Molecular mechanisms of spinal cord plasticity

脊髓可塑性的分子机制

• 批准号: 6552085
• 负责人: JOHN H. BROCK
• 金额: $ 2.85万
• 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/6552085
• 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）：促进中枢神经系统或三七总皂甙损伤的功能恢复需要最大限度地提高神经元存活率，促进轴突生长、髓鞘再生和适当的突触形成。最后一步尤其重要，因为具有不适当目标的新突触的形成可能会产生适应不良的后果。触觉异常性疼痛的特征是对无害的机械刺激过敏，与周围神经病变相关，归因于 A13 纤维（低阈值机械感受器）中央发芽到脊髓浅表背角，在那里它们与伤害性神经元形成功能性突触通常会传递痛苦的刺激。我们感兴趣的是识别分子并阐明使轴突萌芽和异常突触形成的机制。