Eleven of 40 decerebrated cats were found to exhibit periods of sponta
neous or sensory induced myoclonus and locomotion beginning 24 h after
decerebration. Histological analysis showed that the cats generating
myoclonus had hemorrhagic lesions in the retrorubral nucleus (RRN) and
ventral mesopontine junction (vMPJ). However, animals with intact RRN
and vMPJ never showed myoclonus. To verify that the lesions were resp
onsible for myoclonus, 6 additional cats received N-methyl-D-aspartate
(NMDA, 0.5 M/0.5 mu l) injections in the areas of RRN and vMPJ to pro
duce bilateral lesions. Coordinated rhythmic leg movement (locomotion)
or myoclonic twitches developed in all of these cats beginning 3 hour
s after NMDA injection. These NMDA lesion-induced movements appeared e
ither 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, myoclon
ic 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.