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