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Elife. 2018 Aug 14;7. pii: e36726. doi: 10.7554/eLife.36726.

The adipocyte hormone leptin sets the emergence of hippocampal inhibition in mice.

Author information

1
Aix-Marseille University UMR 1249, INSERM (Institut National de la Santé et de la Recherche Médicale) Unité 1249, INMED (Institut de Neurobiologie de la Méditerranée), Marseille, France.
2
Plateforme Post-Génomique, INMED, Marseille, France.
3
Program in Neuroscience, Department of Integrative Physiology and Neuroscience, Washington State University, Pullman, United States.
4
Institute of Biochemical and Clinical Sciences, Hatherly Laboratory, University of Exeter Medical School, Exeter, United Kingdom.

Abstract

Brain computations rely on a proper balance between excitation and inhibition which progressively emerges during postnatal development in rodent. γ-Aminobutyric acid (GABA) neurotransmission supports inhibition in the adult brain but excites immature rodent neurons. Alterations in the timing of the GABA switch contribute to neurological disorders, so unveiling the involved regulators may be a promising strategy for treatment. Here we show that the adipocyte hormone leptin sets the tempo for the emergence of GABAergic inhibition in the newborn rodent hippocampus. In the absence of leptin signaling, hippocampal neurons show an advanced emergence of GABAergic inhibition. Conversely, maternal obesity associated with hyperleptinemia delays the excitatory to inhibitory switch of GABA action in offspring. This study uncovers a developmental function of leptin that may be linked to the pathogenesis of neurological disorders and helps understanding how maternal environment can adversely impact offspring brain development.

KEYWORDS:

GABA; KCC2; chloride homeostasis; hippocampus; maternal obesity; mouse; neuroscience

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