Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.
Inescapably shocked rats perform poorly on a two-way shuttle box escape task 24 hr after the shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hr after inescapable shock, they are likely to be analgesic during the shuttle box escape task. Subjects receiving an equivalent amount of escapable shock display neither the escape dificit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia ("long-term analgesia") may cause the inescapable-shock-produced escape deficit. However, the present experiments demonstrated that two pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of inescapable shock but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by inescapable shock does not cause the deficit in shuttle box escape performance displayed by inescapably shocked rats. Furthermore, these results indicate that the pituitary is not essential in the production of this escape deficit.
D000698:Analgesia; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D004597:Electroshock / Q000009:adverse effects; D004723:Endorphins / Q000502:physiology; D004924:Escape Reaction / Q000187:drug effects / Q000502:physiology*; D007016:Hypophysectomy; D008297:Male; D010902:Pituitary Gland / Q000503:physiopathology; D051381:Rats; D013312:Stress, Physiological / Q000503:physiopathology
D004723:Endorphins; D003907:Dexamethasone