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Early Life Inflammation Increases CA1 Pyramidal Neuron Excitability in a Sex and Age Dependent Manner through a Chloride Homeostasis Disruption

Gomez, Carlos D., Read, Justin, Acharjee, Shaona and Pittman, Quentin J. 2019, Early Life Inflammation Increases CA1 Pyramidal Neuron Excitability in a Sex and Age Dependent Manner through a Chloride Homeostasis Disruption, Journal of Neuroscience, vol. 39, no. 37, pp. 7244-7259, doi: 10.1523/jneurosci.2973-18.2019.

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Title Early Life Inflammation Increases CA1 Pyramidal Neuron Excitability in a Sex and Age Dependent Manner through a Chloride Homeostasis Disruption
Author(s) Gomez, Carlos D.
Read, Justin
Acharjee, Shaona
Pittman, Quentin J.
Journal name Journal of Neuroscience
Volume number 39
Issue number 37
Start page 7244
End page 7259
Total pages 16
Publisher Society for Neuroscience
Place of publication Washington, D.C.
Publication date 2019-09-11
ISSN 0270-6474
1529-2401
Keyword(s) GABA reversal potential
hippocampus
inflammation
intrinsic membrane properties
lipopolysaccharide
sex differences
Summary Early life, systemic inflammation causes long-lasting changes in behavior. To unmask possible mechanisms associated with this phenomenon, we asked whether the intrinsic membrane properties in hippocampal neurons were altered as a consequence of early life inflammation. C57BL/6 mice were bred in-house and both male and female pups from multiple litters were injected with lipopolysaccharide (LPS; 100 μg/kg, i.p.) or vehicle at postnatal day (P)14, and kept until adolescence (P35–P45) or adulthood (P60–P70), when brain slices were prepared for whole-cell and perforated-patch recordings from CA1 hippocampal pyramidal neurons. In neurons of adult male mice pretreated with LPS, the number of action potentials elicited by depolarizing current pulses was significantly increased compared with control neurons, concomitant with increased input resistance, and a lower action potential threshold. Although these changes were not associated with changes in relevant sodium channel expression or differences in capacitance or dendritic architecture, they were linked to a mechanism involving intracellular chloride overload, revealed through a depolarized GABA reversal potential and increased expression of the chloride transporter, NKCC1. In contrast, no significant changes were observed in neurons of adult female mice pretreated with LPS, nor in adolescent mice of either sex. These data uncover a potential mechanism involving neonatal inflammation-induced plasticity in chloride homeostasis, which may contribute to early life inflammation-induced behavioral alterations.
Language eng
DOI 10.1523/jneurosci.2973-18.2019
Indigenous content off
Field of Research 111499 Paediatrics and Reproductive Medicine not elsewhere classified
11 Medical and Health Sciences
17 Psychology and Cognitive Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2019, the authors
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30135243

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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.