ION CURRENTS AND MECHANISMS OF MODULATION IN THE RADULA OPENER MUSCLES OF APLYSIA

Numerous studies of plasticity in the feeding behavior of Aplysia have shown that substantial plasticity is due to peripheral neuromodulatio n of the feeding musculature. Extensive previous work focusing on the accessory radula closer (ARC) muscle has led to the realization that a major function of the modulation in that muscle may be to ensure effi cient coordination between its contractions and those of its antagonis t muscles. For a more complete understanding, therefore, we must study these muscles also. Here we have studied the radula opener muscles 17 -I10. Using single isolated muscle fibers under voltage clamp, we have characterized ion currents gated by voltage and by the physiological contraction-inducing neurotransmitter acetylcholine (ACh) and the effe cts of the physiological modulators serotonin, myomodulins A and B, an d FMRFamide. Our results explain significant aspects of the electrophy siological behavior of the whole opener muscles, as well as why the op ener and ARC muscles behave similarly in many ways yet differently in some key respects. Opener muscles express four types of K currents: in ward rectifier, A-type [I-K(A)], delayed rectifier [I-K(V)], and Ca2+- activated [I-K(Ca)] They also express an L-type Ca current [I-Ca] and a leakage current. ACh activates a positive-reversing cationic current [I-ACh(cat]) and a negative-reversing Cl current [I-ACh(Cl)] The open er muscles differ from the ARC in that, in the openers, activation of I-K(A) occurs similar to 9 mV more positive and there is much less I-A Ch(Cl). In both muscles, I-ACh(cat) most likely serves to depolarize t he muscle until I-Ca activates to supply Ca2+ for contraction, but fur ther depolarization and spiking is opposed by coactivation of I-K(A), I-K(V), I-K(Ca), and I-ACh(Cl). Thus the differences in I-K(A) and I-A Ch(Cl) may well be key factors that prevent spikes in the ARC but ofte n allow them in the opener muscles. As in the ARC, the modulators enha nce I-Ca and so potentiate contractions. They also activate a modulato r-specific K current, which causes hyperpolarization and depression of contractions. Finally, in the opener muscles but not in the ARC, the modulators activate a depolarizing cationic current that may help phas e-advance the contractions. Each modulator exerts these effects to dif ferent degrees and thus has a distinct effect on voltage and contracti on size and shape. The overall effect then will depend on the specific combinations of modulators released in different behaviors. By unders tanding the modulation in the opener muscles, as well as in the ARC, w e are now in a position to understand how the behavior of the two musc les is coordinated under a variety of circumstances.