ACTIVITY DEPENDENT REFINEMENT OF INHIBITORY NETWORKS IN BARREL CORTEX

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这一建议的目的是了解大脑发育抑制回路能够适应感觉输入的机制，并维持它们与发育中的兴奋回路的平衡。在大脑发育的早期，大脑皮层中的神经元建立连接，然后通过经验依赖的机制进行微调。虽然关于谷氨酸能神经网络形成的谷氨酸能神经突触的成熟和活性依赖性修饰的过程已知很多，但新皮质GABA能突触的出生后发育及其在活性依赖性修饰中的作用仍不清楚。这项拟议的研究将利用电生理记录和显微分析相结合的方法，研究抑制性突触和神经元间网络特性的发育变化如何转化为成熟的、功能正常的皮质系统。这项研究将为皮质发育和经验依赖性可塑性的机制提供新的信息。它将帮助我们进一步深入了解几种与发育相关的神经疾病的机制，如皮质发育不良、精神分裂症、癫痫和阅读障碍，在这些疾病中，早期的内源性和外源性不利条件会对成熟的皮质造成长期的影响。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The aim of this proposal is to understand the mechanisms by which developing inhibitory brain circuits are able to adapt to sensory inputs, and to maintain their balance with the developing excitatory circuits. During early brain development, neurons in the cerebral cortex establish connections that are then fine tuned by experience-dependent mechanisms. Although much is now known regarding processes of glutamatergic maturation and activity-dependent modification of glutamatergic synapses for network formation, postnatal development of neocortical GABAergic synapses and their role in activity-dependent modification remains unclear. The proposed research will utilize a combination of electrophysiologic recording and microscopic analyses to examine how developmental changes of inhibitory synapses and interneuron network properties are translated into a mature, functional cortical system. This research will provide new information about mechanisms of cortical development and experience-dependant plasticity. It will help us gain further insights into mechanisms underlying several developmental related neurological disorders such as cortical dysplasia, schizophrenia, epilepsy and dyslexia, in which early endogenous and exogenous unfavorable conditions create long-lasting impacts on the mature cortex.