Nitric oxide stimulates γ-aminobutyric acid release and inhibits glycine release in retina
Article first published online: 28 JAN 2005
Copyright © 2005 Wiley-Liss, Inc.
Journal of Comparative Neurology
Volume 483, Issue 3, pages 278–291, 14 March 2005
How to Cite
Yu, D. and Eldred, W. D. (2005), Nitric oxide stimulates γ-aminobutyric acid release and inhibits glycine release in retina. J. Comp. Neurol., 483: 278–291. doi: 10.1002/cne.20416
- Issue published online: 28 JAN 2005
- Article first published online: 28 JAN 2005
- Manuscript Accepted: 11 OCT 2004
- Manuscript Revised: 29 SEP 2004
- Manuscript Received: 15 JUL 2004
- National Eye Institute
- National Institutes of Health. Grant Number: EY 04785
- release, uptake;
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.