Johnston Michael V
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.
Dev Disabil Res Rev. 2009;15(2):94-101. doi: 10.1002/ddrr.64.
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.
神经元可塑性使中枢神经系统能够学习技能、记忆信息,响应环境刺激重组神经网络,并从脑和脊髓损伤中恢复。神经元可塑性在发育中的大脑中增强,通常具有适应性且有益,但在某些情况下也可能具有适应不良性并导致神经障碍。可塑性所涉及的基本机制包括神经发生、程序性细胞死亡和活动依赖性突触可塑性。对突触的重复刺激可导致神经传递的长期增强或长期抑制。这些变化与树突棘和神经回路的物理变化有关。儿童出生后发育过程中突触的过度产生通过提供在青春期早期被修剪的过量突触,有助于增强可塑性。适应性神经元可塑性的临床实例包括,响应练习弹奏弦乐器对手指皮层图谱进行重组,以及采用强制性运动疗法改善中风或脑瘫所致的偏瘫。这些可塑性形式与大脑的结构和功能变化相关,可通过磁共振成像、正电子发射断层扫描或经颅磁刺激(TMS)检测到。TMS和其他形式的脑刺激也正在进行实验性应用,以增强脑可塑性和功能恢复。可塑性还受遗传因素影响,如脑源性神经营养因子的突变。了解脑可塑性为开发更好的疗法以改善后天性脑损伤的预后提供了基础。