BLOCKING NEURAL CONDUCTION ROSTRAL TO AN INJURY IN RATS HAS A PROTECTIVE EFFECT THAT REDUCES THE ADVERSE CONSEQUENCES OF NOCICEPTIVE STIMULATION.

A.C. Bopp*¹, A.R. Ferguson¹, R.C. Miranda², J.W. Grau¹. ¹Dept. of Psychology, ²Dept. of Medical Anatomy, Texas A&M University, TX, USA

We have shown that 6 minutes of uncontrollable nociceptive stimulation (intermittent tailshock) undermines the recovery of function after a contusion injury. Tailshock could hurt recovery by inducing a destructive effect below the injury,reducing the sparing of white matter at the injury site, or by enlisting brain-dependent processes that influence recovery. If brain-dependent processes contribute, blocking neural conduction rostral to the injury should reduce the adverse effect of shock on recovery. We tested this using the Na+ channel blocker lidocaine microinjected rostral to the injury site. A pilot study verified that our injection procedure saturated approximately 2 cm above the injury site. Rats received a moderate contusion injury using a 12.5 mm weight drop with the MASCIS device and had a catheter implanted rostral to the injury. The next day, rats were treated with either 30 uL of 10% lidocaine or saline. Subjects then received 6 min of uncontrollable intermittent tailshock or nothing (unshocked). Recovery of function was evaluated over 21 days using the BBB open field locomotor scale (Basso et al., 1995, J. Neurotrauma, 12, 1-21). Saline treated shocked rats exhibited poor recovery (lower BBB scores) relative to the unshocked controls. Pretreatment with lidocaine prior to shock had a protective effect that reduced the adverse consequences of nociceptive stimulation. The results suggest that brain-dependent processes contribute to the delterious effects of uncontrollable nociceptive stimulation. Further studies are being conducted to determine the extent to which nociceptive input has a direct, versus brain-dependent, impact on recovery. Supported by MH60157 and NS41548 to JWG & RCM.