Interleukin-16 inhibits sodium channel function and GluA1 phosphorylation via CD4- and CD9-independent mechanisms to reduce hippocampal neuronal excitability and synaptic activity

Hridi, Shehla U. and Franssen, Aimée J.P.M. and Jiang, Hui-Rong and Bushell, Trevor J. (2019) Interleukin-16 inhibits sodium channel function and GluA1 phosphorylation via CD4- and CD9-independent mechanisms to reduce hippocampal neuronal excitability and synaptic activity. Molecular and Cellular Neuroscience, 95. pp. 71-78. ISSN 1044-7431

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    Abstract

    Interleukin 16 (IL-16) is a cytokine that is primarily associated with CD4+ T cell function, but also exists as a multi-domain PDZ protein expressed within cerebellar and hippocampal neurons. We have previously shown that lymphocyte-derived IL-16 is neuroprotective against excitotoxicity, but evidence of how it affects neuronal function is limited. Here, we have investigated whether IL-16 modulates neuronal excitability and synaptic activity in mouse primary hippocampal cultures. Application of recombinant IL-16 impairs both glutamate-induced increases in intracellular Ca2+ and sEPSC frequency and amplitude in a CD4- and CD9-independent manner. We examined the mechanisms underlying these effects, with rIL-16 reducing GluA1 S831 phosphorylation and inhibiting Na+ channel function. Taken together, these data suggest that IL-16 reduces neuronal excitability and synaptic activity via multiple mechanisms and adds further evidence that alternative receptors may exist for IL-16.

    Author(s):Hridi, Shehla U. ORCID logoORCID: https://orcid.org/0000-0001-7906-6763, Franssen, Aimée J.P.M. ORCID logoORCID: https://orcid.org/0000-0001-6399-1663, Jiang, Hui-Rong and Bushell, Trevor J. ORCID logoORCID: https://orcid.org/0000-0003-4145-9670
    Item type:Article
    ID code:66531
    Keywords:IL-16, CD4, neuron, calcium signalling, na+ channels, sEPSCs, Pharmacy and materia medica, Cellular and Molecular Neuroscience, Cell Biology, Molecular Biology
    Subjects:Medicine > Pharmacy and materia medica
    Department:Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
    Depositing user: Pure Administrator
    Date deposited:10 Jan 2019 14:44
    Last modified:05 Dec 2019 04:57
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    URI:https://strathprints.strath.ac.uk/id/eprint/66531
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