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

• Published in: The European journal of neuroscience Vol. 49; no. 11; pp. 1418 - 1435
• Main Authors: Bastos, André E. P., Costa, Pedro F., Varderidou‐Minasian, Suzy, Altelaar, Maarten, Lima, Pedro A.
• Format: Journal Article
• Language: English
• Published: France Wiley Subscription Services, Inc 01.06.2019
• Subjects: Biophysics; CA1 neurones; Energy balance; Excitability; Feeding; feeding cycle; Hippocampus; Information processing; ion channels; Mass spectroscopy; rat hippocampus; Satiety; Sodium; Sodium channels (voltage-gated); Sodium conductance; voltage‐gated sodium currents; Western blotting; CA1 neurones; feeding cycle; ion channels; rat hippocampus; voltage-gated sodium currents
• ISSN: 0953-816X; 1460-9568; 1460-9568
• DOI: 10.1111/ejn.14331

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. Impact of feeding and fasting on the biophysical properties and molecular expression of Na+ currents of rat hippocampal CA1 neurones. In fed neurones, the higher single channel Na+ conductance and increased Na+ channel density at the plasma membrane will determine a larger inward flux of Na+ ions, and, consequently, significant differences in the whole‐cell Na+ current density. Na+ channels are presented as key modulators in the regulation of food intake and energy balance by the hippocampus.