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鼠前额叶皮质中的angiotensin IV受体:神经元表达和NMDA抑制

Zsolt Tamás Papp^1,2, Polett Ribiczey^1,2, Erzsébet Kató²

¹Department of Oral Biology, Semmelweis University, H-1089 Budapest, Hungary.

|January 25, 2025

概括

ангиотензин IV (Ang IV) 抑制了前额叶皮层 (PFC) 中的N-甲基-D-酸盐 (NMDA) 受体活性. 这一发现表明Ang IV/IRAP途径是认知障碍和神经精神疾病的潜在治疗标.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
神经生物学神经生物学神经生物学

背景情况:

N-甲基-D-酸盐受体 (NMDARs) 对神经元功能和功能障碍至关重要,特别是在前额叶皮质 (PFC),这是一个涉及神经精神疾病的区域.
虽然AT₁受体激活增强了NMDAR活性,但其他血管新生素通路,可能通过AT₄受体 (AT4Rs),可能会抑制NMDAR功能.
ангиотензин IV (Ang IV) 和它的类似物在动物模型中改善认知缺陷方面表现有前途.

研究的目的:

确定AT4受体 (AT4R) 的细胞类型特定局部,该AT4受体与胰岛素调节氨基酶 (IRAP) 相同.
为了研究Ang IV对NMDAR功能的调节作用,在老鼠PFC的V层金字塔神经元中.

主要方法:

利用免疫组织化学测绘大鼠PFC中的AT4R/IRAP表达.
采用全细胞补丁电生理学来评估Ang IV对V层金字塔神经元中的NMDAR电流的影响.
用Ang IV和IRAP抑制剂 (LVVYP-H7) 来评估对NMDA诱导电流的抑制作用.

主要成果:

在年轻和成年大鼠的PFC层V的金字塔细胞和GABAergic内部神经元中发现了AT4R/IRAP.
在PFC金字塔神经元的一个子集中,Ang IV以剂量依赖的方式显著抑制NMDA诱导的电流.
IRAP抑制剂LVVYP-H7复制了Ang IV的抑制作用,即使在突触隔离后,这种抑制仍然存在.

结论:

通过AT4R/IRAP作用的Ang IV抑制了PFC层V金字塔神经元中的NMDAR活性.
这种抑制机制为调节认知功能提供了潜在的途径.
格IV/IRAP途径代表了治疗认知障碍和相关神经精神疾病的有希望的药理学标.

关键词:

在AT4血管增生素受体.在N-甲基-D-阿斯巴甜酸盐受体.胰岛素调节的氨基酶.通过神经调节进行神经调节.前额叶皮层前额叶皮层.阳氨素系统阳氨素

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