Table 1.
Cx43 expression and phosphorylation changes associated with human epilepsies.
| Epileptic Condition |
Brain Region (vs. Control Tissue) |
∆ mRNA Expression | ∆ Protein Expression, Phosphorylation |
|---|---|---|---|
| Intractable seizures of structural etiology [65] Cerebral tumors with acute seizures [65] |
Temporal lobe neocortex Neocortex (vs. cerebral tumors without seizures) |
↑ ↑ |
|
| Complex partial seizures (mesial temporal lobe epilepsy (MTLE)) (structural etiology) [73] | Hippocampus (vs. temporal lobectomy) | ↓ | = |
| Epilepsy associated brain tumors [66] | Brain tumor and perilesional epileptic cortex (vs. normal cortex) | ↑ in low-grade gliomas, perilesional cortex (≠ isoforms); ↓ in high-grade gliomas (P0 isoform) |
|
| Generalized seizures in progression of MTLE (structural etiology) [70] | Hippocampus (vs. post-mortem tissue) | ↑ CA1 and CA4 | |
| MTLE (structural etiology) [68] |
Hippocampus (vs. post-mortem tissue) | ↑ | |
| TLE (structural etiology) [65,67] |
Hippocampus (vs. post-mortem tissue) | ↑ | |
| Cryptogenic epilepsy or epilepsy secondary to focal cortical dysplasia (FCD) (structural etiology) [71] | Cortex (vs. tissue resected during tumor surgery and autopsy tissue) | ↑ in 25% of cryptogenic epilepsy | ↑ in FCD type IIB (large Cx43 aggregates around balloon cells and astrocytes); = in cryptogenic epilepsy and FCD type IA/IIA |
| Refractory epilepsy of structural etiology [72] | Epileptic foci (vs. tissue traumatic brain injury) | ↑ | |
| MTLE-hippocampal sclerosis (HS) (structural etiology) [74] |
Sclerotic hippocampus (MTLE-HS vs. MTLE non-HS tissue) | ↑ total (whole cell); = in plasma membrane, large Cx43 plaques around blood vessels (↑ number and size), ↑ phosphorylation S255 |
∆, changed; =, unaltered; ≠, different; ↑, increase(d); ↓, decrease(d); CA, cornu ammonis; FCD, focal cortical dysplasia; HS, hippocampal sclerosis; (M)TLE, (mesial) temporal lobe epilepsy.