Table 2.
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.