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Nitric oxide stimulates γ‐aminobutyric acid release and inhibits glycine release in retina
Author(s) -
Yu Dou,
Eldred William D.
Publication year - 2005
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20416
Subject(s) - gabaergic , glycine , nipecotic acid , glutamate receptor , chemistry , cyclic guanosine monophosphate , glycine receptor , biochemistry , gamma aminobutyric acid , microbiology and biotechnology , biophysics , nitric oxide , neurotransmitter , biology , receptor , amino acid , organic chemistry
Nitric oxide (NO) modulates the uptake and/or release of neurotransmitters through a variety of cellular mechanisms. However, the pharmacological and biochemical processes underlying these neurochemical effects of NO often remain unclear. In our study, we used immunocytochemical methods to study the effects of NO, cyclic guanosine monophosphate (cGMP), and peroxynitrite on the uptake and release of γ‐aminobutyric acid (GABA) and glycine in the turtle retina. In addition, we examined the involvement of glutamate receptors, calcium, and the GABA transporter in this GABA uptake and release. We also tested for interactions between the GABAergic and glycinergic systems. In general, we show that NO stimulated GABA release and inhibited glycine release. The NO‐stimulated GABA release involved calcium‐dependent or calcium‐independent synaptic release or reversal of the GABA transporter. Some effects of NO on GABA release involved glutamate, cGMP, or peroxynitrite. NO promoted glycine uptake and inhibited its release, and this inhibition of glycine release was influenced by GABAergic modulation. These findings indicate that NO modulates the levels of the inhibitory transmitters GABA and glycine through several specific biochemical mechanisms in different retinal cell types and layers. Thus it appears that some of the previously described reciprocal interactions between GABA and glycine in the retina function through specific NO signaling pathways. J. Comp. Neurol. 483:278–291, 2005. © 2005 Wiley‐Liss, Inc.