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Anteromesial Temporal Lobectomy for Medically Intractable Temporal Lobe Epilepsy: An Operative Study
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Changes in synaptic AMPA receptor concentration and composition in chronic temporal lobe epilepsy
Daniel L Egbenya1, Suleman Hussain1, Yi-Chen Lai2
1Laboratory for Synaptic Plasticity, Division of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
Molecular and Cellular Neurosciences
|August 1, 2018
Summary
Chronic epilepsy alters AMPA receptor subunits in synapses, reducing key proteins like GluA1 and GluA2. This synaptic change may increase neuronal vulnerability to excitotoxicity and impact cognitive function.
Area of Science:
- Neuroscience
- Molecular Biology
- Epilepsy Research
Background:
- Excitotoxicity, driven by excessive glutamate receptor stimulation and calcium influx, is implicated in neurodegenerative diseases.
- Chronic epilepsy involves plastic changes in synaptic AMPA receptors, which are crucial for calcium regulation.
- Understanding these changes is vital to determine their adaptive or detrimental roles.
Purpose of the Study:
- To investigate long-term alterations in synaptic AMPA receptor subunits in a rat model of chronic temporal lobe epilepsy (TLE).
- To assess the impact of chronic epilepsy on the concentration and localization of AMPA receptor subunits (GluA1, GluA2) and NMDA receptor subunit (NR2B).
- To evaluate the functional implications of these synaptic changes on neuronal excitability and cognitive function.
Main Methods:
- Utilized a kainic acid (KA)-induced rat model of chronic temporal lobe epilepsy (TLE).
- Employed hippocampal synaptosomes to quantify synaptic concentrations of AMPA receptor subunits (GluA1, GluA2) and NMDA receptor subunit (NR2B).
- Performed postembedding immunogold electron microscopy (EM) on Schaffer collateral synapses in the hippocampal CA1 area to localize GluA1 and GluA2 at the postsynaptic density (PSD).
Main Results:
- Significant reductions were observed in synaptic concentrations of AMPA receptor subunits GluA1 (28%) and GluA2 (27%), and NMDA receptor subunit NR2B.
- Electron microscopy revealed substantial reductions of GluA1 (32%) and GluA2 (52%) subunits at the postsynaptic density (PSD) of CA1 synapses.
- Chronic epilepsy led to a relative increase in GluA2-lacking AMPA receptors within the synapse.
Conclusions:
- Chronic TLE induces lasting changes in glutamatergic neurotransmission, characterized by reduced synaptic AMPA receptor subunits.
- The observed increase in GluA2-lacking AMPA receptors may enhance neuronal excitotoxic vulnerability.
- These synaptic alterations have significant implications for hippocampal cognitive functions in epilepsy.
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