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Review
. 2002 Mar;135(5):1079-95.
doi: 10.1038/sj.bjp.0704569.

NO as a signalling molecule in the nervous system

Juan V Esplugues  1
Affiliations
Review

NO as a signalling molecule in the nervous system

Juan V Esplugues. Br J Pharmacol. 2002 Mar.
No abstract available

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Figures

Figure 1
Figure 1
Activation of nNOS in the CNS. Release of glutamate activates NMDA receptors (NMDAr), and the consequent flux of Ca2+ entering the ion channel activates nNOS, which is linked to the receptor via the postsynaptic density protein PSD-95. It is possible that NO bioactivity feeds back to control the presynaptic neuron and the activity of the channel. The protein CAPON is thought to be selectively associated with nNOS and regulates NO formation in neurones.
Figure 2
Figure 2
nNOS in mysenteric neurones is regulated by the flux of Ca2+ through voltage-dependent calcium channels (VDCC). NO relaxes the adjacent smooth muscle following activation of sGC.
Figure 3
Figure 3
Activation of nNOS in the skeletal muscle follows the influx of Ca2+ through voltage-dependent calcium channels (VDCC) induced by activation of ACh receptors (AChr) and membrane depolarization. The release of Ca2+ from the sarcoplasmic reticulum (SR) is also implicated. nNOS targets the membrane due to its association with α1-syntropin, a component of the dystrophin complex (DC).
Figure 4
Figure 4
Representative microphotograph of basal nNOS immunoreactivity (monoclonal antibody) in the dorsal vagal complex (DVC) of the brainstem. Scale bar=100 μm.
Figure 5
Figure 5
Selective destruction of nitrergic nerves in a model of portal hypertension results in supersensitivity of vascular tissue to the effects of exogenously administered NO. The graph shows cumulative concentration-response to SNAP in isolated mesenteric veins from control and portal hypertensive rats. Relaxations induced by SNAP are expressed as % of decrease induced by KCL (30 mM), and each point is the mean±s.e.mean of at least five experiments.
See this image and copyright information in PMC

References

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