Regulation of transmitter release by presynaptic receptors at a cholinergic neuro-neuronal synapse.

Abstract

The modulation of evoked transmitter release by presynaptic receptors was studied at an identified cholinergic synapse in the buccal ganglion of Aplysia. Two auto-receptors affecting acetylcholine release in opposite ways were identified. Additionally acetylcholine (ACh) release was found to be facilitated by the peptide FLRFamide and inhibited by histamine. Ca2+ channels appeared as the final effectors controlled by these non-cholinergic presynaptic receptors whereas the activation of cholinergic presynaptic receptors did not affect the Ca2+ influx. The intracellular pathway activated by FLRFamide receptors was investigated in detail. The facilitation of transmitter release induced by this peptide was prevented by bath application of H-7, a protein kinase C inhibitor. Moreover, a diacylglycerol analog mimicked the action of FLRFamide. These results suggest that activation of protein kinase C leading to the phosphorylation of Ca2+ channels could be the mechanism through which presynaptic FLRFamide receptors increase evoked quantal release of acetylcholine at this synapse.

• Authors: L Tauc, P Fossier, G Baux
• Journal: Acta biologica Hungarica (Acta Biol Hung) Vol. 43 Issue 1-4 Pg. 49-58 ( 1992) ISSN: 0236-5383 [Print] Hungary
• PMID: 1338557 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Calcium Channels
• Invertebrate Hormones
• Isoquinolines
• Neuropeptides
• Piperazines
• FMRFamide
• Histamine
• 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
• Protein Kinase C
• Acetylcholine

Topics

• 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
• Acetylcholine (metabolism)
• Animals
• Aplysia (physiology)
• Calcium Channels (drug effects, metabolism)
• FMRFamide
• Histamine (pharmacology)
• Invertebrate Hormones (pharmacology)
• Isoquinolines (pharmacology)
• Neuropeptides (pharmacology)
• Piperazines (pharmacology)
• Protein Kinase C (antagonists & inhibitors, metabolism)
• Synapses (drug effects, metabolism)