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Fast extensor tibiae (FETi) activity has been implicated as a crucial element underlying the locust kick motor programme with regard to four circuits, (i) A positive feedback reflex from extensor tibiae (ETi) muscle tension helps maintain FETi spiking during co-contraction, (ii) A central connection from FETi to flexor tibiae (FITi) motor neurones helps initiate FITi spiking at the start of cocontraction, (iii) Reflex feedback from ETi tension to FITi motor neurones helps maintain the latter spiking during co-contraction after the central connection has decremented, (iv) A proprioceptive gate controlled by ETi tension ensures that FITi trigger activity does not occur until sufficient ETi tension has developed to allow an effective kick.
The hypotheses concerning these circuits have been tested in two ways. First, FETi was phasically inhibited for varying periods during co-contraction, abolishingits spikes and hence its central output, and reducing ETi tension. Second, the nerve containing the FETi axon was cut in the femur, thus partially denervating the ETi muscle, and reducing its tension without directly affecting FETi activity. In both cases, kicks were analysed to see whether the motor programme changed in accordance with the circuit model. The overall conclusion is that the model isnot correct, since considerable experimentally induced changes in FETi activity and ETi tension had no obvious effects on the motor programme. The circuits may play a supplementary role in generating the programme, but they are not crucial to it.