Membrane potential responses of the mouse anococcygeus muscle to ionophoretically applied noradrenaline

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Abstract
Membrane potential responses to ionophoretically applied noradrenaline [norepinephrine, NE] and to field stimulation were studied in the mouse anococcygeus muscle using intracellular recording techniques. The ionophoretic application of NE produced charge-dependent depolarizations (total duration was 1-2 s at room temperature) which were characterized by a delay between the start of the ionophoretic pulse and the onset of depolarization (termed the latency of the responses). On occasion ionophoresis of NE did not depolarize the muscle even though it seemed that successful ejection of NE had occurred as small localized contractions were seen. The characteristics of these depolarizations were unaffected by tetrodotoxin (10-7 M) and could not be reproduced when the ionophoretic pipette contained 2 M-NaCl rather than NE. NE still produced depolarizations in denervated muscle. The responses were evidently caused by NE released from the ionophoretic micropipette and not from the intrinsic noradrenergic nerves. Field stimulation of innervated muscle usually evoked excitatory junction potentials (e.j.p.), but sometimes inhibitory junction potentials (i.j.p.), or a mixture of e.j.p. and i.j.p. were observed. The time course of the e.j.p. was slightly longer than that of the ionophoretic depolarizations, which was accounted for by a smaller latency of the ionophoretically induced responses. The pharmacology of the nerve-evoked e.j.p. and the ionophoretically induced depolarizations were similar as both types of responses were antagonized by .alpha.1-adrenoceptor blocking agents (phentolamine and prazosin), but were unaffected by the .beta.-adrenoceptor antagonist, propranolol. NE released from the intrinsic nerves and from the ionophoretic micropipette were apparently acting on the same adrenoceptors. The latency and, to a lesser extent, the rise-time of the depolarization produced by the ionophoretic application of NE were highly sensitive to changes in temperature of the bathing fluid (Q10 > 2), whereas the half-decay time was relatively insensitive to temperature changes (Q10 .apprx. 1.5). The latency of the depolarizations was not altered by inhibiting the NE-uptake mechanism with cocaine (2 .times. 10-6 M) or by .alpha.-adrenoceptor blocking agents. The latency of the responses may be a property of the NE-receptor interaction rather than being caused by other phenomena such as diffusion of NE.

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