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The effect of morphine microinjection (5 microgram/0.5 microliter) and focal electrical stimulation on the animal's response to radiant heat and noxious pinch was studied concurrently at 117 brain loci extending from the medial thalamus caudally to the periaqueductal gray area (PAG). Three populations of brain sites were discernible based on their responsiveness to focal electrical stimulation and morphine microinjection in the production of antinociception: (a) sites which support stimulation-produced analgesia (SPA, n = 24), (b) sites which were sensitive to the direct application of morphine (n = 8), (c) sites responsive to both manipulations (n = 8). With a few exceptions, all morphine sensitive sites were located within the anatomical boundaries of the PAG while sites supporting SPA were located not only within the PAG but also in the brain regions peripheral to this structure. Sites responsive to both manipulations were generally distributed throughout thf lateral aspect of the posteroventral PAG. Stimulation strength-effect curves for sites subserving SPA were also obtained. No differences were discovered between curves obtained from morphine-sensitive and -insensitive brain loci.

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1. Electrolytic lesions were made in various brain regions of the rat, and the effects of these lesions on nociceptive threshold and the antinociceptive actions of morphine were tested using a shock titration technique. 2. Lesions in the medial thalamus, the periaqueductal grey area, or the caudate nucleus, had no effect on the nociceptive threshold; whereas, lesions in the posterior hypothalamus resulted in a small but statistically significant increase in this threshold. 3. Morphine administered intraperitoneally to rats having histologically verified lesions in the posterior hypothalamus, the caudate nucleus or the periaqueductal grey area resulted in a 15-30% increase in the nociceptive threshold. This increase was similar to that observed in unoperated control rats. On the other hand, injections of morphine into animals having greater than 50% of the medial thalamus destroyed produced a highly significant increase of 95% in the threshold. This potentiation of the antinociceptive action of morphine was not observed in rats having less than 50% destruction of the medial thalamus.

No abstract