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Long-term plasticity expressed in layer 2/3 cortical microcircuits

2/3 层皮质微电路表达的长期可塑性

基本信息

批准号：
8940344
负责人：
Hyungbae Kwon
金额：
$ 47.75万
依托单位：
MAX PLANCK FLORIDA CORPORATION
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-05-18 至 2020-02-29
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8940344
关键词：
Action Potentials Address Animals Area Autistic Disorder Brain Brain Diseases Brain Injuries Cells Characteristics Code Complex Cortical Column Development Disease Disinhibition Electrophysiology (science)Elements Epilepsy Foundations Functional disorder Glutamates Goals Image Individual Laboratories Lead Learning Mediating Mental disorders Methods Modification Molecular Monitor Neurons Optics Pathogenesis Pattern Population Process Resolution Rodent Schizophrenia Sensory Somatosensory Cortex Structure Study models Symptoms Synapses Techniques Testing Time Training Transgenic Animals Vertebral column Vibrissae Work awake barrel cortex base cell type design excitatory neuron hippocampal pyramidal neuron improved functioning in vivo insight nervous system disorder neural circuit neuronal excitability neuropsychiatry novel novel strategies optogenetics photolysis public health relevance relating to nervous system restoration sensory cortex spatiotemporal two-photon

项目摘要

DESCRIPTION (provided by applicant): Normal brain function requires proper neuronal connections. Layer 2/3 cortical pyramidal neurons in a mammalian brain have similar morphological and functional characteristics, but they tend to form functionally distinct microcircuits by making specialized connections. The cellular and molecular mechanisms by which one neuron finds specific target neurons and eventually forms functional subnetworks are not fully understood. A growing body of evidence indicates that the functional microcircuit formation is largely influenced by the activity pattern arising in local circuits. Presumably, the exact timing of action potential firing, the degree of excitability, and the level of inhibition ar important, but how these factors are operated together and are expressed at the level of multiple neurons have not yet been precisely defined. We propose to address these questions by using electrophysiological and optical approaches to visualize and manipulate neuronal activities at individual cell level. In the Aim 1, we seek to determine how spikes generated in multiple neurons within a short time window influence circuit reorganization by varying three factors: spike timing and number, distance between neurons, and the number of neurons. In Aim 2, cellular mechanisms such as neuronal excitability and the involvement of disinhibition will be examined. Lastly, Aim 3 is designed to test whether circuit assembly can be manipulated in awake behaving animals. Completion of the proposed work will provide mechanistic insight during cortical circuit plasticity and would establish experimental evidence for non-random features of neural connectivity in the mammalian brain. Abnormal neuronal connectivity has been implicated in various neuropsychiatric diseases such as schizophrenia, epilepsy, and autism spectrum diseases, and can directly influence the symptoms of other brain disorders or injuries. Thus, understanding cellular mechanisms of activity-dependent redistribution of local circuits could also help inform the development of novel strategies for circuit dysfunction.