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Gap Junctions Contribute to Ictal/Interictal Genesis in Human Hypothalamic Hamartomas
Jie Wu1, Ming Gao2, Stephen G Rice3
1The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China; Division of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA; Department of Pharmacology, Shantou University of Medical College, Guangdong, Shantou 815041, China.
Ebiomedicine
|July 19, 2016
Summary
Neuronal gap junctions in human hypothalamic hamartoma (HH) tissue contribute to epilepsy. Blocking these junctions reduced seizure-like activity, suggesting a potential new therapy for HH patients.
Area of Science:
- Neuroscience
- Cellular Biology
- Epileptology
Background:
- Human hypothalamic hamartoma (HH) is a rare brain lesion linked to difficult-to-treat epilepsy.
- The precise cellular mechanisms driving epileptogenesis in HH remain unclear.
Purpose of the Study:
- To investigate the role of neuronal gap junctions in epileptogenesis within HH tissue.
- To test the hypothesis that synchronous neuronal activity via gap junctions contributes to seizures in HH.
Main Methods:
- Western blot and immunohistochemistry to analyze connexin expression (Cx36, Cx43).
- Electron microscopy and biocytin microinjection to visualize neuronal connections.
- Patch-clamp recordings and field potential recordings in HH tissue slices.
- Pharmacological blockade of gap junctions using mefloquine.
Main Results:
- Increased expression of Cx36 and Cx43 in HH tissue compared to controls.
- Evidence of neuronal gap junctions between small neurons in HH tissue.
- Gap junction blockade significantly reduced spontaneous seizure-like discharges without affecting neuronal firing.
Conclusions:
- Neuronal gap junctions, particularly between small GABAergic neurons, play a role in generating epileptic discharges in HH.
- Targeting neuronal gap junctions offers a potential therapeutic strategy for managing seizures in HH patients.
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