The behavioral deficit observed following noncontingent shock in spinalized rats is prevented by the protein synthesis inhibitor cycloheximide.

Spinalized rats that receive shock when 1 hind limb is extended (contingent shock) exhibit an increase in flexion duration, a simple form of instrumental learning. Rats that receive shock independent of leg position (noncontingent shock) do not exhibit an increase in flexion duration and fail to learn when tested with contingent shock 24 hr later. It appears that noncontingent shock induces an intraspinal modification that inhibits the capacity to learn. The authors propose that the mechanisms that underlie this effect depend on de novo protein synthesis. To evaluate this hypothesis, the authors gave spinalized rats the protein synthesis inhibitor Cycloheximide (CXM) or saline intrathecally prior to, or immediately after, noncontingent shock exposure. Twenty-four hours later, rats were tested with contingent shock. Rats that received the vehicle and noncontingent shock failed to learn. CXM-treated shocked rats learned normally, suggesting that the learning deficit depends on protein synthesis within the spinal cord.