An exploration of the mechanisms that underlie environmentally induced hyperalgesia

Abstract

Prior studies have shown that exposure to mild shock can produce a decrease in pain reactivity (hypoalgesia) in rats. For example, it increases the latency at which rats withdraw their tail froma noxious thermal stimulus. Recently, our laboratory discovered thatthe opposite is observed if pain reactivity is assessed in another way:by measuring the shock intensity needed to elicit a vocalization or motor response. Using these measures, previously shocked rats appear more responsive (hyperalgesic) to the test stimulus. The present series of experiments explore the mechanisms that mediate this hyperalgesia. Experiments 1 and 2 showed that neither testing subjects outside of the shock context, nor the presentation of a distracting stimulus, affects the magnitude of hyperalgesia. This suggests that the hyperalgesia is an unconditioned response and that memorial mechanisms play little role in its production. Experiment 3 showed that exposure to shock lowers vocalization thresholds to a thermal stimulus applied to the tail while it increases tail-flick latencies. Experiment 4 compared the motor responses observed when either shock or heat is used as the test stimulus. It was found that shocked rats were hypoalgesic to heat, but hyperalgesic to shock, even when the same response criteria are employed. Experiment 5 looked at whether prior exposure to shock affects the acquisition of conditioned fear in a different context. It was found that previously shocked rats exhibited greater conditioned freezing after a test shock was presented in a novel context, shock suggests the test shock was perceived as more aversive.