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Published on: January 9, 2019
Microglia induce auditory dysfunction after status epilepticus in mice
Tasuku Araki1, Toshimitsu Hiragi1, Nahoko Kuga1,2
1Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Abstract:
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.
Insights
Microglia contribute to auditory pathway dysfunction after seizures in mice by reducing inhibitory synapses. Targeting these glial cells in the thalamus may improve auditory processing in epilepsy.
Area of Science:
- Neuroscience
- Immunology
- Epilepsy Research
Background:
- Auditory dysfunction and hyperactivity in auditory pathways are observed in temporal lobe epilepsy.
- The underlying cellular mechanisms, particularly the role of glia, remain unclear.
Purpose of the Study:
- To investigate the role of microglia in auditory pathway disinhibition following status epilepticus in a mouse model.
- To elucidate the cellular mechanisms linking microglia to auditory dysfunction in epilepsy.
Main Methods:
- Induction of status epilepticus in mice.
- Electrophysiological recordings and neuronal activity assessments in auditory pathways (auditory cortex, medial geniculate body).
- Microglial manipulation (local removal) and assessment of synaptic changes and auditory discrimination.
Main Results:
- Status epilepticus led to increased neuronal activity and impaired auditory discrimination.
- Microglia were found to reduce inhibitory synapses on medial geniculate body (MGB) relay neurons post-seizure.
- Removal of microglia from the MGB normalized neuronal activity and improved auditory discrimination.
Conclusions:
- Thalamic microglia play a critical role in the development of auditory pathway hyperactivity and dysfunction after epilepsy.
- Microglial-mediated reduction of inhibitory synapses contributes to epilepsy-associated auditory deficits.
- Targeting thalamic microglia presents a potential therapeutic strategy for auditory dysfunction in epilepsy.
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