Plasticity in the developing brain: implications for rehabilitation.
Neuronal plasticity allows the central nervous system to learn skills and remember information, to reorganize neuronal networks in response to environmental stimulation, and to recover from brain and spinal cord injuries. Neuronal plasticity is enhanced in the developing brain and it is usually adaptive and beneficial but can also be maladaptive and responsible for neurological disorders in some situations. Basic mechanisms that are involved in plasticity include neurogenesis, programmed cell death, and activity-dependent synaptic plasticity. Repetitive stimulation of synapses can cause long-term potentiation or long-term depression of neurotransmission. These changes are associated with physical changes in dendritic spines and neuronal circuits. Overproduction of synapses during postnatal development in children contributes to enhanced plasticity by providing an excess of synapses that are pruned during early adolescence. Clinical examples of adaptive neuronal plasticity include reorganization of cortical maps of the fingers in response to practice playing a stringed instrument and constraint-induced movement therapy to improve hemiparesis caused by stroke or cerebral palsy. These forms of plasticity are associated with structural and functional changes in the brain that can be detected with magnetic resonance imaging, positron emission tomography, or transcranial magnetic stimulation (TMS). TMS and other forms of brain stimulation are also being used experimentally to enhance brain plasticity and recovery of function. Plasticity is also influenced by genetic factors such as mutations in brain-derived neuronal growth factor. Understanding brain plasticity provides a basis for developing better therapies to improve outcome from acquired brain injuries.
Johnston
Michael V
MV
Departments of Neurology, Pediatrics and Physical Medicine and Rehabilitation, Kennedy Krieger Institute and Johns Hopkins University School of Medicine, 707 North Broadway, Baltimore, MD 21205, USA. Johnston@kennedykrieger.org
D000293:Adolescent; D000818:Animals; D001925:Brain Damage, Chronic / Q000503:physiopathology* / Q000534:rehabilitation*; D001930:Brain Injuries / Q000503:physiopathology* / Q000534:rehabilitation*; D019208:Brain-Derived Neurotrophic Factor / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D002658:Developmental Disabilities / Q000503:physiopathology* / Q000534:rehabilitation; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D017774:Long-Term Potentiation / Q000502:physiology; D008279:Magnetic Resonance Imaging; D009415:Nerve Net / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D049268:Positron-Emission Tomography; D011247:Pregnancy; D051381:Rats; D017470:Receptors, Glutamate / Q000502:physiology; D018009:Receptors, Glycine / Q000502:physiology; D013569:Synapses / Q000502:physiology; D050781:Transcranial Magnetic Stimulation
D019208:Brain-Derived Neurotrophic Factor; D017470:Receptors, Glutamate; D018009:Receptors, Glycine