Loss of the zinc receptor ZnR/GPR39 in mice enhances anxiety-related behavior and motor deficits, and modulates KCC2 expression in the amygdala
Our findings indicate that loss of ZnR/GPR39 enhances anxiety-related behavior in both male and female mice. Moreover, ZnR/GPR39 KO mice exhibit impaired motor coordination, which may be associated with increased anxiety. Finally, we demonstrate that loss of ZnR/GPR39 modulates the expression of KCC2 in the amygdala. Thus, we propose that ZnR/GPR39 can serve as a target for regulating GABAergic signaling in anxiety treatment.
Authors
- Moumita Chakraborty (ORCID: https://orcid.org/0000-0001-7509-1777)
- Hagit Cohen (ORCID: https://orcid.org/0000-0002-4762-1969)
- Milos Bogdanovic (ORCID: https://orcid.org/0000-0002-7130-2394)
- Michal Hershfinkel (ORCID: https://orcid.org/0000-0003-1652-1989)
- Ora Kofman (ORCID: https://orcid.org/0000-0001-6498-3534)
- Hila Asraf (ORCID: https://orcid.org/0000-0003-4134-1218)
- Israel Sekler (ORCID: https://orcid.org/0000-0002-7550-1550)
- Romi Sagi
Institutions
- Ben-Gurion University of the Negev (IL)
- Bar-Ilan University (IL)
- National Institute of Diabetes and Digestive and Kidney Diseases (US)
- Geha Mental Health Center (IL)
Publication Details
- Journal
- Behavioral and Brain Functions
- Published
- 2024-11-24
- DOI
- https://doi.org/10.1186/s12993-024-00254-x
- Citations
- 3
- Primary Topic
- Neuroscience and Neuropharmacology Research
- Type
- article
- Field-Weighted Citation Impact
- 0.80
Funders
- Israel Science Foundation