Central and peripheral control of the trigger mechanism for kicking and jumping in the locust.

A crucial stage of the locust kick motor program is the trigger activity that inhibits the flexor motorneurons at the end of flexor-extensor coactivation and releases the tibia. One source of this inhibition is the M interneuron, which produces a spike burst at the time of the trigger activity. Previous work has suggested that sensory input resulting from extensor muscle tension may contribute to the M spike burst. We find that extensor muscle tension produced during thrusting behavior or by direct electrical stimulation with the tibia held fixed results in the depolarization of M, but this is not of sufficient amplitude to account for the M spike burst during the trigger activity. Furthermore, M still produces a spike burst after ablating the sensory systems that produce the response to the muscle stimulation. It is concluded that the major component of the M trigger activity is central in origin, although sensory feedback from extensor muscle tension makes some contribution. The combination of both central and peripheral paths for M activation may enhance the robustness of the behavior.