| First Author | Hridi SU | Year | 2019 |
| Journal | Mol Cell Neurosci | Volume | 95 |
| Pages | 71-78 | PubMed ID | 30738184 |
| Mgi Jnum | J:294076 | Mgi Id | MGI:6446330 |
| Doi | 10.1016/j.mcn.2019.01.002 | Citation | Hridi SU, et al. (2019) Interleukin-16 inhibits sodium channel function and GluA1 phosphorylation via CD4- and CD9-independent mechanisms to reduce hippocampal neuronal excitability and synaptic activity. Mol Cell Neurosci 95:71-78 |
| abstractText | 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 Ca(2+) 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. |
