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Published on: August 5, 2017
Microglial activation drives neuronal dysregulation in alcohol-induced seizure susceptibility
Shiyong Zhang1, Yuting Zhou2, Yue Ren3
1School of Clinical Medicine, Bengbu Medical University, Bengbu, 233030, People's Republic of China.
Abstract:
Excessive alcohol drinking can induce seizures, but the mechanisms underlying acute alcohol-induced seizures remained to be extensively investigated. To investigate this, we established an acute alcohol-treated model and observed a microglial response in the hippocampal CA1 region of mice, which was associated with the enhancement of seizure susceptibility. Furthermore, we found an increased abundance of GABAergic interneurons and a decrease in the activity of CaMKII in the hippocampal CA1 region. Minocycline-mediated microglial depletion fully inhibited the increase in GABAergic interneurons and GABAergic inhibitory synapse formation, and the decrease in glutamatergic neurons and glutamatergic excitatory synapse formation induced by acute alcohol treatment. In conclusion, our findings indicate that dysregulation of synapse formation via microglial activation contributes to acute alcohol-induced enhancement of seizure susceptibility.
Insights
Acute alcohol intake increases seizure susceptibility by activating microglia in the brain. This leads to altered neuron activity and synapse formation, highlighting a new target for preventing alcohol-induced seizures.
Area of Science:
- Neuroscience
- Neuropharmacology
- Cellular Biology
Background:
- Excessive alcohol consumption is a known cause of seizures.
- The precise mechanisms behind acute alcohol-induced seizures are not fully understood.
- Microglial activation in the hippocampus is implicated in neurological disorders.
Purpose of the Study:
- To investigate the role of microglial response in acute alcohol-induced seizures.
- To elucidate the impact of alcohol on neuronal and synaptic changes in the hippocampus.
- To explore potential therapeutic interventions targeting microglial pathways.
Main Methods:
- Establishment of an acute alcohol-treated mouse model.
- Observation of microglial response in the hippocampal CA1 region.
- Assessment of GABAergic and glutamatergic neuron and synapse changes.
- Utilizing minocycline for microglial depletion.
Main Results:
- Acute alcohol treatment enhanced seizure susceptibility and activated microglia in the hippocampal CA1 region.
- Alcohol increased GABAergic interneurons and decreased CaMKII activity.
- Minocycline treatment reversed alcohol-induced changes in neuron and synapse formation.
Conclusions:
- Microglial activation contributes to acute alcohol-induced seizures by disrupting synapse formation.
- Dysregulation of GABAergic and glutamatergic pathways is a key mechanism.
- Targeting microglial activation may offer a novel therapeutic strategy for alcohol-related seizures.
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