Increased expression of the growth-associated protein-43 gene after primary motor cortex lesion in macaque monkeys

Yumi Murata1, Noriyuki Higo2, Takao Oishi3

  • 1Human Informatics Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Umezono, Tsukuba, Ibaraki 305-8568, Japan.

Insights

Axonal remodeling, indicated by growth-associated protein-43 (GAP-43) gene expression, supports functional recovery after primary motor cortex (M1) lesions. This remodeling occurs in specific brain regions and at different times during recovery of manual dexterity.

Area of Science:

  • Neuroscience
  • Motor control research
  • Molecular biology

Background:

  • Functional recovery after primary motor cortex (M1) lesions involves brain activity changes in the ventral premotor cortex (PMv) and perilesional M1.
  • The role of axonal remodeling in these recovery processes remains unclear.

Purpose of the Study:

  • To investigate the association between axonal remodeling and M1 lesion-induced brain activity changes.
  • To determine if gene expression related to axonal growth correlates with functional recovery of manual dexterity.

Main Methods:

  • Gene expression of growth-associated protein-43 (GAP-43) was assessed in motor and premotor cortices of macaque monkeys following M1 lesions.
  • Expression levels were analyzed in relation to the recovery phase of manual dexterity.

Main Results:

  • Increased GAP-43 expression was observed in the ventral premotor cortex (PMv) shortly after functional recovery.
  • Elevated GAP-43 expression was detected in the perilesional primary motor cortex (M1) during the plateau phase of recovery.

Conclusions:

  • Time-dependent and brain region-specific axonal remodeling, evidenced by GAP-43 expression, likely contributes to functional recovery after M1 lesions.
  • These findings highlight the dynamic nature of neural plasticity in motor cortex repair.

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