Non-depolarizing neuromuscular blocking drugs such as tubocurarine, pancuronium and vecuronium, are potent inhibitors of muscle nicotinic acetylcholine receptors (nAChRs) and are commonly used as muscle relaxants during abdominal surgery. Previous studies have reported adverse effects of these drugs on heart rate and other cardiovascular parameters (Son & Waud, 1980; Narita et al. 1992). The effects of muscle relaxants on neuronal nAChRs were investigated in dissociated neurons from rat (5-14 days old) intracardiac ganglia (ICG), which mediate vagal parasympathetic control of the heart. Amphotericin B perforated-patch clamp technique was employed to determine firing properties of ICG neurons and their response to 3 s rapid, focal application of nicotine alone (100 μM) or together with vecuronium, tubocurarine or pancuronium. There was significant variation in peak amplitude, time course and recovery of nicotine-evoked responses among ICG neurons. The mean peak amplitude of nicotine-evoked inward currents at -60 mV was significantly larger (approximately 4-fold) in neurons exhibiting tonic (-26.4 pA/pF; n=6) and accommodating (-25.8 pA/pF; n=6) firing patterns compared to phasic (-6.9 pA/pF; n=17; P < 0.0001). Vecuronium, tubocurarine and pancuronium at 1 μM inhibited nicotine-evoked currents by 80%, 55% and 37% with approximate IC₅₀ values of 0.9, 9.6 and 100 nM, respectively. Pancuronium modulation of nicotine-evoked currents was biphasic in 7 of 11 neurons tested whereby potentiation was observed at low concentrations (<10 nM) and inhibition at higher concentrations with maximum inhibition of 40% at 10 μM. Concentration-response curves of inhibition by muscle relaxants were shifted left by ~10-fold in tonic or accommodating neurons compared to the phasic neurons. Taken together, these data indicate that nAChR-mediated currents in ICG neurons and their modulation by muscle relaxants are closely correlated with neuronal firing patterns.