糖尿病小鼠模型初级躯体感觉皮层突触可塑性受损

IF 4.2 3区 医学 Q2 NEUROSCIENCES
Nuria García-Magro, Alberto Mesa-Lombardo, Natali Barros-Zulaica, Ángel Nuñez
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引用次数: 0

摘要

1 型和 2 型糖尿病患者的中枢神经系统会发生变化,从而导致认知障碍。在糖尿病动物模型中也观察到认知缺陷,如感官知觉受损、工作记忆和空间记忆功能缺陷。有研究认为,胰岛素样生长因子-I(IGF-I)和/或胰岛素水平的降低可能会诱发这些神经系统疾病。我们研究了幼年链脲佐菌素(STZ)糖尿病小鼠初级体感皮层的突触可塑性。我们重点研究了大脑 IGF-I 水平降低对皮层突触可塑性的影响。在异氟醚麻醉下,我们对对照组和 STZ-糖尿病小鼠初级躯体感觉皮层(S1)的 2/3 层神经元进行了单元记录。通过重复刺激胡须诱导突触可塑性。结果显示,在对照组小鼠的S1皮层第2/3层神经元中,胡须的重复刺激(8赫兹诱导训练)引起了长期电位(LTP)。相比之下,同样的诱导训练在 STZ 糖尿病小鼠中引起了长期抑制(LTD),这种抑制依赖于 NMDA 和代谢型谷氨酸能受体。糖尿病患者脑内 IGF-I 水平的降低可能是导致突触可塑性受损的原因,这一点从 STZ-糖尿病小鼠应用 IGF-I 后反应促进的改善可以得到证明。免疫化学技术进一步支持了这一假设,免疫化学技术显示 STZ 糖尿病动物 S1 皮层 2/3 层的 IGF-I 受体减少。在 STZ-糖尿病动物中观察到的突触可塑性损伤伴随着胡须辨别任务中表现的下降,以及免疫化学研究中观察到的 IGF-I、GluR1 和 NMDA 受体的减少。总之,S1 大脑皮层突触可塑性受损可能源于 IGF-I 信号传导减少,导致细胞内信号通路减少,从而减少了细胞膜上谷氨酸能受体的数量。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impairment of synaptic plasticity in the primary somatosensory cortex in a model of diabetic mice
Type 1 and type 2 diabetic patients experience alterations in the Central Nervous System, leading to cognitive deficits. Cognitive deficits have been also observed in animal models of diabetes such as impaired sensory perception, as well as deficits in working and spatial memory functions. It has been suggested that a reduction of insulin-like growth factor-I (IGF-I) and/or insulin levels may induce these neurological disorders. We have studied synaptic plasticity in the primary somatosensory cortex of young streptozotocin (STZ)-diabetic mice. We focused on the influence of reduced IGF-I brain levels on cortical synaptic plasticity. Unit recordings were conducted in layer 2/3 neurons of the primary somatosensory (S1) cortex in both control and STZ-diabetic mice under isoflurane anesthesia. Synaptic plasticity was induced by repetitive whisker stimulation. Results showed that repetitive stimulation of whiskers (8 Hz induction train) elicited a long-term potentiation (LTP) in layer 2/3 neurons of the S1 cortex of control mice. In contrast, the same induction train elicited a long-term depression (LTD) in STZ-diabetic mice that was dependent on NMDA and metabotropic glutamatergic receptors. The reduction of IGF-I brain levels in diabetes could be responsible of synaptic plasticity impairment, as evidenced by improved response facilitation in STZ-diabetic mice following the application of IGF-I. This hypothesis was further supported by immunochemical techniques, which revealed a reduction in IGF-I receptors in the layer 2/3 of the S1 cortex in STZ-diabetic animals. The observed synaptic plasticity impairments in STZ-diabetic animals were accompanied by decreased performance in a whisker discrimination task, along with reductions in IGF-I, GluR1, and NMDA receptors observed in immunochemical studies. In conclusion, impaired synaptic plasticity in the S1 cortex may stem from reduced IGF-I signaling, leading to decreased intracellular signal pathways and thus, glutamatergic receptor numbers in the cellular membrane.
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来源期刊
CiteScore
7.90
自引率
3.80%
发文量
627
审稿时长
6-12 weeks
期刊介绍: Frontiers in Cellular Neuroscience is a leading journal in its field, publishing rigorously peer-reviewed research that advances our understanding of the cellular mechanisms underlying cell function in the nervous system across all species. Specialty Chief Editors Egidio D‘Angelo at the University of Pavia and Christian Hansel at the University of Chicago are supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
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