Previous studies in our laboratory have indicated that anesthetic block of neural activity at discrete sites within the limbic system, including the lateral hypothalamus and anterior cingulum bundle, causes a significant long-lasting analgesia during the formalin test. In this experiment, the local anesthetic lidocaine was microinjected into the dentate region of the hippocampus, an important limbic structure presumed to subserve the affective-motivational aspects of pain. The dentate gyrus is strategically situated at a point of convergence of widespread polysensory cortical input to the hippocampus, to allow modulation of cortical signals before they diverge into numerous limbic circuits. The results indicate that anesthetic block of the anterior region of the dentate gyrus produces analgesia in the rat during the formalin test. The analgesia produced by this procedure became apparent 30 minutes after regional block contralateral to the site of injury and persisted for the duration of the test period. These data provide further evidence that limbic forebrain structures are involved in pain and analgesia.

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This series of experiments examined the neural mechanisms of analgesia caused by local anaesthetic blockade or selective blockade of N-methyl- scD-aspartate (NMDA) receptors at sites in the rat forebrain. Microinjections of the local anaesthetic lidocaine were made into the medial or lateral thalamic nuclei. The results indicate that the medial thalamic nuclei mediate the expression of pain behavior after peripheral injury, whereas the lateral thalamic nuclei influence phasic withdrawal responses, but are not critical for injury-induced pain responses. Electrolytic lesions made in the lateral thalamus verified this latter finding. Intracranial microinjections of the NMDA antagonist AP5 were used to determine if NMDA receptors in the forebrain participate in pain-related central processing. The intralaminar thalamic nuclei, the striatum and the dentate gyrus of the hippocampal formation were indicated as forebrain sites where antagonism of NMDA-sensitive neural mechanisms significantly reduced the expression of pain-related behavior in the formalin test.