Presynaptic modulation of ganglionic ACh release by muscarinic and nicotinic receptors.

Abstract

The present experiments were undertaken to investigate the effects of atropine and d-tubocurarine on acetylcholine (ACh) release and ganglionic synaptic transmission in the isolated cat stellate ganglion. Ganglionic release of picomole amounts of ACh was measured by radioenzymatic assay, and ganglionic transmission was estimated on the basis of the compound action potential recorded from the postganglionic stellate cardiac nerve. Atropine (5 microM) produced a significant increase in both spontaneous and evoked ACh release from the ganglion while depressing synaptic transmission. d-Tubocurarine (20 microM) also caused a significant, though smaller, increase in spontaneous release of ACh but had little effect on evoked release of ACh. These results suggest that ACh release and synaptic transmission in the cat stellate ganglion are subject to cholinergic feedback regulation, which appears to be mediated predominantly via muscarinic presynaptic receptors.

• Authors: Z Dujic, D L Roerig, H K Schedewie, J P Kampine, Z J Bosnjak
• Journal: The American journal of physiology (Am J Physiol) Vol. 259 Issue 2 Pt 2 Pg. R288-93 (Aug 1990) ISSN: 0002-9513 [Print] United States
• PMID: 2386239 (Publication Type: Journal Article)

Chemical References

• Receptors, Muscarinic
• Receptors, Nicotinic
• Atropine
• Physostigmine
• Acetylcholine
• Tubocurarine

Topics

• Acetylcholine (metabolism)
• Action Potentials (drug effects)
• Animals
• Atropine (pharmacology)
• Cats
• Dose-Response Relationship, Drug
• Electric Stimulation
• Female
• Ganglia, Sympathetic (metabolism)
• Male
• Physostigmine (pharmacology)
• Receptors, Muscarinic (metabolism)
• Receptors, Nicotinic (metabolism)
• Synapses (physiology)
• Tubocurarine (pharmacology)