Abstract

1. The anatomical and neurophysiological basis of limb elevation at the basiischiopodite joint during locomotion, resistance reflexes, activation of cuticular stress detector 1 (CSL1) and production of the autotomy fracture was studied. 2. Scanning electron micrographs of the basi-ischiopodite interior revealed that the fracture plane consists of a line of tiny perforations in the cuticle (Fig. 3 A and B), which render the limb particularly susceptible to a distorting force concentrated at a single point along the plane. 3. Both the larger anterior levator (AL) and the smaller posterior levator (PL) can elevate the basi-ischiopodite. Force applied to the AL tendon is transmitted via elastic elements to a thin region of cuticle along the fracture plane and can cause the limb to fracture; force applied to the PL tendon is not transmitted to the fracture plane. The levator tendons are mechanically linked at their insertions so that contraction of PL alters the manner in which the force of AL is applied at its tendon insertion (Fig. 5). 4. AL and PL are simultaneously active in walking and resistance reflexes although they possess no shared innervation. The levators are antagonized in both motor patterns by the depressor muscle group. 5. Autotomy elicited by injury to the limb activates large phasic units in the AL nerve; activity in the PL nerve is simultaneously suppressed. In structural terms the inactivity of PL would result in the AL tendon bracing against the internal fulcrum (Fig. 4 A) in an orientation favorable for the transmission of force to the fracture plane. 6. Both levators are activated by stimulation of CSD1. This receptor does not evoke autotomy and instead may regulate the force exerted by the levators in such a way as to relieve stress in the cuticle distal to the AL tendon insertion when the integrity of the fracture plane is threatened.

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