Hammond D L, Proudfit H K
Brain Res. 1980 Apr 21;188(1):79-91. doi: 10.1016/0006-8993(80)90558-2.
These studies were designed to examine the role of the norepinephrine-containing cells comprising the nucleus locus coeruleus (LC) in the mediation of pain perception and morphine-induced antinociception. Nociceptive threshold and morphine-induced analgesia were measured following monosodium-L-glutamate lesions of the LC and adjacent tegmentum (nucleus parabrachialis ventralis; PBV) at 17, 24 and 31 days after surgery. Nociceptive thresholds assessed by the tail flick and hot plate assays were not altered following lesions which included both the LC and PBV (Group 1) or by lesions of the PBV (Group 2) alone. Examination of lesion-induced effects on the capacity of morphine to induce analgesia revealed that damage which included both LC and PBV as well as that confined primarily to the PBV resulted in attenuation of analgesia induced by morphine. Those lesions which involved the LC altered norepinephrine content in the cortex, spinal cord and medial brain stem; however, no correlation could be demonstrated between the attenuation of morphine-induced analgesia and the changes in norepinephrine content of the brain regions examined. Thus, destruction of the LC does not appear to be responsible for the decreased effectiveness of morphine. The only region consistently damaged in both groups 1 and 2 was the ventral parabrachial nucleus. Therefore, we tentatively conclude that destruction of the PBV was responsible for the observed attenuation of morphine analgesia.
