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ORIGINAL RESEARCH article

Front. Cell. Neurosci.
Sec. Cellular Neurophysiology
Volume 18 - 2024 | doi: 10.3389/fncel.2024.1444395

IMPAIRMENT OF SYNAPTIC PLASTICITY IN THE PRIMARY SOMATOSENSORY CORTEX IN A MODEL OF DIABETIC MICE

Provisionally accepted
Angel Nuñez Angel Nuñez 1*Nuria García Magro Nuria García Magro 2Alberto Mesa-Lombardo Alberto Mesa-Lombardo 1Natalí Barros Zulaica Natalí Barros Zulaica 3
  • 1 Anatomy, Histology and Neuroscience, Autonomous University of Madrid, Madrid, Spain
  • 2 Universidad Francisco de Vitoria, Pozuelo de Alarcón, Madrid, Spain
  • 3 Swiss Federal Institute of Technology Lausanne, Lausanne, Vaud, Switzerland

The final, formatted version of the article will be published soon.

    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 insulinlike 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.

    Keywords: synaptic plasticity, IGF-I, GluR1 receptor, NMDA receptor, PI3-kinase, mTOR, Somatosensory Cortex, diabetes

    Received: 05 Jun 2024; Accepted: 17 Jul 2024.

    Copyright: © 2024 Nuñez, García Magro, Mesa-Lombardo and Barros Zulaica. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Angel Nuñez, Anatomy, Histology and Neuroscience, Autonomous University of Madrid, Madrid, 28029, Spain

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