PT  - JOURNAL ARTICLE
AU  - Eyo, Ukpong B.
AU  - Peng, Jiyun
AU  - Murugan, Madhuvika
AU  - Mo, Mingshu
AU  - Lalani, Almin
AU  - Xie, Ping
AU  - Xu, Pingyi
AU  - Margolis, David J.
AU  - Wu, Long-Jun
TI  - Regulation of Physical Microglia–Neuron Interactions by Fractalkine Signaling after Status Epilepticus
AID  - 10.1523/ENEURO.0209-16.2016
DP  - 2016 Nov 01
TA  - eneuro
PG  - ENEURO.0209-16.2016
VI  - 3
IP  - 6
4099  - http://www.eneuro.org/content/3/6/ENEURO.0209-16.2016.short
4100  - http://www.eneuro.org/content/3/6/ENEURO.0209-16.2016.full
SO  - eNeuro2016 Nov 01; 3
AB  - Microglia, the resident immune cells of the brain, perform elaborate surveillance in which they physically interact with neuronal elements. A novel form of microglia–neuron interaction named microglial process convergence (MPC) toward neuronal axons and dendrites has recently been described. However, the molecular regulators and pathological relevance of MPC have not been explored. Here, using high-resolution two-photon imaging in vivo and ex vivo, we observed a dramatic increase in MPCs after kainic acid– or pilocarpine-induced experimental seizures that was reconstituted after glutamate treatment in slices from mice. Interestingly, a deficiency of the fractalkine receptor (CX3CR1) decreased MPCs, whereas fractalkine (CX3CL1) treatment increased MPCs, suggesting that fractalkine signaling is a critical regulator of these microglia–neuron interactions. Furthermore, we found that interleukin-1β was necessary and sufficient to trigger CX3CR1-dependent MPCs. Finally, we show that a deficiency in fractalkine signaling corresponds with increased seizure phenotypes. Together, our results identify the neuroglial CX3CL1–CX3CR1 communication axis as a modulator of potentially neuroprotective microglia–neuron physical interactions during conditions of neuronal hyperactivity.