Search

Injection of 0.5 microliter L-sodium glutamate (60 mM) into the periaqueductal gray matter of the rat resulted in a short-lived analgesia as assessed by the tail-flick method. Naloxone (1 mg/kg) attenuated glutamate-induced analgesia when injected 30 min but not 5 min before testing. Paradoxically, a higher dose of naloxone (10 mg/kg) significantly potentiated glutamate analgesia when injected 5 min but not 30 min before testing. Moreover, this higher dose also potentiated analgesia when injected 5 min prior to 12 mM glutamate, a dose of glutamate previously found to be ineffective in causing analgesia. Microinjections of either 60 mM or 1 M KCl failed to elicit analgesia, indicating the specificity of the glutamate effect. Taken together with several other lines of evidence, the present findings suggest that glutamate-induced analgesia may be mediated by processes quite different from those underlying morphine analgesia. It is further suggested that a dose-related naloxone antagonism is not a necessary criterion for assessing endogenous opioid activity.

The activity of lumbar spinal dorsal horn lamina I neurons with afferent drive from the sciatic nerve was studied in intact cats and in cats with acute sciatic nerve transection or chronic sciatic nerve transection with neuroma formation. The majority (51 of 75) of neurons recorded in lamina I ipsilateral to a neuroma had no receptive field and could only be identified by their responses to electrical stimulation of the sciatic nerve. The remainder could be activated by the sciatic nerve, but their responses to mechanical stimulation were irregular in comparison to the stable responses of cells recorded in control animals and to the responses of cells contralateral to chronic nerve lesions. Animals with acute nerve transections demonstrated a loss of sciatic nerve-innervated cells with receptive fields except for those cells located on the lateral edge of the dorsal horn, which had normal, proximal receptive fields and response characteristics. In addition, the characteristic somatotopy of lamina I cells was not observed in some cats with chronic neuromata. The mediolateral distribution of cell types indicated that some cells had altered receptive fields following chronic nerve transection. The data presented for lamina I neurons agrees with the observation of spinal cord plasticity first presented for cat dorsal horn cells. Since there is no evidence for a redistribution of intact afferent fibers following chronic nerve transection in adult mammals, the mechanism of altered somatotopy may involve alterations in synaptic efficacy at existing synapses.

The peptidergic content of rat spinothalamic tract neurons was investigated by combining the retrograde transport of the fluorescent dye Fluoro-gold with immunocytochemistry for enkephalin, dynorphin or vasoactive intestinal polypeptide. Evidence is presented for the existence of enkephalin and dynorphin in a subpopulation of spinothalamic neurons terminating in the medial thalamus and vasoactive intestinal polypeptide in a subpopulation terminating primarily in the lateral thalamus.

The distribution of gamma-aminobutyric acid (GABA) neurons was examined in the retroinsular cortex (Ri) and area 7b of the monkey. GABA-immunoreactive somata and puncta were observed in all layers of Ri and area 7b. The densest concentration of these neurons was located in layers I and II. The vast majority (98.9%) of GABA-immunoreactive somata were less than 15 microns in major diameter. These data demonstrate that high concentrations of GABAergic neurons are located in those cortical layers that have been shown to receive afferent projections from corticocortical fibers.

Neurons adjacent to the central canal in the rat spinal cord were retrogradely labeled bilaterally after injection of horseradish peroxidase into the bulbar reticular formation. Lesions restricted to parts of the ventral lateral funiculus in thoracic or high lumbar segments on the side ipsilateral to the injections produced significant bilateral reductions in labeling. Lesions that included the entire ipsilateral ventral lateral funiculus greatly reduced the number of labeled neurons surrounding the central canal caudal to the lesion. Lesions of either the dorsal lateral funiculus, or midline lesions encompassing both the dorsal and ventral columns had no significant effect on labeling. Spinoreticular tract neurons on both sides of the central canal issue axons that ascend in the ventral lateral funiculus of the side ipsilateral to their termination.

The synaptic relationship between spinal cord central gray projection neurons and immunocytochemically identified afferents in the rat were examined at the light microscopic level using the combined techniques of retrogradely transported True blue and serotonin (5-HT), enkephalin (ENK), and substance P (SP) immunocytochemistry. At L4-L6, numerous retrogradely labeled neurons could be identified around the central canal after large bulbar injections of True blue. Of these projection neurons, 75% were apposted by 5-HT varicosities, 57% by ENK varicosities and 58% by SP varicosities. Hemisection of the spinal cord produced a marked reduction in the amount of 5-HT immunoreactivity and the number of putative 5-HT contacts observed on neurons of the spinal cord central gray. A small decrease in SP immunoreactivity and putative contacts was seen after dorsal rhizotomy. Neither rhizotomy nor hemisection produced discernable changes in ENK immunofluorescence. Based on the distributions of 5-HT, ENK and SP in the spinal cord, we suggest that a more precise delineation of lamina X in the rat can be made according to immunocytochemical rather than strictly morphological criteria.