Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/56895
Title: Specific Deletion of the Astrocyte Leptin Receptor Induces Changes in Hippocampus Glutamate Metabolism, Synaptic Transmission and Plasticity.
Authors: 
Keywords: 
Mesh: 
Issue Date: 6-Nov-2019
Citation: Neuroscience.2020;(447):182-190
Abstract: The aim of this study was to indentify the involvement of leptin receptors (LepR) in astrocytes in hippocampal synaptic transmission and plasticity and metabolism. To this end we used a genetic mouse model (GFAP-LepR-/-) of specific LepR ablation in GFAP positive cells and recorded excitatory postsynaptic potentials (fEPSPs) within the CA1 area. Glutamate (Glu) uptake and the expression of Glu transporters (EEAT3, GLT-1 and GLAST) and enzymes involved in Glu metabolism (glutamine synthase, GABA decarboxylase 65 and 67) were quantified. Modifications in the expression of GFAP, the glucose transporter (GLUT)-1, and the monocarboxylate transporters MCT-2 and MCT-4, were also analyzed. The results show that depletion of LepR in GFAP positive cells reduced basal synaptic transmission within the CA1 area and impaired N-methyl-d-aspartate (NMDA)-evoked long-term depression (NMDA-LTD). Hippocampal slices from GFAP-LepR-/- mice displayed lower Glu uptake efficacy together with up-regulation of GLT-1, glutamine synthase, GFAP and GLUT-1. In conclusion, astrocyte LepRs are involved in the maintenance of Glu homeostasis and Glu neurotransmission within the hippocampus. Our findings support a role of hippocampal LepRs in synaptic plasticity, which could have an impact on memory and learning processes.
PMID: 31705891
URI: https://hdl.handle.net/20.500.12530/56895
Appears in Collections:Fundaciones e Institutos de Investigación > FIB H. Infantil U. Niño Jesús > Artículos

Files in This Item:
The file with the full text of this item is not available due to copyright restrictions or because there is no digital version. Authors can contact the head of the repository of their center to incorporate the corresponding file.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.