An analysis of neuronal elements within the median nucleus of the raphe that mediate lesion-induced increases in locomotor activity.

Electrolytic lesions of the median nucleus of the raphe (MR) are known to result in large increases in motor activity. The present studies were concerned with identifying the neuronal elements within or near the MR (e.g. fibers of passage, serotonergic or non-serotonergic cells) which, when destroyed, lead to these increases in ambulation. Groups of rats were given either an electrolytic MR lesion or were injected locally with the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or the excitotoxin ibotenic acid, and their subsequent locomotor activities were compared in the open field and in photocell cages. In a 5 min open field test, rats with either electrolytic or ibotenate lesions of the MR were more active compared to all other groups, although rats in the former group were also more active than those in the latter. In a longer activity test conducted in photocell cages, rats with electrolytic lesions were more active than all other groups during the first 20 min period, after which their activity did not differ from the ibotenate group; however, both of these groups were hyperactive compared to all others. Both electrolytic and ibotenate groups showed exaggerated hyperactivity in response to D-amphetamine. Lesions produced by 5,7-DHT failed to significantly increase either spontaneous or D-amphetamine-induced locomotor activity. When the results from all of the activity measures are considered, it appears that damage to at least two different neuronal populations may be responsible for the hyperactivity observed in MR lesioned rats. However, damage to the serotonergic system does not appear to contribute to these locomotor effects.