Long-Term Gliosis and Molecular Changes in the Cervical Spinal Cord of the Rhesus Monkey after Traumatic Brain Injury

This study investigates the long-term effects of traumatic brain injury (TBI) on the spinal cord of rhesus monkeys, focusing on changes in glial cells and molecules that might contribute to recovery of motor skills. The researchers lesioned part of the motor cortex in monkeys, which initially impaired their hand function. However, the animals eventually regained some of their motor skills, allowing the researchers to study the underlying cellular and molecular changes during this recovery process. The study found that after TBI, there were long-term increases in specific molecules (MHC-II and ERK1/2) and proteins (GAP-43, Nogo receptor, and glutamate transporters) in the cervical spinal cord. These changes suggest that microglia, a type of immune cell in the brain and spinal cord, play a role in helping the nervous system recover after TBI by supporting the survival of neurons, promoting axonal growth, and regulating glutamate levels.

• 1
  There were significant increases in MHC-II and ERK1/2 immunoreactivity in the lateral corticospinal tract (LCST) of the cervical spinal cord up to 12 months post-lesion, indicating long-term microglial activation.
• 2
  Phosphorylated ERK1/2 colocalized within MHC-II positive microglia, suggesting a trophic role for these activated microglia in the long-term recovery process.
• 3
  Increased immunoreactivity to GAP-43 was observed in the LCST and spinal gray matter of the lesioned animals, indicating active sprouting of axons.