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. 2020 Dec 30;22(1):339. doi: 10.3390/ijms22010339

Table 2.

Abnormalities of Cx43 expression and function of Cx43 in experimental models of depression.

Model Region (Cell) Effect Reference
(In Vivo)
chronic unpredictable stress prefrontal cortex
(rat, in vivo)
decrease (mRNA and protein)
suppresses gap junction permeability
[59,60,61]
Hippocampus
(rat, in vivo)
decrease (protein)
suppresses gap junction permeability
[62]
acute restraint stress
(2 h)
Hippocampus
(mouse, in vivo)
No effect (protein)
enhances hemichannel permeability
[63]
chronic restraint stress
(2 h × 10 times)
Hippocampus
(mouse, in vivo)
No effect (protein)
enhances hemichannel permeability
[63]
Mouse corticosterone
(5 mg/kg/day for 28 days)
Hippocampus
(mouse, in vivo)
No effect (protein)
increase (phosphorylated protein)
[64]
(In Vitro)
corticosterone
(50 µM for 24 h)
cortical astrocyte
(rat, in vitro)
decrease (protein in total lysate and plasma membrane) increase phosphorylated Cx43 in plasma membrane supresses gap junction permeability [68]
Corticosterone
(50 µM for 24 h)
hippocampal astrocyte
(rat, in vitro)
decrease (protein in total lysate and plasma membrane)
increase phosphorylated Cx43 in plasma membrane supresses gap junction permeability
[68]
corticosterone (5‒50 µM for 16 days) cortical astrocyte
(rat, in vitro)
decrease (protein) [65]
Mouse lipopolysaccharide
(1 µg/mL for 24 h)
cortical astrocyte
(mouse, in vitro)
augmentation of hemichannel permeability [75]

We searched MEDLINE using the keywords “(((connexin) OR (hemichannel) OR (gap junction)) AND ((unpredictable stress) OR (restraint stress) OR (corticosterone)))” for papers published by 1 November 2020.