Department of Physiology and Neuroscience, New York University, School of Medicine, New York, NY, USA.
Prog Brain Res. 2012;197:153-68. doi: 10.1016/B978-0-444-54299-1.00008-X.
Intellectual disability (ID) affects 1-3% of the general population and is defined by an intelligence quotient score under 70 and the presence of two or more adaptive behaviors. Learning and memory involves the change in the transmission efficacy at the synapse (synaptic plasticity). Synaptic plasticity is the ability of the connection, or synapse, between two functional neurons to change in strength. Many molecular mechanisms are involved in the change in synaptic strength, which can result in changes in spine morphology. Spines are specialized dendritic protrusions and their change in morphology is implicated in learning and memory. In several cases of ID, the link between spine abnormalities (abnormal in number, size, and shape) and ID is well described, including nonsyndromic ID and Down, Fragile X, and Rett syndromes. This chapter discusses the underlying molecular mechanisms of this altered spine phenotype.
智力障碍(ID)影响一般人群的 1-3%,其定义为智商得分低于 70,以及存在两个或更多适应性行为。学习和记忆涉及突触(突触可塑性)传递效能的变化。突触可塑性是两个功能神经元之间连接或突触强度变化的能力。许多分子机制参与了突触强度的变化,这可能导致棘突形态的变化。棘突是专门的树突突起,其形态的变化与学习和记忆有关。在几种智力障碍病例中,棘突异常(数量、大小和形状异常)与智力障碍之间的联系得到了很好的描述,包括非综合征性智力障碍和唐氏综合征、脆性 X 综合征和雷特综合征。本章讨论了这种改变的棘突表型的潜在分子机制。