Brainstem-mediated locomotion and myoclonic jerks. I. Neural substrates.
|Title||Brainstem-mediated locomotion and myoclonic jerks. I. Neural substrates.|
|Publication Type||Journal Article|
|Year of Publication||1997|
|Authors||Lai YY, Siegel JM|
|Date Published||1997 Jan 16|
|Keywords||Animals, 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 Journal||Brain Res|
|Grant List||HL41370 / HL / NHLBI NIH HHS / United States|