INSTRUMENTAL LEARNING OF A FLEXION RESPONSE IN SPINALIZED RATS: EVIDENCE FOR BEHAVIORAL IMMUNIZATION AND THERAPY. E. D. Crown*, & J. W. Grau, Dept. of Psychology, Texas A&M Univ., College Station, TX 77843.

We have shown that spinal cord neurons can support a simple form of instrumental learning (Grau et al., 1998, Behav. Neuro., 112, 1366). Rats are spinalized at the second thoracic vertebra (T2) and given shock to one hindleg. One group (Master) receives shock whenever the leg is extended. This response-contingent shock causes an increase in flexion duration that decreases net shock exposure. This instrumental learning is not observed in yoked controls that receive the same amount of shock independent of leg position (noncontingent shock). Interestingly, rats that have received noncontingent shock also fail to learn when they are subsequently exposed to response-contingent shock. We have shown that just 6 min of noncontingent shock to the leg or tail causes the behavioral deficit, undermining spinal cord function for 24-48 hrs.

The present experiments explored whether a form of behavioral therapy can prevent and/or reverse the behavioral deficit. In an attempt to prevent the deficit, spinalized rats received 30 min of training with contingent or noncontingent shock prior to noncontingent tailshock. They were then tested with contingent shock to the contralateral hindleg. Rats that had received noncontingent shock both times failed to learn while prior exposure to contingent shock had an immunizing effect, preventing the development of the deficit. We have previously shown that intrathecal naltrexone can temporarily attenuate the deficit. The next experiment examined whether this pharmacological treatment, when combined with a form of behavioral therapy (contingent shock), would restore behavioral potential following noncontingent shock. Subjects were tested 24 hrs after this therapy treatment with contingent shock to the contralateral leg. We found that naltrexone combined with contingent shock therapy restored spinal cord function. This work was funded by MH 60157 to J.W.G.

Published in Society for Neuroscience Abstracts, 26, 2000, 2207.

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