title: Nitric oxide inhibits the release of acetylcholine in the isolated retina.
abstract: BACKGROUND
  Recent studies have revealed that administration of nitric oxide (NO) donors increases the release of neurotransmitters in various brain regions. In the retina, NO synthetase (NOS) is found in retinal amacrine and ganglion cells, and it is evident that NO is involved in encoding visual information. In the present study, therefore, NO donors were used to study the effect of exogenous NO on the high K(+)-evoked release of endogenous acetylcholine (ACh) in the rat retina.
  
  
  METHODS
  Isolated rat retinal preparations were superfused with modified Krebs-Ringer bicarbonate buffer solution. In each experiment, stimulation for 10 min with 30 mM KCl was done twice. The amounts of ACh released by the first or second KCl stimulation were termed S1 and S2 respectively. Test agents were applied just before the second KCl stimulation. The effects of test agents were evaluated as S2 divided by S1. ACh was converted to hydrogen peroxide and electrochemically assayed by high-performance liquid chromatography.
  
  
  RESULTS
  S-Nitro-N-acetyl-DL-penicillamine (SNAP), an NO donor, dose-dependently inhibited the high K(+)-evoked release of endogenous ACh. Such inhibition by NO was confirmed also by another NO donor, (+/-)-(E)-4-ethyl-2-[(E)-hydroxy imino]-5-nitro-3-hexenamide (NOR3). The inhibitory effect of SNAP was abolished by both carboxy-PTIO, an NO scavenger, and bicuculline, an antagonist of GABAA receptors.
  
  
  CONCLUSIONS
  The NO-induced decrease of ACh release is probably due to an NO-induced increase of GABAergic system inhibition.
authors.affiliation: Department of Ophthalmology, Kochi Medical School, Nankoku, Kochi 783-8505, Japan. okadam@kochi-ms.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Okada
authors.forename: Y
authors.initials: Y
authors.lastname: Osumi
authors.forename: Y
authors.initials: Y
authors.lastname: Okuma
authors.forename: H
authors.initials: H
authors.lastname: Ueno
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D003497:Cyclic N-Oxides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D009574:Nitro Compounds / Q000494:pharmacology; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects* / Q000378:metabolism
chemical_list: D003497:Cyclic N-Oxides; D016166:Free Radical Scavengers; D018756:GABA Antagonists; D007093:Imidazoles; D020030:Nitric Oxide Donors; D009574:Nitro Compounds; C110881:S-nitro-N-acetylpenicillamine; C079391:2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide; D009569:Nitric Oxide; D011189:Potassium Chloride; C061872:FK 409; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D010396:Penicillamine; D000109:Acetylcholine; D001640:Bicuculline