INTRATHECAL ADMINISTRATION OF THE NMDA ANTAGONIST MK - 801 PREVENTS THE BEHAVIORAL DEFICIT OBSERVED AFTER NONCONTINGENT SHOCK IN SPINALIZED RATS. A.R.Ferguson*; E.D.Crown; B.C.Patton; J.W.Grau . Psychol Dept, Texas A & M Univ, College Station, TX, USA.
Previously we found that the spinal cord can demonstrate a simple form of instrumental learning. In a typical experiment, rats are spinally transected (spinalized) and tested 24 h later. During testing, subjects receive response-contingent shock to one hindleg whenever their leg falls below a preset criterion. Spinalized rats rapidly learn to maintain the leg in a flexed position, thereby decreasing net shock exposure. Subjects that have previously received shock independent of leg position (noncontingent shock) fail to learn. This behavioral deficit can be induced by as little as 6 min of noncontingent shock to the tail and lasts for 48 h. Recent work suggests that subcutaneous injection of the inflammatory agent carrageenan is sufficient to induce a behavioral deficit. This suggests that the phenomenon may be related to central sensitization, a NMDA-mediated process. The present study explores the role of NMDA receptors in the behavioral deficit. Subjects were given an intrathecal administration of the NMDA antagonist MK-801 at one of 4 doses (0, 0.1, 1.0, or 10 nmol) immediately prior to noncontingent shock, and were tested 24 h later. MK-801 was found to dose dependently block the induction of the behavioral deficit. This finding suggests that the behavioral deficit reflects a NMDA-mediated saturation that blocks the development of response-selective synaptic modifications.
Supported by: MH60157 to JWG & RCM
Citation: A.R.Ferguson, E.D.Crown, B.C.Patton, J.W.Grau. INTRATHECAL ADMINISTRATION OF THE NMDA ANTAGONIST MK - 801 PREVENTS THE BEHAVIORAL DEFICIT OBSERVED AFTER NONCONTINGENT SHOCK IN SPINALIZED RATS. Program No. 166.7. 2002 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience, 2002. CD-ROM.