Abstract

A previous study demonstrated that microinjection of carbachol (CCh) into the dorsal periaqueductal gray matter (dPAG) of rats increases the latency for the tail flick reflex. Several other studies have implicated the raphe magnus (NRM) and the reticularis paragigantocellularis (NRPG) nuclei as relay stations through which descending pathways from the PAG project to the spinal cord via the dorsolateral funiculus (DLF). In the present study, the effects of microinjecting CCh into the dPAG on the tail flick test were examined in rats in which the ipsilateral DLF was previously lesioned, or saline or lidocaine (2%) was microinjected into the NRM or ipsilateral NRPG. The DLF lesion did not change the baseline threshold of the animals in the test, but abolished the CCh-induced increase in the tail flick latency from the dPAG. The neural block of the NRM or NRPG with lidocaine also did not change significantly the latency for the tail flick reflex. The increase in the tail flick latency produced by CCh from the dPAG was not changed by the neural block of the NRPG, but was significantly reduced by the neural block of the NRM. These results are interpreted as indicative that the central antinociceptive mechanisms activated by CCh from the dPAG depend on a descending pathway that projects to the spinal cord via DLF utilizing at least the NRM, but not the NRPG, as an intermediary relay station.

Full Text
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