Brainstem-mediated locomotion and myoclonic jerks. I. Neural substrates.

TitleBrainstem-mediated locomotion and myoclonic jerks. I. Neural substrates.
Publication TypeJournal Article
Year of Publication1997
AuthorsLai YY, Siegel JM
JournalBrain Res
Date Published1997 Jan 16
KeywordsAnimals, Brain Stem, Cats, Cerebral Hemorrhage, Decerebrate State, Electric Stimulation, Female, Locomotion, Male, Myoclonus, Neurons, Physical Stimulation, Sleep, REM

Eleven of 40 decerebrated cats were found to exhibit periods of spontaneous or sensory myoclonus and locomotion beginning 24 h after decerebration. Histological analysis showed that the cats generating myoclonus hemorrhagic lesions in the retrorubral nucleus (RRN) and ventral mesopontine junction (vMPJ). However, with intact RRN and vMPJ never showed myoclonus. To verify that the lesions were responsible for myoclonus, 6 additional cats received N-methyl-D-aspartate (NMDA, 0.5 M/0.5 microliter) injections in the areas of RRN and vMPJ to produce bilateral lesions. Coordinated rhythmic leg movement (locomotion) or myoclonic twitches developed in all of these cats beginning 3 hours after NMDA injection. These NMDA lesion-induced movements appeared either spontaneously (5 out of 6 cats) or after sensory stimulation (1 cat). Four cats received saline control injections in the RRN and vMPJ and did not have spontaneous, or sensory stimulation-induced, myoclonic twitches during the 48 h observation period. These results indicate that the RRN and vMPJ have a suppressive effect on myoclonic twitches and rhythmic leg movement. Dysfunction of these regions could release motor activity into sleep and waking states.

Alternate JournalBrain Res
PubMed ID9037417
Grant ListHL41370 / HL / NHLBI NIH HHS / United States