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

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....

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Published inThe 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
LanguageEnglish
Published France Wiley Subscription Services, Inc 01.06.2019
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Abstract 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.
AbstractList 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.
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.
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.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.
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.
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.
Author Bastos, André E. P.
Lima, Pedro A.
Costa, Pedro F.
Varderidou‐Minasian, Suzy
Altelaar, Maarten
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Keywords CA1 neurones
feeding cycle
ion channels
rat hippocampus
voltage-gated sodium currents
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Snippet 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...
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StartPage 1418
SubjectTerms 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
Title Feeding cycle alters the biophysics and molecular expression of voltage‐gated Na+ currents in rat hippocampal CA1 neurones
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fejn.14331
https://www.ncbi.nlm.nih.gov/pubmed/30588669
https://www.proquest.com/docview/2331795003
https://www.proquest.com/docview/2161065137
Volume 49
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