Opiate modulation of the active and inactive components of the postshock reaction: parallels between naloxone pretreatment and shock intensity.
Electric footshock elicited an immediate burst of activity followed by a period of immobility termed freezing. Naloxone, an opiate antagonist, enhanced both of these postshock reactions (Experiment 1). Naloxone's effects on the active and inactive components of the postshock reaction paralleled those of increasing shock intensity (Experiment 2). This finding suggests that the drug caused these results by enhancing the perceived intensity of shock. The facilitatory effects of naloxone on the active and inactive reactions to shock appear to be specific to nociceptive stimuli, as naloxone decreased the activity burst elicited by a nonnociceptive startling stimulus and had no effect on the freezing that followed that nonnociceptive stimulus (Experiment 3). Naloxone could accomplish its alteration of perceived intensity by antagonizing endogenous opioid analgesic systems. However, as hypophysectomy did not block the drug's action, the effects are not mediated by pituitary opioids (Experiment 4).
D000818:Animals; D004597:Electroshock; D004723:Endorphins / Q000502:physiology*; D005260:Female; D007016:Hypophysectomy; D009043:Motor Activity / Q000502:physiology*; D009270:Naloxone; D010146:Pain / Q000503:physiopathology*; D010902:Pituitary Gland / Q000502:physiology*; D051381:Rats; D013216:Reflex, Startle / Q000502:physiology; D013045:Species Specificity
D004723:Endorphins; D009270:Naloxone