An evaluation of the role of identified interneurons in triggering kicks and jumps in the locust.

Abstract

1. We have used intracellular recording and staining techniques to examine the importance of certain identified interneurons within the system responsible for triggering kicks and jumps in the locust, Locusta migratoria. In particular, our study focused on a pair of metathoracic interneurons called the M-neurons. These cells make strong inhibitory connections to hind-leg flexor motoneurons and are thought to play a key role in the termination of flexor activity which causes kicks and jumps to be triggered (8, 20, 24). 2. Simultaneous recordings from M-neurons and flexor motoneurons during bilateral hindleg kicks revealed that in most cases the onset of the M-neuron's high-frequency discharge coincided precisely with the start of the flexor's rapid repolarization. This result demonstrated that M's activity had the correct timing to be involved in the triggering process and so confirmed suggestions made in previous studies. At times, however, the flexor motoneurons began to repolarize slowly prior to the first spike in the M-neuron, indicating that triggering must involve other neurons and perhaps also an additional mechanism such as a reduction of flexor excitation. 3. The sufficiency and necessity of the M-neurons for triggering kicks were tested by experiments involving intracellular current injections. The application of a brief pulse of depolarizing current to an M-neuron, in order to evoke a burst of spikes in the cell prior to the time it would normally have become active, caused extension of the ipsilateral leg to be triggered prematurely but did not influence the motor program in the contralateral leg. This effect was only observed when the discharge frequency evoked artificially in the M-neuron was greater than that seen during natural performance of the behavior. Even then, the repolarization produced in the flexor motoneurons by the current pulses was not the same as occurs normally. We conclude that under natural circumstances the M-neurons, by themselves, are not sufficient to trigger kicks. 4. When the usual discharge in an M-neuron was prevented by the injection of hyperpolarizing current, both legs were still able to kick. This lack of necessity of the M-neurons confirms that additional neurons must be involved in the triggering process. The rate of repolarization of the flexor motoneurons during kicks in which M activity had been abolished was slower and more variable than is seen in normal kicks but this did not appear to alter the timing of leg extension.(ABSTRACT TRUNCATED AT 400 WORDS)