Impact of shock on pain reactivity: I. Whether hypo- or hyperalgesia is observed on how pain reactivity is tested.

Abstract

Prior research has shown that exposure to shock can induce a decrease in pain reactivity (hypoalgesia). The present experiments show that, at the same time points that subjects are less responsive to radiant heat applied to the tail (the tail-flick test), tailshock elicits enhanced motor reactivity and vocalization. This enhanced responsiveness, or hyperalgesia, is observed with both magnitude (Experiment 1) and threshold (Experiment 2) measures and decays within 32 min (Experiment 2). Experiment 3 shows that the hyperalgesia decays irrespective of whether or not subjects remain in the shock context, which suggests that the loss of hyperalgesia does not reflect extinction of the context-shock association. Neither removing subjects from the shock context (Experiment 4) nor the presentation of a postshock distractor (Experiment 5) affected the hyperalgesia.

The effects of age and isolation period on two phases of behavioral response to foot shock in isolation‐reared rats

“…On the other hand, all subjects that were isolated from 26 to 40 days of age showed similar scores for the jumping threshold, which were lower than 0.30 mA irrespective of other differences in the rearing conditions. These facts suggest that isolation during the postweaning stage does not produce stress-induced hyperalgesia, reflected in the increased responsivity to nociceptive stimulus following exposure of a stressor (Illich, King, & Grau, 1995;Jørum, 1988;Vidal & Jacob, 1982, 1986Viken et al, 1982), but rather prevents the increase of the jumping threshold, which should increase with age under natural rearing conditions.…”

Effects of contextual cues previously paired with footshock or illness on behavior and pain sensitivity in the rat

“…Although the results from the hotplate and formalin tests (Experiments 2 and 3) are consistent with the PDR model, the results from the tailflick test (Experiment 1B) are not. It could be argued that decreased tailflick latencies are not indicative of increased pain sensitivity (see, e.g., Illich, King, & Grau, 1995;King, Joynes, Meagher, & Grau, 1996;but see McNally, 1999), and therefore are not relevant to the PDR model. Further experiments are required to address this issue and to determine whether exposure to the LiCl-associated context provokes additional behavioral and autonomic changes consistent with conditioned arousal of a fear or defensive motivational system.…”

The impact of morphine after a spinal cord injury

“…Separate groups received nothing (0 s) or 30 min of uncontrollable, intermittent tailshock. The shocks were 1.5 mA, 0.08 s in duration, and occurred on a variable time schedule (range 0.2 to 3.8 s) with a mean interstimulus interval of 2.0 s. (Shock at an intensity of 1.5 mA [AC, constant current] is known to engage antinociceptive mechanisms within the spinal cord [18,19], vigorous defensive behavior in intact rats, and pain in humans [see 8,9].) An experimenter blind to the subject's drug treatment recorded whether the shocked rats vocalized during the first minute of stimulation.…”

“…Intermittent tailshock elicits a variety of behaviors in intact rats indicative of pain, including vocalization, struggling, escape behaviors, and conditioned freezing [8,9]. A moderate contusion injury greatly reduces these behaviors but does not eliminate shock-elicited movement or vocalization.…”