Table 2.
Cx43 expression and phosphorylation changes in the hippocampus in rodent models of seizures and epilepsy.
| Seizure/Epilepsy Model | ∆ mRNA Expression | ∆ Protein Expression, Phosphorylation, Coupling | ||||
|---|---|---|---|---|---|---|
| Ex vivo epileptiform Activity | ||||||
| Repetitive tetanization of Schaffer collaterals in CA1 (slices) from post-natal day (PD)25–40 rats [110] | = total, ↓ non-phosphorylated (P0) (redistribution from P0 to phosphorylated (P)) |
|||||
| Co2+ in whole hippocampal isolates from PD15 mice [62] | ↑ | P1 ↑ P2 and P0 slightly ↑ |
||||
| Chronic (18 h) bicuculline in organotypic hippocampal slice cultures of PD7 rats [96] | ↑ | ↑ in membrane fractions also ↑ coupling |
||||
| In Vivo Models | ||||||
| Acute | Latent | Chronic | Acute | Latent | Chronic | |
| Status epilepticus (SE) Models | ||||||
| I.p. Li+-pilocarpine SE in rats [98] | ↑ 2–12 h, most at 24 h post-SE (CA1-3) | = 30 d and 60d post-SE | ||||
| I.p. pilocarpine SE in rats (200–250 g) [95] |
↑ after focal seizures | |||||
| I.p. pilocarpine SE in rats (270–300 g) [114] |
total =, but ≠ distribution 2 h post-SE: ↑ str.pyramidale, ↓ str.radiatum |
total ↑, but = distribution 3 d post-SE |
||||
| I.p. lithium-pilocarpine SE in rats (180–200 g, 6 w old) [108] | Total ↓ 24 h post-SE, gradually ↑ from 7 to 60 d after SE; ↓ P-Cx43 (S368) 24 h post-SE, gradually ↑ from 7 to 30 d after SE, peak at 60 d |
|||||
| I.p. pilocarpine SE in mice (25–30 g) [100] |
= 4 h, 1 d post-SE | ↑ 1 w post-SE |
↑ 2 m post-SE |
= 4 h and 1 d post-SE | ↑ 1 w post-SE |
↑ 2 m post-SE |
| I.p. pilocarpine SE in mice (22–28 g, 8 w old) [102] |
↑ 3 h, peak between 1 and 3 d post-SE | ↑ 7 d, ↑ 15 d post-SE | = as baseline 30 d post-SE | |||
| I.p. kainic acid (KA) SE in rats (150–180 g) [99] | ↑ 1 w post-SE, also ↑ coupling | |||||
| I.p. KA SE in PD26-33 rats [112] | = 4 w post-SE |
= 4 w post-SE | ||||
| Intracortical KA in mice (3–4 m old) [72] |
3 m post-SE: ↑ total, ↑ P2 (whole-cell); = plasma membrane, shift to P2, Cx43 accumulates around blood vessels | |||||
| I.c.v. KA in rats (280 ± 300 g) [103] | 24 h: ↓ CA3-4 pyr.layer, ↑ other regions |
48–72 h: ↓ CA3-4 pyr.layer, ↑ other regions | 48 h: ↑ layer oriens, molecular, lacunosum molecular | |||
| Chemical kindling models | ||||||
| I.p. pentylenetetrazol (PTZ)-kindled rats (180–200 g) [91] | ↑ CA3 (after 2 w, in fully kindled rats) | |||||
| Electrical kindling models | ||||||
| Amygdala kindling in PD83-95 rats (230–250 g) [112] | slight↓/= 2–6 w after last stage 5 seizure | = 2–6 w after last stage 5 seizure | ||||
| Amygdala kindling in rats (300–350 g) [109] |
= 24 h after stage 2 seizures | = 24 h after stage 5 seizures | = 24 h after stage 2 seizures | = 24 h after stage 5 seizures | ||
| Hippocampal kindling in adult rats (275–300 g) (escalating stimulations until after discharges) [111] | = after 3 h, 12 h, 24 h | = after 3 h, 12 h, 24 h | ||||
| Other seizure/epilepsy models | ||||||
| PTZ in rats (14 w old) [101] | ↑ after 2 h, most 8 h | |||||
| Genetic mouse model of tuberous sclerosis complex [Tsc1GFAPCKO mice (gene Tsc1 inactivated in glia)] [107] | ↓ in mice 2–3 w old (precedes seizure onset) and mice 4–5 w (seizure onset) (also ↓ coupling) | |||||
| Experimental febrile seizures induced by hyperthermia (HT) in PD14-15 mice [115] | 5 d post-HT: total ↓, ↑ P1/P2 (↓coupling) |
|||||
| Chronic i.c.v. administered lipopolysaccharide (LPS) in adult rats (280–320 g) [106] | = | = | = | = | ↓ after 7 LPS injections | = |
| Intrahippocampal 4-aminopyridine (4-AP) in rats (250–300 g) [94] | trend towards ↑ after 1 h | ↑ | ||||
∆, changed; =, unaltered; ≠, altered; ↑, increase(d); ↓, decrease(d); 4-AP, 4-aminopyride; CA, cornu ammonis; d, days; i.c.v., intracerebroventricular; i.p., intraperitoneal, h, hours; HT, hyperthermia; KA, kainic acid; LPS, lipopolysaccharide; m, months; P(1/2), phosphorylated isoform (1/2); PD, post-natal day; PTZ, pentylenetetrazole; SE, status epilepticus; w, weeks.