RT Journal Article
SR Electronic
T1 Temporal Plasticity Involved in Recovery from Manual Dexterity Deficit after Motor Cortex Lesion in Macaque Monkeys
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 84
OP 95
DO 10.1523/JNEUROSCI.1737-14.2015
VO 35
IS 1
A1 Murata, Yumi
A1 Higo, Noriyuki
A1 Hayashi, Takuya
A1 Nishimura, Yukio
A1 Sugiyama, Yoko
A1 Oishi, Takao
A1 Tsukada, Hideo
A1 Isa, Tadashi
A1 Onoe, Hirotaka
YR 2015
UL http://www.jneurosci.org/content/35/1/84.abstract
AB The question of how intensive motor training restores motor function after brain damage or stroke remains unresolved. Here we show that the ipsilesional ventral premotor cortex (PMv) and perilesional primary motor cortex (M1) of rhesus macaque monkeys are involved in the recovery of manual dexterity after a lesion of M1. A focal lesion of the hand digit area in M1 was made by means of ibotenic acid injection. This lesion initially caused flaccid paralysis in the contralateral hand but was followed by functional recovery of hand movements, including precision grip, during the course of daily postlesion motor training. Brain imaging of regional cerebral blood flow by means of H215O-positron emission tomography revealed enhanced activity of the PMv during the early postrecovery period and increased functional connectivity within M1 during the late postrecovery period. The causal role of these areas in motor recovery was confirmed by means of pharmacological inactivation by muscimol during the different recovery periods. These findings indicate that, in both the remaining primary motor and premotor cortical areas, time-dependent plastic changes in neural activity and connectivity are involved in functional recovery from the motor deficit caused by the M1 lesion. Therefore, it is likely that the PMv, an area distant from the core of the lesion, plays an important role during the early postrecovery period, whereas the perilesional M1 contributes to functional recovery especially during the late postrecovery period.