Microglia induce auditory dysfunction after status epilepticus in mice

Auditory dysfunction and increased neuronal activity in the auditory pathways have been reported in patients with temporal lobe epilepsy, but the cellular mechanisms involved are unknown. Here, we report that microglia play a role in the disinhibition of auditory pathways after status epilepticus in mice. We found that neuronal activity in the auditory pathways, including the primary auditory cortex and the medial geniculate body (MGB), was increased and auditory discrimination was impaired after status epilepticus. We further demonstrated that microglia reduced inhibitory synapses on MGB relay neurons over an 8-week period after status epilepticus, resulting in auditory pathway hyperactivity. In addition, we found that local removal of microglia from the MGB attenuated the increase in c-Fos+ relay neurons and improved auditory discrimination. These findings reveal that thalamic microglia are involved in auditory dysfunction in epilepsy. In mice after status epilepticus, neuronal activity in the medial geniculate body (MGB) increased in parallel with an impairment in auditory discrimination.MGB microglia depletion suppressed neural hyperactivity and improved auditory discrimination.image

Automated summary

This study found that microglia play a role in the hyperactivity of auditory pathways after status epilepticus. The researchers discovered that microglia reduce inhibitory synapses on MGB relay neurons, leading to auditory dysfunction. Local removal of microglia from the MGB can suppress neural hyperactivity and improve auditory discrimination.