The physiological role of acetylcholine in the neuromuscular system ofascaris lumbricoides

Abstract

1. the effect of acetylcholine, d-tubocurarine and neostigmine on the electrical activity of Ascaris muscle cells, has been studied with intracellular microelectrodes. 2. Acetylcholine depolarizes the membrane surrounding the syncytial region of the muscle cells. the rest of the cell surface is not affected by this compound. It appears, therefore, that the acetylcholine receptors are located in the same area of the muscle where the rhythmic spontaneous spike potentials are generated. 3. Between 15 and 40 mV, the frequency of the spike potentials is an inverse function of the resting potential; no spike activity occurs outside those potential levels. 4. Although d-tubocurarine prevents the effect of externally applied acetylcholine, it does not block the firing of rhythmic spontaneous spike potentials, even at concentrations as high as 10⁻³ (w/v). 5. the effects of neostigmine are comparable to those of small concentrations of acetylcholine. On the other hand, the administration of d-tubocurarine in the absence of externally applied acetylcholine increases slightly the resting potential, and may decrease the frequency and amplitude of the spike potentials. 6. the pharmacological actions of neostigmine and d-tubocurarine suggest that small amounts of acetylcholine, or a closely related choline ester, act most of the time on the muscle syncytium, decreasing the resting potential and increasing the rate of the spike potentials. 7. These results suggest: (a) that the spike potentials recorded from Ascaris muscle are due the oscillatory activity of the muscle membrane itself, rather than being generated by nervous pacemakers; (b) that acetylcholine plays the role of a modulatory “accelerating”, neurohormone, rather than that of a chemical transmitter involved in the one-to-one transfer of impulses from nerve cord to muscle.