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Journal of Experimental Biology 61,655-666 (1974)
Published by Company of Biologists 1974

Interactions Between Neurones Mediating Tuft Withdrawal in Tritonia Hombergi

D. A. DORSETT ¹ and A. O. D. WILLOWS ²

¹ Marine Science Laboratories, Menai Bridge, Anglesey
² Marine Science Laboratories, Menai Bridge, Anglesey; Friday Harbor Laboratories, University of Washington, Washington, 98250, U.S.A.

The seven neurones that command the three stages of branchial tuft withdrawal interact by electrotonic and chemically mediated polysynaptic pathways.

The pleural tuft retractors, L and R Pl 6, make electrotonic synapses with the ipsilateral neuronesPd2, which cause retraction of the tips of the tufts.

The chemically transmitting pathways, between these and other retractor neurones, are mostly reciprocal and can be classified as weak or strong. The former are small in amplitude, with long latencies (1-3 sec) and are labile to repeated activation; the latter are of large amplitude and shorter latency (0·5-0·8 sec), but may still show decrement with repeated use. Frequently the p.s.p. shows indications of 1:1 correlation with the spike pattern in the driven neurone, but the long latencies require the presence of at least one interneurone in the pathway.

The progressive spread of the behavioural response (withdrawal of the tips, complete unilateral withdrawal, complete bilateral withdrawal of all tufts), which occurs with increasing stimulus intensity, is not dependent on a central hierarchy in the activation of the tuft retractor neurones. Reciprocal feedback leads to a general increase in central excitability, the threshold for more extensive responses being probably determined largely by the sensory input to individual neurones.

The unique pleural cell R Pl 5 is exceptional, both in the variety of motor activity it commands and in the absence of reciprocal connexions from other retractor neurones.