Hm. Cousins et al., CHOLINERGIC NEUROMUSCULAR-TRANSMISSION IN THE LONGITUDINAL MUSCLE OF THE GUINEA-PIG ILEUM, Journal of physiology, 471, 1993, pp. 61-86
1. Brief transmural stimuli, 0.5-1 ms, initiated contractions of the l
ongitudinal muscle taken from the guinea-pig ileum that were recorded
isometrically. In separate preparations similar stimuli were found to
initiate excitatory junction potentials which were recorded using intr
acellular recording electrodes. All of these responses were abolished
by either tetrodotoxin, omega-conotoxin or hyoscine. 2. The contractio
ns produced by increasing [K+]o were blocked by nifedipine, 1 x 10(-7)
M; nicardipine, 1 x 10(-7) M; verapamil, 1 x 10(-5) M or diltiazem, 1
x 10(-5) M. In these solutions brief stimuli continued to initiate co
ntractions: this indicates that neuronally released acetylcholine. con
tinues to trigger a contraction when muscle voltage-dependent calcium
channels appear to have been blocked. 3. When membrane potential recor
dings were made from the smooth muscle layer, brief transmural stimuli
initiated excitatory junction potentials that triggered muscle action
potentials. Although muscle action potentials were abolished by low c
oncentrations of a range of organic calcium antagonists, excitatory ju
nction potentials persisted and continued to initiate contractions of
reduced amplitude. 4. When the internal concentration of calcium ions,
[Ca2+]i, was measured using fura-2, brief transmural stimuli caused a
n increase in [Ca2+]i. Part of this response, which occurred at a time
corresponding to the unblocked excitatory junction potential, persist
ed in the presence of the organic calcium antagonist nifedipine. 5. Tw
o explanations appear possible. Neuronally released acetylcholine may
simultaneously activate non-selective cation channels and cause the re
lease of Ca2+ from an internal store. Alternatively, neuronally releas
ed acetylcholine may cause an increase in [Ca2+]i which is separate fr
om that which accompanies the activation of voltage-dependent calcium
channels. At this stage there is little other anatomical or electrophy
siological evidence to support this view.