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中文摘要
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这是对SC2分数奖助金家长奖助金的多样性补充 2型糖尿病小鼠星形胶质细胞Kir4.1通道功能:对神经元超兴奋性的影响“。 这项请求的目的是提供补充资金,以支持和加强 培训博士候选人Luis A.Rojas-Colón先生 将允许我们的实验室纳入神经炎症研究,这将大大增加 家长资助和实验室团队。通过他的神经炎博士训练,他将评估 促炎介质是否会影响星形胶质细胞缓冲钾离子的能力 在海马体中,如果这些促炎介质影响神经元癫痫样活动。 让Luis A.Rojas-Colón先生在实验室呆两年是合适的,因为 路易斯在神经炎症方面的研究、天赋和兴趣。因为他会分享他的知识 与我们的实验室成员一起,他将直接增强我们的 为这一任命获得多样性补充的资格提供便利的工作室。 通过集中讨论,Miguel P.Méndez-González博士(父方赠款的PI)和Miguel P.Méndez-González先生 路易斯·A·罗哈斯-科隆共同制定了新的具体目标,这些目标将利用我们的 最近发表的调查结果和父母赠款的具体目标。2020年,我们发表了糖尿病患者 雄性小鼠表现出神经元过度兴奋和星形胶质细胞钾电导降低。另外,它 已经证明,肿瘤坏死因子-a降低星形胶质细胞的钾电导(Köler et al.,1998),而 神经元暴露于IL-1b会导致神经元癫痫样活动(Schäfers&Sorkin,2008)。通过 利用电生理学,他们将确定星形细胞和神经元的电生理学 糖尿病和非糖尿病雌性(对照)小鼠的特性。总体而言,开发的实验 将提供有关高血糖如何影响的其他机制 与癫痫样活动有关。
英文摘要
This is a diversity supplement to an SC2 Score grant parent grant entitled: “Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability”. The purpose of this request is to provide supplemental funding to support and enhance the training of Ph.D. candidate, Mr. Luis A. Rojas-Colón. The recruitment of Mr. Luis A. Rojas-Colón will allow our laboratory to incorporate neuroinflammation studies that will substantially add to the parent grant and to the laboratory team. With his neuroinflammation Ph.D. training, he will assess if pro-inflammatory mediators could be affecting the ability of astrocytes to buffer potassium ions in the hippocampus and if those pro-inflammatory mediators affect neuronal epileptiform activity. Having Mr. Luis A. Rojas-Colón in the laboratory for the next 2 years would be fitting because of Luis’ research, talent, and interest in neuroinflammation. Since he would share his knowledge with our laboratory members, he will be directly enhancing the diversity environment in our workroom facilitating the qualification of this appointment for a diversity supplement. Through focused discussions, Dr. Miguel P. Méndez-González (PI of the parent grant) and Mr. Luis A. Rojas-Colón, together, have developed new specific aims that will take advantage of our recent published findings and of the parent grant specific aims. In 2020, we published that diabetic male mice display neuronal hyperexcitability and decreased astrocytic K+ conductance. Also, it has been shown that TNF-a reduces astroglia potassium conductance (Köller et al., 1998), while neuronal exposure to IL-1b results in neuronal seizure like activity (Schäfers & Sorkin, 2008). By using Electrophysiology, they will determine the astrocytic and neuronal electrophysiological properties in diabetic and non-diabetic female (control) mice. Overall, the developed experiments in this supplement will provide insight of additional mechanism of how hyperglycemia contributes to epileptiform activity.
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Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability
Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability
Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability
Hippocampal astrocytic Kir4.1 channel function in Type 2 diabetic mice: impact on neuronal hyperexcitability
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