Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons

Research output: Contribution to journalJournal articlepeer-review

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Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons. / Sørensen, Andreas T; Ledri, Marco; Melis, Miriam; Nikitidou Ledri, Litsa; Andersson, My; Kokaia, Merab.

In: eNeuro, Vol. 4, No. 6, e0172-17.2017 1–10, 07.12.2017.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Sørensen, AT, Ledri, M, Melis, M, Nikitidou Ledri, L, Andersson, M & Kokaia, M 2017, 'Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons', eNeuro, vol. 4, no. 6, e0172-17.2017 1–10. https://doi.org/10.1523/ENEURO.0172-17.2017

APA

Sørensen, A. T., Ledri, M., Melis, M., Nikitidou Ledri, L., Andersson, M., & Kokaia, M. (2017). Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons. eNeuro, 4(6), [e0172-17.2017 1–10]. https://doi.org/10.1523/ENEURO.0172-17.2017

Vancouver

Sørensen AT, Ledri M, Melis M, Nikitidou Ledri L, Andersson M, Kokaia M. Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons. eNeuro. 2017 Dec 7;4(6). e0172-17.2017 1–10. https://doi.org/10.1523/ENEURO.0172-17.2017

Author

Sørensen, Andreas T ; Ledri, Marco ; Melis, Miriam ; Nikitidou Ledri, Litsa ; Andersson, My ; Kokaia, Merab. / Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons. In: eNeuro. 2017 ; Vol. 4, No. 6.

Bibtex

@article{75c91502e8a345d19c91752c95bae86d,
title = "Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons",
abstract = "Chloride ions play an important role in controlling excitability of principal neurons in the central nervous system. When neurotransmitter GABA is released from inhibitory interneurons, activated GABA type A (GABAA) receptors on principal neurons become permeable to chloride. Typically, chloride flows through activated GABAA receptors into the neurons causing hyperpolarization or shunting inhibition, and in turn inhibits action potential (AP) generation. However, in situations when intracellular chloride concentration is increased, chloride ions can flow in opposite direction, depolarize neurons, and promote AP generation. It is generally recognized that altered chloride homeostasis per se has no effect on the AP threshold. Here, we demonstrate that chloride overload of mouse principal CA3 pyramidal neurons not only makes these cells more excitable through GABAA receptor activation but also lowers the AP threshold, further aggravating excitability. This phenomenon has not been described in principal neurons and adds to our understanding of mechanisms regulating neuronal and network excitability, particularly in developing brain and during pathological situations with altered chloride homeostasis. This finding further broadens the spectrum of neuronal plasticity regulated by ionic compositions across the cellular membrane.",
author = "S{\o}rensen, {Andreas T} and Marco Ledri and Miriam Melis and {Nikitidou Ledri}, Litsa and My Andersson and Merab Kokaia",
year = "2017",
month = dec,
day = "7",
doi = "10.1523/ENEURO.0172-17.2017",
language = "English",
volume = "4",
journal = "eNeuro",
issn = "2373-2822",
publisher = "Society for Neuroscience",
number = "6",

}

RIS

TY - JOUR

T1 - Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons

AU - Sørensen, Andreas T

AU - Ledri, Marco

AU - Melis, Miriam

AU - Nikitidou Ledri, Litsa

AU - Andersson, My

AU - Kokaia, Merab

PY - 2017/12/7

Y1 - 2017/12/7

N2 - Chloride ions play an important role in controlling excitability of principal neurons in the central nervous system. When neurotransmitter GABA is released from inhibitory interneurons, activated GABA type A (GABAA) receptors on principal neurons become permeable to chloride. Typically, chloride flows through activated GABAA receptors into the neurons causing hyperpolarization or shunting inhibition, and in turn inhibits action potential (AP) generation. However, in situations when intracellular chloride concentration is increased, chloride ions can flow in opposite direction, depolarize neurons, and promote AP generation. It is generally recognized that altered chloride homeostasis per se has no effect on the AP threshold. Here, we demonstrate that chloride overload of mouse principal CA3 pyramidal neurons not only makes these cells more excitable through GABAA receptor activation but also lowers the AP threshold, further aggravating excitability. This phenomenon has not been described in principal neurons and adds to our understanding of mechanisms regulating neuronal and network excitability, particularly in developing brain and during pathological situations with altered chloride homeostasis. This finding further broadens the spectrum of neuronal plasticity regulated by ionic compositions across the cellular membrane.

AB - Chloride ions play an important role in controlling excitability of principal neurons in the central nervous system. When neurotransmitter GABA is released from inhibitory interneurons, activated GABA type A (GABAA) receptors on principal neurons become permeable to chloride. Typically, chloride flows through activated GABAA receptors into the neurons causing hyperpolarization or shunting inhibition, and in turn inhibits action potential (AP) generation. However, in situations when intracellular chloride concentration is increased, chloride ions can flow in opposite direction, depolarize neurons, and promote AP generation. It is generally recognized that altered chloride homeostasis per se has no effect on the AP threshold. Here, we demonstrate that chloride overload of mouse principal CA3 pyramidal neurons not only makes these cells more excitable through GABAA receptor activation but also lowers the AP threshold, further aggravating excitability. This phenomenon has not been described in principal neurons and adds to our understanding of mechanisms regulating neuronal and network excitability, particularly in developing brain and during pathological situations with altered chloride homeostasis. This finding further broadens the spectrum of neuronal plasticity regulated by ionic compositions across the cellular membrane.

U2 - 10.1523/ENEURO.0172-17.2017

DO - 10.1523/ENEURO.0172-17.2017

M3 - Journal article

C2 - 29379872

VL - 4

JO - eNeuro

JF - eNeuro

SN - 2373-2822

IS - 6

M1 - e0172-17.2017 1–10

ER -

ID: 189370157