Hm. Cousins et al., NEURONALLY RELEASED AND APPLIED ACETYLCHOLINE ON THE LONGITUDINAL MUSCLE OF THE GUINEA-PIG ILEUM, Neuroscience, 65(1), 1995, pp. 193-207
Brief transmural stimuli, which selectively excited cholinergic fibres
, initiated contractions and excitatory junction potentials in prepara
tions of longitudinal muscle isolated from the guinea-pig ileum: these
responses were associated with an increase in the internal concentrat
ion of calcium ions. When muscle voltage-dependent calcium channels we
re blocked using the organic calcium antagonist nifedipine, brief stim
uli continued to initiate contractions, evoke excitatory junction pote
ntials and cause an increase in the intracellular calcium concentratio
n. Ionophoretically applied acetylcholine caused depolarizations which
resembled the excitatory junction potentials evoked by cholinergic ne
rve stimulation. Both responses had slow time courses and were abolish
ed by muscarinic receptor antagonists. However, the depolarizations pr
oduced by ionophoretically applied acetylcholine, unlike those produce
d by nerve stimulation, were frequently interrupted by transient hyper
polarizations. The transient hyperpolarizations were abolished by bari
um ions or charybdotoxin. High concentrations of the calcium antagonis
ts nicardipine, verapamil or diltiazem had a tendency to preferentiall
y abolish the excitatory junction potential. When the effects of the c
holinesterase inhibitor, eserine, on excitatory junction potentials we
re examined, it became apparent that when the destruction of acetylcho
line was prevented it initiated an additional conductance change to th
at initiated by acetylcholine in untreated tissues. The results are di
scussed in relation to the idea that neuronally released acetylcholine
and applied acetylcholine might activate different subsets of muscari
nic receptors on longitudinal ileal smooth muscle.