4.6 Article

Output Properties and Organization of the Forelimb Representation of Motor Areas on the Lateral Aspect of the Hemisphere in Rhesus Macaques

期刊

CEREBRAL CORTEX
卷 20, 期 1, 页码 169-186

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhp084

关键词

corticospinal neurons; EMG; forelimb; frontal lobe; motor control; premotor areas; primate

资金

  1. National Institute of Health [NS39023, NS051825]
  2. National Institute of Health Center [HD02528]
  3. Les Fonds de la Recherche en Sante du Quebec [FRSQ6389]
  4. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P30HD002528] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS051825, R01NS039023] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Motor output capabilities of the forelimb representation of dorsal motor area (PMd) and ventral motor area (PMv) were compared with primary motor cortex (M1) in terms of latency, strength, sign, and distribution of effects. Stimulus-triggered averages (60 mu A) of electromyographic activity collected from 24 forelimb muscles were computed at 314 tracks in 2 monkeys trained to perform a reach-to-grasp task. The onset latency and magnitude of facilitation effects from PMd and PMv were significantly longer and 7- to 9-fold weaker than those from M1. Proximal muscles were predominantly represented in PMd and PMv. A joint-dependent flexor or extensor preference was also present. Distal and proximal muscle representations were intermingled in PMd and PMv. A gradual increase in latency and decrease in magnitude of effects were observed in moving from M1 surface sites toward more anterior sites in PMd. For many muscles, segregated areas producing suppression effects were found along the medial portion of PMd and adjacent M1. Although some facilitation effects from PMd and PMv had onset latencies as short as those from M1 in the same muscle, suggesting equal direct linkage, the vast majority had properties consistent with a more indirect linkage to motoneurons either through corticocortical connections with M1 and/or interneuronal linkages in the spinal cord.

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