The Effect of Carbachol and α‐Bungarotoxin on the Frequency of Miniature Endplate Potentials at the Frog Neuromuscular Junction

Abstract

The effects of an acetylcholine analogue, carbachol (CCh), and a purified irreversible nicotinic antagonist, -bungarotoxin (BTX), on the frequency of the miniature endplate potentials (mEPPs) at the neuromuscular junction of the frog were tested at 20 and 10 C. CCh (5 10-6 m) reduced the frequency of mEPPs to about 60 %; this reduction was not affected by 1 10-7 g ml-1 BTX. BTX also reversibly decreased the mEPP frequency by 40 %, but not in the presence of CCh or in Ringer solution with 0 or 8 mM Ca2+. The present data show that BTX, which inhibits a class of nicotinic ACh receptors, does not block the decrease of mEPP frequency evoked by CCh and can itself suppress the frequency of spontaneous quantal release.

Negative cross‐talk between presynaptic adenosine and acetylcholine receptors

“…Experiments were carried out on frog sartorius muscle preparations in vitro at room temperature (for details see Giniatullin et al ., 1997, 2005; Bukharaeva et al ., 2000). Briefly, muscles were dissected from ether‐anaesthetized frogs killed by decapitation and by double pithing.…”

“…At the neuromuscular junction, acetylcholine (ACh) and ATP are coreleased from motor nerve terminals (Silinsky & Redman, 1996) with breakdown of ATP to adenosine (Cunha & Sebastiao, 1991; Ribeiro et al ., 1996; Zimmermann, 2000). Previous studies demonstrated that neurotransmitter release at the neuromuscular junction is modulated by cholinergic (Slutsky et al ., 1999, 2001, 2002; Bukharaeva et al ., 2000) and purinergic receptors in presynaptic terminals (Ribeiro et al ., 1996; Giniatullin & Sokolova, 1998; Sebastiao & Ribeiro, 2001). While adenosine and ATP inhibit quantal release via A1 and P2Y receptors, respectively (Giniatullin & Sokolova, 1998; Sokolova et al ., 2003a), ACh acts in an inhibitory manner via presynaptic muscarinic receptors (Slutsky et al ., 2001; Giniatullin et al ., 2002).…”