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. ![]() ![]() ![]() | Item type: | Article |
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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 |
Related URLs: | |
URI: | https://strathprints.strath.ac.uk/id/eprint/66531 |
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