Behavioural Brain Research 100 (1999) 33-42
Research report

Shock-induced hyperalgesia: Evidence forebrain systems play an essential role

Tamara E. King, Eric D. Crown, Amy N. Sieve, Robin L. Joynes, James W. Grau,
Mary W. Meagher * Department of Psychology, Texas A&M University, College Station, TX 77843, USA
Received 6 April 1998; received in revised form 9 July 1998; accepted 9 July 1998

Abstract

Exposure to a few moderately intense (1-mA) tailshocks has opposite effects on two measures of pain reactivity in rats. Tail-withdrawal to radiant heat is inhibited (antinociception) while vocalization thresholds are lowered (hyperalgesia) to both heat and shock (King et al., 1996). Prior work indicates that this hyperalgesia represents an unconditioned response and that it enhances the acquisition of both conditioned freezing and an avoidance response to thermal pain. The present experiments begin to explore the neural mechanisms that underlie hyperalgesia. Experiments 1 and 2 demonstrated that hyperalgesia is eliminated by both decerebration and pentobarbital anesthesia. Lesions limited to the frontal pole had a similar effect (Experiment 3). Experiment 4 showed that lesioning the frontal pole also disrupted the acquisition of conditioned fear.

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