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Glutamate receptor mechanisms in human epileptic dysplastic cortex
1Department of Neurosciences, The Cleveland Clinic Foundation, OH 44195, USA. babbt@cesmtp.ccf.org
Epilepsy Research
|October 7, 1998
Summary
This study reveals that specific glutamate receptor subunits, NMDAR2A/B and NMDAR1, are highly expressed in dysplastic neurons, contributing to epilepsy in cortical dysplasia. AMPA receptors also play a role.
Area of Science:
- Neuroscience
- Molecular Biology
- Neuropathology
Background:
- Cortical dysplasia, a developmental brain disorder, involves neuronal migration defects.
- Current understanding of cortical dysplasia lacks detailed investigation into glutamate receptor mechanisms.
Purpose of the Study:
- To investigate the expression of glutamate receptor subunits (NMDAR2A/B, NMDAR1, AMPA Glu-R2/3) in human brain tissue with cortical dysplasia.
- To explore the role of these receptors in the hyperexcitability associated with epilepsy in cortical dysplasia.
Main Methods:
- Immunocytochemistry was employed to detect glutamate receptor subunit protein expression.
- Human brain tissue resected for intractable epilepsy and cortical dysplasia was analyzed.
- Adjacent 30-micrometer sections from seventeen patients were examined using batch-matched reagents.
Main Results:
- Dysplastic neurons showed intense NMDAR2A/B labeling in cell bodies and dendrites, unlike non-dysplastic neurons.
- Dysplastic neurons were also immunoreactive to NMDAR1 antibodies.
- Both dysplastic and non-dysplastic neurons expressed AMPA Glu-R2/3.
Conclusions:
- The epileptic hyperexcitability in cortical dysplasia may stem from NMDAR2A/B and NMDAR1 subunit coassembly in dysplastic neurons.
- AMPA receptors are implicated but likely insufficient alone to explain the epileptic properties of these neurons.