Insulin decreases epileptiform activity in rat layer 5/6 prefrontal cortex in vitro


Por: Villalobos, N., Ramirez-Sanchez, E., Mondragon-Garcia, A., Garduño J., Castillo-Rolon, D., Trujeque-Ramos, S., Hernandez-Lopez, S.

Ahead of Print: 1 feb 2023
Resumen:
Accumulating evidence indicates that insulin-mediated signaling in the brain may play important roles in regulating neuronal function. Alterations to insulin signaling are associated with the development of neurological disorders including Alzheimer's disease and Parkinson's disease. Also, hyperglycemia and insulin resistance have been associated with seizure activity and brain injury. In recent work, we found that insulin increased inhibitory GABA(A)-mediated tonic currents in the prefrontal cortex (PFC). In this work, we used local field potential recordings and calcium imaging to investigate the effect of insulin on seizure-like activity in PFC slices. Seizure-like events (SLEs) were induced by perfusing the slices with magnesium-free artificial cerebrospinal fluid (ACSF) containing the proconvulsive compound 4-aminopyridine (4-AP). We found that insulin decreased the frequency, amplitude, and duration of SLEs as well as the synchronic activity of PFC neurons evoked by 4-AP. These insulin effects were mediated by the PI3K/Akt signaling pathway and mimicked by gaboxadol (THIP), a delta GABA(A) receptor agonist. The effect of insulin on the number of SLEs was partially blocked by L-655,708, an inverse agonist with high selectivity for GABA(A) receptors containing the alpha 5 subunit. Our results suggest that insulin reduces neuronal excitability by an increase of GABAergic tonic currents. The physiological relevance of these findings is discussed.

Filiaciones:
Villalobos, N.:
 Academia de Fisiología, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, Ciudad de México, Mexico

 Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina del IPN, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, Ciudad de México, Mexico

Ramirez-Sanchez, E.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

Mondragon-Garcia, A.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

Garduño J.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

Castillo-Rolon, D.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

Trujeque-Ramos, S.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico

 Translational Neurogenetics Unit, Wallenberg Neuroscience Center, Lund University, Lund, Sweden

Hernandez-Lopez, S.:
 Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
ISSN: 08874476





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Tipo de documento: Article
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WOS Id: 000942348600001
ID de PubMed: 36732015