journal
03604012 → ACNP
Volume
58
Issue
1
Year of publication
1999
Pages
139 - 151
Database
ISI
SICI code
0360-4012(19991001)58:1<139:NOATCI>2.0.ZU;2-Y
Abstract
Recent neuroanatomical studies, neurochemical coding and physiological find ings of multiple cotransmitter actions and/or receptor patterns, and the ch aracterization of synaptic molecules and nitrergic (NOergic) signaling mech anisms may help for a better understanding of target-organ control in the a utonomic nervous system, Thus, nitric oxide (NO) synthase, which generates the freely diffusible and short-lived messenger NO and expression of neurot rophic proteins (e.g., neurotrophins, glial cell-line-derived neurotrophic factor, fibroblast growth factors) in autonomic neural pathways or target o rgans suggest unique actions in autonomic neurotransmission, In central NOe rgic pathways, NO may serve as spatial (volume) messenger within hierarchic ally ordered autonomic neuron pools and convergent/divergent pathways for s ynchronized autonomic outflow. Likewise, NO modulates intraganglionic and i nteraxonal transmission and postganglionic activity including long-term pot entiation. In the visceral targets, NO appears to be a spatial modulator in local intrinsic networks or at varicose terminals. In endocrine glands, NO possibly acts as synaptic coactivator or inhibitor, as a cotransmitter aff ecting stimulus-coupled exocytosis, or as a local vasoactive signal. The sh ort-term neural messenger NO may also induce diffusible target-derived long -term neurotrophic signals, thereby supporting neuroeffector maintenance an d plasticity, if not synaptic efficacy, in autonomic target-organ control. (C) 1999 Wiley-Liss, Inc.