BRIEF RESEARCH REPORT article
Front. Cell. Neurosci.
Sec. Cellular Neurophysiology
Volume 19 - 2025 | doi: 10.3389/fncel.2025.1638550
GLP-1 selectively enhances tonic GABAA receptor-mediated currents in mouse dentate gyrus granule cells of the ventral hippocampus
Provisionally accepted
- Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
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Glucagon-like peptide-1 (GLP-1) is a metabolic hormone secreted by L-cells in the gut and it stimulates insulin secretion in the pancreatic islets by activating GLP-1 receptors (GLP-1Rs). In the brain, the GLP-1Rs are expressed in many regions including the hippocampus. We examined whether GLP-1 modulation of GABA-activated currents in the mouse hippocampus varied along the hippocampal dorsal-ventral axis. We recorded spontaneous inhibitory postsynaptic (sIPSCs) and tonic extrasynaptic currents in dorsal and ventral hippocampal dentate gyrus (DG) granule cells in brain slices from 2-month-old mice. GLP-1 (100 pM) did not modulate the GABA-activated fast or slow phasic postsynaptic currents in either the dorsal or the ventral hippocampal slices. In contrast, the tonic extrasynaptic current was potentiated by GLP-1 but, only consistently in the DG granule cells of the ventral hippocampus. Thus, GLP-1 modulation of the DG neurons depends on the dorso-ventral longitudinal hippocampal axis and further, with the subcellular location (synaptic vs. extrasynaptic) of the GABAA receptors (GABAAR) in the DG granule cells. The results are consistent with GLP-1 enhancing the tonic inhibitory extrasynaptic current by a postsynaptic mechanism.
Keywords: GABA, inhibition, GABAA receptor, Glucagon-like peptide-1, hormone
Received: 30 May 2025; Accepted: 29 Aug 2025.
Copyright: © 2025 Netsyk, Korol, Birnir and Jin. 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: Zhe Jin, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
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