Miniature Excitatory Junction Potentials

Neuromuscular transmission of excitation in invertebrates has been studied extensively by many investigators (cf. Bullock & Horridge, 1963). Miniature inhibitory junction potentials (m.i.j.p.s) and miniature excitatory junction potentials (m.e.j.p.s) could be recorded from the longitudinal layer of the somatic muscle in the earthworm. Field stimulation to the peripheral nerves elicited inhibitory junction potentials (i.j.p.s) and excitatory junction potentials (e.j.p.s). Generation of the m.i.j.p. and i.j.p. was blocked by treatment with picrotoxin (icr g./ml.) and the equilibrium potentials for them ranged between —52 and —58 mV. The m.e.j.p.s and e.j.p.s were blocked by d-tubocurarine (io~ g./ml.) and the equilibrium potential for them was o mV. The former was thought to be due to release of y-aminobutyric acid (GABA) from the peripheral inhibitory nerves and to selective increase of chloride permeability. The latter was thought to be due to release of acetylcholine which increases the sodium and potassium permeabilities of the postsynaptic muscle membrane. Generation of the m.e.j.p. was less common than that of the m.i.j.p., in spite of the double innervation to the muscle fibres. However, when the external sodium (Na)0 was replaced with (Tris)0, the membrane was hyperpolarized from — 35 mV. to — 55 mV. and frequently generated the m.e.j.p. (Hidaka et al. 1969b, c). The present experiments were intended to investigate the ionic mechanism involved in generation of the m.e.j.p.s in sodiumfree solution, and the results indicated that, in sodium-free solution, generation of the m.e.j.p in a depolarizing direction is due mainly to increase in calcium permeability and, to a lesser extent, to increase in potassium permeability, brought about by the release of acetylcholine from the nerve terminals.