Table 3.
Cx43 expression and phosphorylation changes in other seizure-relevant regions in rodent models of seizures and epilepsy.
| Seizure/Epilepsy Model | ∆ mRNA Expression | ∆ Protein Expression, Phosphorylation |
|---|---|---|
| Amygdala kindling in rats (180–250 g) [109] |
↓ in amygdala after 4 w, but normalization with increasing numbers of stimulations | same as mRNA |
| Tetanus-toxin in amygdala of rats (180–250 g) [109] |
↓ or = in amygdala after 4, 8, 10 w | same as mRNA |
| Tetanus-toxin in amygdala of rats (250–320 g) [110] | ↓ or = in amygdala and posterior cerebral cortex (no distinct temporal profile of Cx43 expression during epileptogenesis) | |
| Local in vivo 4-aminopyridine (4-AP) in post-natal day (PD)40–50 rats [102] | ↑ in somatosensory cortex (primary focus (Pf) and mirror focus (Mf)) (60 min after intensive seizure activity) |
|
| Local in vivo 4-AP in PD30-40 rats [95] | ↑ in Pf and Mf (60 min after seizure onset) | |
| I.p. 4-AP in adult rats (200–250 g) [118] | = 1, 3, 24 h in neocortex after seizure induction | same as mRNA, 50% ↓ in phosphorylated (P1, P2) to non-phosphorylated (P0) Cx43 at 3 h |
| FeCl3 injection in sensimotor cortex in frontal lobe of rats (6–8 w) (model posttraumatic epilepsy) [119] | ↑ in cortex after 14 d | ↑ in cortex after 14 d |
| Pentylenetetrazol in rats (14 w) [106] | ↑ in cortex after 8 h | |
| Genetic model of tuberous sclerosis complex [Tsc1GFAPCKO mice of 4–5 w] [112] | ↓ in neocortex | |
| Genetic rat model of autosomal dominant sleep-related hypermotor epilepsy (ADSHE) with S284-L mutation [76] | ↑ in thalamus and frontal cortex |
∆, changed; =, unaltered; ↑, increase(d); ↓, decrease(d); 4-AP, 4-aminopyride; ADSHE, autosomal dominant sleep-related hypermotor epilepsy; i.p., intraperitoneal, h, hours; Mf, mirror focus; P0, non-phosphorylated; P(1/2), phosphorylated isoform (1/2); PD, post-natal day; Pf, primary focus; w, week.