Opposite effects of nitric oxide on identified inhibitory and excitatory cholinergic synapses of Aplysia californica
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9200208
Knihovny.cz E-resources
- MeSH
- Acetylcholine metabolism pharmacology MeSH
- Action Potentials MeSH
- Aplysia MeSH
- Arginine pharmacology MeSH
- Cholinergic Agonists pharmacology MeSH
- Cholinergic Antagonists pharmacology MeSH
- Potassium Channels drug effects MeSH
- Ganglia, Invertebrate drug effects metabolism MeSH
- Ganglia, Parasympathetic drug effects metabolism MeSH
- Cyclic GMP analogs & derivatives pharmacology MeSH
- Guanylate Cyclase metabolism MeSH
- Molsidomine analogs & derivatives pharmacology MeSH
- Synaptic Transmission drug effects MeSH
- Nitric Oxide pharmacology MeSH
- Synapses drug effects metabolism MeSH
- Nitric Oxide Synthase metabolism MeSH
- Calcium Channels drug effects MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 8-bromocyclic GMP MeSH Browser
- Acetylcholine MeSH
- Arginine MeSH
- Cholinergic Agonists MeSH
- Cholinergic Antagonists MeSH
- Potassium Channels MeSH
- Cyclic GMP MeSH
- Guanylate Cyclase MeSH
- linsidomine MeSH Browser
- Molsidomine MeSH
- Nitric Oxide MeSH
- Nitric Oxide Synthase MeSH
- Calcium Channels MeSH
The effects of nitric oxide on evoked acetylcholine (ACh) release were studied at two identified cholinergic neuro-neuronal synapses of the nervous system of the mollusc Aplysia californica. The NO-donor, 3-morpholinosydnonimine (SIN-1), decreased the amplitude of evoked inhibitory postsynaptic currents (buccal ganglion) and potentiated that of evoked excitatory postsynaptic currents (abdominal ganglion). SIN-1 acted by modulating the number of ACh quanta released. 8Br-cGMP mimicked the effects of NO on ACh release in both types of synapses thus pointing to the involvement of a NO-sensitive guanylate cyclase. Presynaptic voltage-dependent Ca2+ and K+ (IA and late outward rectifier) currents were not modified by SIN-1 suggesting another final target for NO/cGMP. The labelling of a NO-synthase by immunostaining in several neurones as well as the modulation of ACh release by L-arginine indicate that an endogenous NO-synthase is involved in the modulation of synaptic efficacy in both buccal and abdominal ganglia.
