THE GENERALITY OF SHOCK-INDUCED HYPERALGESIA IN RATS. M. W. Meagher, S. McLemore, T. K. King, & J. W. Grau. Psychology Dept., Texas A&M University, College Station, TX 77843.
Exposure to moderately intense tail-shocks (3, 0.75-s, 1 mA) has opposite effects on spinal and forebrain mediated measures of pain reactivity: it induces antinociception on the tail-flick test while it lowers vocalization thresholds to both heat and shock (hyperalgesia). Although prior work indicates that shock-induced antinociception can be elicited by a variety of shock schedules (Meagher et al., Behavioral Neuroscience, 107, 1993), little is known about the generality of hyperalgesia. Experiment 1 examined the emergence of hyperalgesia and antinociception by exposing separate groups of rats to either 0, 0.1, 0.3, or 1.0 mA shocks and measuring tail-withdrawal to radiant heat and vocalization thresholds to shock. Both antinociception and hyperalgesia emerged after exposure to the 0.3 mA intensity. Experiment 2 evaluated whether more severe shock schedules elicit hyperalgesia by testing the impact of longer (3, 25-s, 1 mA) or more intense (3, 2-s, 3 mA) shock conditions on subsequent shock reactivity. Prior research has shown that longer shocks engage a brainstem mediated nonopioid antinociception, while brief but more intense shocks (3, 2-s, 3 mA) engage a spinally mediated opioid antinociception on the tail-flick test. In contrast, both shock conditions lowered vocalization thresholds, suggesting enhanced pain. The duration of the hyperalgesia depended on the shock condition: hyperalgesia persisted for 32 min in the intense condition and 128 min in the long shock condition. We are currently assessing the impact of these shock schedules on startle and the acquisition of conditioned freezing. Supported by MH54557 to J.W.G. and M.W.M.
Society for Neuroscience Abstracts, 24 (1998), 1901.