Plasticity-associated molecular and structural events in the injured brain.
Injury to the brain appears to create a fertile ground for functional and structural plasticity that is, at least partly, responsible for functional recovery. Increases in dendritic arborization, spine density, and synaptogenesis in both peri-injury and intact cortical areas are the potential morphological strategies that enable the brain to reorganize its neuronal circuits. These injury-initiated alterations are time-dependent and frequently proceed in interaction with behavior-related signals. A complex concert of a variety of genes/proteins is required to tightly control these changes. Two broad categories of molecules appear to be involved. First, regulatory molecules or effector molecules with regulatory function, such as immediate early genes/transcription factors, kinase network proteins, growth factors, and neurotransmitter receptors, and second, structural proteins, such as adhesion molecules and compounds of synapses, growth cones, and cytoskeleton. A better understanding of the processes contributing to postinjury plasticity may be an advantage for developing new and more effective therapeutic approaches. This knowledge might also shed light on other forms of brain plasticity, such as those involved in learning processes or ontogeny.
Keyvani
Kathy
K
Institute of Neuropathology, University of Muenster, Germany.
Schallert
Timothy
T
D000818:Animals; D001921:Brain / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology*; D006801:Humans; D009414:Nerve Growth Factors / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000502:physiology*; D009473:Neuronal Plasticity
D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins