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389 perineal probing ("distraction" control). The panel-press latency was signifi- cantly shorter in the CP group than in the perineal group. Latency in a con- trol group, in which shock was terminated as soon as the rats pressed the panel, did not differ significantly from the CP group. Latency in another control group, in which the shock persisted for 7 sec after the rots pressed the panel with no probing being applied was not significantly different from that of the perineal probing group but was significantly longer than latency in the CP group. Thus the present studies suggest that CP is indeed analgesic and that this effect of CP is mediated by neither movement inhibition nor distraction. Naloxone and shock~licited freezing in the rat.- M.S. Fanselow and R.C. Bolles, J. comp. physiol. Psychol., 93 (1979) 736--744. The freezing behavior of the rat that occurs following painful electric shock was found to increase when the animal was pretreated with the opiate antagonist naloxone. Freezing was a positive linear function of drug dose and shock intensity (experiment 2). Naloxone pretreatment enhanced freezing only when the animal was given two or three shocks but did not affect freez- ing when the animal was given only one shock or not shocked at all (experi- ments 3, 4, 5). Naloxone must be present during shock, not just during the observation period, in order to increase freezing (experiment 6). These results suggest that when an animal is shocked, it releases endogenous analge- sics (endorphins) that make a subsequent shock less aversive. Naloxone, by blocking the endorphin system, makes the shock more aversive than it would normally be. Naloxone attenuates rat's preference for signaled shock.- M.S. Fanselow, Physiol. Psychol., 7 (1979)70--74. Rats were confined and given signaled shock on one side of a shuttlebox and unsignaled shock on the other side. Preferehce tests revealed that rats injected with the opiate antagonist nalexone during training showed ,1o sub- sequent side preference, whereas saline control rats preferred the signaled side. The second and third experiments showed that this naloxone effect could not be due to state-dependent learning (generalization decrement), interference with exploratory activity, or the drug making the signal aversive. The results suggest that release of endogenous analge:~ic substances may con- stitute a central nervous system preparatory response which mediates a pref- erence for signaled shock. Opioid and nonopioid mechanisms of stress analgesia.- J.W. Lewis, J.T. Cannon and J.C. Liebeskind, Science, 208 (1980) 623--625. Inescapable foot shock caused profound analgesia in rats that was antago- nized by naloxone or dexamethasone when shock was delivered il~ter- mittently for 30 min, but not when it was delivered continuously for 3 rain. Thus, de.pending only on its temporal characteristics, foot-shock stress appears to activate opioid or non-opioid analgesia mechanisms. Certain forms of stress may act as natural inputs to an endogenous opiate analgesia system.

Opioid and nonopioid mechanisms of stress analgesia

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perineal probing ("distraction" control). The panel-press latency was signifi- cantly shorter in the CP group than in the perineal group. Latency in a con- trol group, in which shock was terminated as soon as the rats pressed the panel, did not differ significantly from the CP group. Latency in another control group, in which the shock persisted for 7 sec after the rots pressed the panel with no probing being applied was not significantly different from that of the perineal probing group but was significantly longer than latency in the CP group. Thus the present studies suggest that CP is indeed analgesic and that this effect of CP is mediated by neither movement inhibition nor distraction.

Naloxone and shock~licited freezing in the r a t . - M.S. Fanselow and R.C. Bolles, J. comp. physiol. Psychol., 93 (1979) 736--744.

The freezing behavior of the rat that occurs following painful electric shock was found to increase when the animal was pretreated with the opiate antagonist naloxone. Freezing was a positive linear function of drug dose and shock intensity (experiment 2). Naloxone pretreatment enhanced freezing only when the animal was given two or three shocks but did not affect freez- ing when the animal was given only one shock or not shocked at all (experi- ments 3, 4, 5). Naloxone must be present during shock, not just during the observation period, in order to increase freezing (experiment 6). These results suggest that when an animal is shocked, it releases endogenous analge- sics (endorphins) that make a subsequent shock less aversive. Naloxone, by blocking the endorphin system, makes the shock more aversive than it would normally be.

Naloxone attenuates rat's preference for signaled s h o c k . - M.S. Fanselow, Physiol. Psychol., 7 (1979)70--74.

Rats were confined and given signaled shock on one side of a shuttlebox and unsignaled shock on the other side. Preferehce tests revealed that rats injected with the opiate antagonist nalexone during training showed ,1o sub- sequent side preference, whereas saline control rats preferred the signaled side. The second and third experiments showed that this naloxone effect could not be due to state-dependent learning (generalization decrement), interference with exploratory activity, or the drug making the signal aversive. The results suggest that release of endogenous analge:~ic substances may con- stitute a central nervous system preparatory response which mediates a pref- erence for signaled shock.

Opioid and nonopioid mechanisms of stress analgesia.- J.W. Lewis, J.T. Cannon and J.C. Liebeskind, Science, 208 (1980) 623--625.

Inescapable foot shock caused profound analgesia in rats that was antago- nized by naloxone or dexamethasone when shock was delivered il~ter- mittently for 30 min, but not when it was delivered continuously for 3 rain. Thus, de.pending only on its temporal characteristics, foot-shock stress appears to activate opioid or non-opioid analgesia mechanisms. Certain forms of stress may act as natural inputs to an endogenous opiate analgesia system.