Journal of affective disorders · 2018
Increased expression of inwardly rectifying Kir4.1 channel in the parietal cortex from patients with major depressive disorder.
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Xiong Zhongwei, Zhang Kai, Ren Qian, Chang Lijia, Chen Jincao, Hashimoto Kenji
Аннотация
BACKGROUND: The inwardly rectifying K+ channel subtype Kir4.1 has been well studied in the astrocyte within brain; however, the precise role of this protein in psychiatric disorders is unknown. Kir4.1 is also known to interact with GABAB receptors which may be implicated in psychiatric disorders. Here we studied whether expression of Kir4.1 and GABAB receptors was altered in the postmortem brain samples (parietal cortex and cerebellum) from patients with major psychiatric disorders.
METHODS: Protein expression of Kir4.1 and GABAB receptors in the parietal cortex and cerebellum from control, major depressive disorder (MDD), schizophrenia (SZ), and bipolar disorder (BD) groups was measured.
RESULTS: Levels of Kir4.1 in the parietal cortex from MDD group, but not SZ and BD groups, were significantly higher than the control group. Furthermore, levels of GABAB receptor subunit 1 in the parietal cortex from MDD group and SZ group, but not BD group, were also significantly higher than the control group. Interestingly, there was a positive correlation between Kir4.1 protein and GABAB receptor subunit 1 in the parietal cortex from control group, but not MDD group.
LIMITATIONS: The small number in each group may limit our interpretation. Only two brain regions were analyzed.
CONCLUSIONS: Abnormalities in the interaction of Kir4.1 and GABAB receptor in the parietal cortex might play a role in the pathophysiology of MDD.
METHODS: Protein expression of Kir4.1 and GABAB receptors in the parietal cortex and cerebellum from control, major depressive disorder (MDD), schizophrenia (SZ), and bipolar disorder (BD) groups was measured.
RESULTS: Levels of Kir4.1 in the parietal cortex from MDD group, but not SZ and BD groups, were significantly higher than the control group. Furthermore, levels of GABAB receptor subunit 1 in the parietal cortex from MDD group and SZ group, but not BD group, were also significantly higher than the control group. Interestingly, there was a positive correlation between Kir4.1 protein and GABAB receptor subunit 1 in the parietal cortex from control group, but not MDD group.
LIMITATIONS: The small number in each group may limit our interpretation. Only two brain regions were analyzed.
CONCLUSIONS: Abnormalities in the interaction of Kir4.1 and GABAB receptor in the parietal cortex might play a role in the pathophysiology of MDD.