No abstract

These experiments were conducted to examine extinction and retention of a classically conditioned response in acute spinal cats. Conditioning was obtained by pairing a mild electrical stimulus to the superficial peroneal sensory nerve (CS) with a stronger electrical stimulus to the ankle skin (US) of the same leg. Subsequent extinction was produced by presenting CS-alone trials. In the first experiment, animals given massed extinction trials showed response decrements to base levels. Response decrements were not found in animals that received distributed extinction trials. In the second experiment, .5-, 1-, 2-, 3-, or 4-hr intervals between acquisition and extinction produced no significant differences in the extinction data. In the third experiment, animals received extinction trials immediately or 30 min after acquisition trials, followed by 20 additional extinction trials 30 min later. Analyses of these data indicated significant acquisition and extinction in the 10- and 20- acquisition trial groups. As in Experiment 2, varying the interval between acquisition and extinction did not produce any group differences in the extinction data. The results of these experiments demonstrate that response increases produced by paired trials in the spinal preparation do not decay spontaneously over time and are not caused by sensitization effects.

Temporal parameters concerning retention of a stimulation-induced hindlimb flexion were investigated. After spinal transection, 60 rats received 10, 20,30, 40, 45, or 50 min of hindlimb stimulation. Consistent persistence of flexion following stimulus cessation was observed in rats that were stimulated for at least 30 min. When the results are compared with previous data, the spinalized rat shows a 10-min reduction in the critical time interval needed to consistently obtain poststimulation persistence of flexion.

Previous studies have shown flexor nerve response increases produced by classical conditioning procedures in spinal cats when the conditioned stimulus (CS) was delivered to the superficial peroneal nerve and the unconditioned stimulus (US) was delivered to the ankle skin. In this study, these effects were produced when the CS was delivered to the whole tibial nerve or to the medial plantar branch. The finding that response increases followed by extinction effects could be obtained when either the superficial peroneal or the tibial nerve was utilized allowed the assessment of the effects of a differential conditioning paradigm. The responses to CS-US presentations on the superficial peroneal nerve increased, whereas responses to CS presentations on the tibial nerve remained unchanged. However, lack of extinction effects in the superficial peroneal data suggested that stimulation of the tibial nerve potentiated superficial peroneal evoked responses. Furthermore, responses evoked by stimulation of either nerve increased when paired trials were given on the tibial nerve. These data demonstrate that stimulation of the tibial nerve potentiates responses to superficial peroneal nerve stimulation but that superficial peroneal nerve stimulation has no effect on responses to CS presentations to the tibial nerve.

Hindlimb flexion induced by direct stimulation of the hindlimb has been observed subsequent to spinal section if an appropriate time interval was allowed to elapse between onset of flexion and spinal cord section. The present series of experiments was conducted to test the possibility that asymmetry persistence is a product of ongoing cutaneous input that continues after stimulation offset and spinal cord section. A local anesthetic (lidocaine) was injected in the general area of stimulation, and its effects on asymmetry were assessed in three experiments. The results generally indicated that ongoing cutaneous input was not a sufficient explanation for persistence of flexion in animals stimulated with intact or severed spinal cords. The data revealed, however, that ongoing cutaneous input may partially explain results of a previous study that employed a "stimulation-wait" preparation to obtain peripherally induced spinal fixation.