The Journal of Neuroscience, March 9, 2005, ():
The Nitric Oxide-cGMP Signaling Pathway Differentially Regulates Presynaptic Structural Plasticity in Cone and Rod Cells
J. Neurosci. Zhang et al.
25: 2761
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplemental material 1. Action sites of reagents used to affect the NO-cGMP signaling pathway. Key enzymes in this pathway are neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC). nNOS is inhibited by L-NAME. sGC is stimulated by YC-1 and the NO donor SNAP, but is inhibited by ODQ. 8Br-cGMP is a membrane-permeant analog of cGMP. cGMP is degraded by phosphodiesterase (PDE). IBMX is a non-specific inhibitor of PDEs. Two other targets of cGMP are cGMP-gated channels, blocked by L-cis-diltiazem, and protein kinase G (PKG), blocked by Rp-pCPT-cGMPS. (*) donor or analog; (+) stimulation; (-) inhibition. In bold, reagents; in italics, enzymes
- supplemental material
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Supplemental material 2. Summary of the effects of NO-cGMP reagents on varicosity formation.
A. In cone cells, stimulation of the NO-cGMP pathway by SNAP, YC-1 and 8Br-cGMP, within a certain range of concentrations, caused a significant increase in varicosity formation.
B. In rod cells, a decrease in varicosity formation was observed after cells were treated with the same reagents at the same concentrations.
