Molecular mechanisms of spinal cord plasticity

脊髓可塑性的分子机制

• 批准号: 6616810
• 负责人: JOHN H. BROCK
• 金额: $ 2.95万
• 依托单位: ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6616810
• 关键词: cadherins; laboratory rat; nerve injury; nervous system regeneration; neural plasticity; predoctoral investigator; sciatic nerve; spinal cord; synaptogenesis

DESCRIPTION (provided by applicant): Promoting functional recovery to CNS or PNS injury requires maximizing neuronal survival, facilitating axon growth, remyelination and appropriate synapse formation. This last step is particularly important since formation of new synapses with inappropriate targets could produce maladaptive consequences. Tactile allodynia, characterized by hypersensitivity to innocuous mechanical stimuli, is associated with peripheral neuropathy and has been attributed to the central sprouting of A13 fibers (low threshold mechanoreceptors) into the superficial dorsal horn of the spinal cord, where they form functional synapses with nociceptive neurons that normally relay painful stimuli. We are interested in identifying the molecules and elucidating the mechanisms that enable axon sprouting and aberrant synapse formation.

描述（由申请人提供）：促进CNS或PNS损伤的功能恢复需要最大化神经元存活，促进轴突生长、髓鞘再生和适当的突触形成。这最后一步特别重要，因为与不合适的目标形成新的突触可能会产生适应不良的后果。触觉异常性疼痛，其特征在于对无害的机械刺激的超敏反应，与周围神经病变相关，并且已经归因于A13纤维（低阈值机械感受器）在脊髓的浅表背角中的中枢出芽，在那里它们与通常传递疼痛刺激的伤害感受神经元形成功能性突触。我们的兴趣在于识别分子并阐明轴突发芽和异常突触形成的机制。