Abstract

The ability of central morphine administration to disrupt established maternal responsiveness in rats was examined. Studies focused on the direct administration of morphine sulfate (M) to the preoptic area (POA), a region known to be involved in the expression of maternal behavior in this species. In the first experiment, crystalline M was administered via bilateral 28 g cannulae to the POA or ventromedial hypothalamus (VMH) of 31 ovariectomized, estrogen-primed, nulliparous, pup-induced, maternal females. All subjects were tested twice for maternal responsiveness; once after M-filled cannulae and once after blank inserts were lowered into place. Behavioral tests lasted for 1 h after foster young were introduced into the test cage, and retrieval, grouping and crouching responses were recorded. Thirteen of 14 females with cannulae placements in the POA showed disruption of maternal responsiveness following morphine treatment. In contrast, only 4 of 17 females with VMH implants showed some deficit in maternal behavior following opiate administration. Results of a second experiment established that M-filled implants placed in the POA of lactating females were capable of disrupting the responsiveness of nursing females toward their own young. Finally, the specificity of morphine's central effects were examined in a third experiment in which lactating females received bilateral POA infusions of morphine (0.5 μg, n= 7), dextrorphan (an inactive stereoisomer of an active opioid compound; 1.0 μg, n= 7) or saline alone (n= 6). Whereas maternal behavior was disrupted in all morphine-treated subjects, infusions of dextrorphan or saline had no effect. Furthermore, the disruptive effects of morphine were negated when subjects received bilateral infusions of a solution that contained morphine plus a 10-fold excess of the opiate antagonist naloxone (n= 6) suggesting that the disruption of maternal responsiveness by direct application of morphine to the POA may involve a receptor-mediated mechanism.

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