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Eur J Neurosci. 2019 Jun;49(11):1418-1435. doi: 10.1111/ejn.14331. Epub 2019 Jan 27.

Feeding cycle alters the biophysics and molecular expression of voltage-gated Na+ currents in rat hippocampal CA1 neurones.

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Department of Chemistry and Biochemistry, Centre of Chemistry and Biochemistry, Faculty of Sciences University of Lisbon, Lisbon, Portugal.
Department of Physiology, Nova Medical School/Faculdade de Ciências Médicas, Lisbon, Portugal.
Sea4Us, Biotechnology and Marine Resources, Lda., Sagres, Portugal.
Biomolecular Mass Spectrometry and Proteomics, Utrecht University, Utrecht, The Netherlands.


The function of hippocampus as a hub for energy balance is a subject of broad and current interest. This study aims at providing more evidence on this regard by addressing the effects of feeding cycle on the voltage-gated sodium (Na+ ) currents of acutely isolated Wistar rat hippocampal CA1 neurones. Specifically, by applying patch clamp techniques (whole cell voltage clamp and single channel in inside-out patches) we assessed the influence of feeding and fasting conditions on the intrinsic biophysical properties of Na+ currents. Additionally, mass spectrometry and western blotting experiments were used to address the effect of feeding cycle over the Na+ channel population of the rat hippocampus. Na+ currents were recorded in neurones obtained from fed and fasted animals (here termed "fed neurones" and "fasted neurones", respectively). Whole cell Na+ currents of fed neurones, as compared to fasted neurones, showed increased mean maximum current density and a higher "window current" amplitude. We demonstrate that these results are supported by an increased single channel Na+ conductance in fed neurones and, also, by a greater Nav1.2 channel density in plasma membrane-enriched fractions of fed samples (but not in whole hippocampus preparations). These results imply fast variations on the biophysics and molecular expression of Na+ currents of rat hippocampal CA1 neurones, throughout the feeding cycle. Thus, one may expect a differentiated regulation of the intrinsic neuronal excitability, which may account for the role of the hippocampus as a processor of satiety information.


CA1 neurones; feeding cycle; ion channels; rat hippocampus; voltage-gated sodium currents


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