Abstract
Intracellular membrane potential recordings were made from circular muscle cells in the guinea-pig ileum in vitro at 30 degrees C in the presence of atropine (1.4 microM). Following transmural nerve stimulation the inhibitory junction potential (i.j.p.) was followed by a post-stimulus depolarization (p.s.d.). Both were abolished by tetrodotoxin. P.s.d. consisted of two phases; (i) an early fast phase (f.p.s.d.) which peaked about 1 s following the stimulus and (ii) a late slow phase (s.p.s.d.) which had a latency of 1-2 s and peaked approximately 4 s following the stimulus. Both f.p.s.d. and s.p.s.d. were observed when the membrane was hyperpolarized by anodal current to the reversal potential of the i.j.p. F.p.s.d. and s.p.s.d. were therefore unlikely to result solely from a decrease in membrane conductance to potassium ions. During f.p.s.d., hyperpolarizing electronic potentials were reduced in amplitude suggesting that f.p.s.d. was associated with an increase in membrane conductance. There were no consistent changes in the amplitude of the electronic potentials during s.p.s.d. When the membrane potential was hyperpolarized by prolonged anodal current, an additional relatively rapid depolarizing potential could be induced by either transmural stimulation or depolarizing electrotonic current pulses.
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