INSTRUMENTAL LEARNING IN SPINALIZED RATS: INFLAMMATION INDUCES A BEHAVIORAL DEFICIT, SIMILAR TO THE ONE INDUCED BY NONCONTINGENT SHOCK. A. R. Ferguson*, E. D. Crown, S. N. Washburn, R. C. Miranda, & J. W. Grau, Depts. of Psychology & Medical Anatomy, Texas A&M University, College Station, TX 77843.
We have previously shown that the spinal cord can support a simple form of instrumental learning. In a typical experiment, rats are transected at the second thoracic vertebra and are tested 24 h later. During testing subjects receive shock to one hindleg when that leg is extended. They quickly learn to maintain the leg in a flexed position, decreasing net shock exposure. Rats that have previously received shock independent of leg position (noncontingent shock) fail to learn. This learning deficit shares many properties with inflammation. Inflammation is associated with tactile allodynia, an increase in GABAergic inhibition and increased expression of kappa opioids. Similarly, following noncontingent shock rats show a local tactile allodynia. Moreover, expression of the learning deficit can be blocked with a kappa opioid antagonist, and a GABAa antagonist blocks both the induction and expression of the deficit.
The present study explores the impact of inflammation on instrumental learning. We hypothesized that inflammation would induce a behavioral deficit similar to that produced by noncontingent shock. To test this spinalized rats were given a subcutaneous injection of the inflammatory agent carrageenan to one hind paw, and were tested for instrumental learning on the contralateral limb at 0, 3, 6, 12, or 24 hours after administration. Rats showed a robust learning deficit that peaked at 3-6 hours and then gradually subsided. These results indicate that a clinically relevant stimulus can induce a behavioral deficit in spinalized animals. Supported by MH60157 to JWG & RCM.
Published in Society for Neuroscience Abstracts, 27, 2001, 2202.
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