SHORT TERM SYNAPTIC PLASTICITY OF CORTICAL INTERNEURONS

皮质中间神经元的短期突触可塑性

• 批准号: 6447377
• 负责人: KATRINA M MACLEOD
• 金额: $ 2.96万
• 依托单位: UNIV OF MARYLAND, COLLEGE PARK
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-12-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6447377
• 关键词: anticholinergic agent; cerebral cortex; cholinergic agents; cholinergic receptors; gamma aminobutyrate; glutamate receptor; interneurons; laboratory rat; neural inhibition; neural plasticity; neuropharmacology; norepinephrine; serotonin; synapses; voltage /patch clamp

Short-term synaptic plasticity has a profound effect on the function of the neural circuit in which it is embedded. Previous work in the Nelson lab has characterized the short-term plasticity in the rat visual cortex using a quantitative (parametric) method, using trains of evoked stimuli delivered over a range of physiological frequencies. extend results previously obtained for pyramidal cells to a characterization of the short-term plasticity of inhibitory inputs to inhibitory interneurons by making whole-cell voltage-clamp recordings of nonpyramidal neurons in layers 2/3 in slices of rat neocortex. These inhibitory interneurons will be characterized and identified physiologically and morphologically. Our goals are: 1) Characterize the interneuron-interneuron synaptic plasticity of evoked IPSCs by extracellular or intracellular presynaptic stimulation; 2) Determine if the synaptic plasticity is differentially expressed depending on the interneuron subtype of the presynaptic or postsynaptic neuron; and 3) Investigate whether the interneuron-interneuron synaptic plasticity can be modified by neuro-modulatory agents such as acetylcholine. By investigating the cholinergic modulation of cortical synaptic plasticity, these results may have implications for behavioral and cognitive brain function, and the neurological disorders, such as Alzheimer's disease, which may be related cholinergic dysfunction.

短期突触可塑性对嵌入其神经回路的功能具有深远的影响。 尼尔森实验室（Nelson Lab）的先前工作已经使用定量（参数）方法来表征大鼠视觉皮层中的短期可塑性，该方法使用了在一系列生理频率上传递的诱发刺激的列车。扩展了先前在锥体细胞中获得的结果，以表征抑制性输入对抑制性中间神经元的短期可塑性，通过在2/3中在大鼠新皮层的切片中2/3中的非锥体神经元记录全细胞电压钳记录。这些抑制性中间神经元将在生理和形态上进行表征和鉴定。 我们的目标是：1）表征通过细胞外或细胞内突触前刺激引起的IPSC的神经元间interneuron突触可塑性； 2）确定突触可塑性是否取决于突触前或突触后神经元的间神经元亚型； 3）研究是否可以通过神经调节剂（如乙酰胆碱）来修饰神经元间神经元的突触可塑性。 通过研究皮质突触可塑性的胆碱能调节，这些结果可能对行为和认知脑功能有影响，以及神经系统疾病，例如阿尔茨海默氏病，这可能是相关的胆碱能功能障碍。