Add like
Add dislike
Add to saved papers

Increased expression of inwardly rectifying Kir4.1 channel in the parietal cortex from patients with major depressive disorder.

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.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app