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Vrk2 deficiency elicits aggressive behavior in female zebrafish
Ryohei Umeda1, Hitoshi Teranishi1, Kazumasa Hada2
1Department of Neurophysiology, Faculty of Medicine, Oita University, Oita, Japan.
Abstract:
Vaccinia-related kinase 2 (VRK2) is a serine/threonine kinase initially identified in highly proliferative cells such as thymocytes and fetal liver cells, and it is involved in cell proliferation and survival. VRK2 is also expressed in the brain; however, its molecular function in the central nervous system is mostly unknown. Many genome-wide association studies (GWASs) have reported that VRK2 is a potential candidate molecule for neuropsychiatric diseases such as schizophrenia in humans. However, the pathophysiological relationship between VRK2 and neuropsychiatric disorders has not been fully investigated. In this study, we evaluated vrk2-deficient (vrk2-/- ) zebrafish and found that vrk2-/- female zebrafish showed aggressive behavior and different social preference compared with control (vrk2+/+ ) zebrafish, with low gamma-aminobutyric acid (GABA) content in the brain and high density of neuronal dendrites when compared to vrk2+/+ zebrafish. These findings suggest that female vrk2-/- zebrafish were indeed a model of malbehavior characterized by aggression and social interaction, which can be attributed to the low levels of GABA content in their brain.
Insights
Vaccinia-related kinase 2 (VRK2) deficiency in female zebrafish caused aggressive behavior and altered social interaction. This malbehavior is linked to reduced brain gamma-aminobutyric acid (GABA) levels.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Vaccinia-related kinase 2 (VRK2) is a kinase involved in cell proliferation and survival, also found in the brain.
- Genome-wide association studies suggest VRK2's role in neuropsychiatric disorders like schizophrenia.
- The precise function of VRK2 in the central nervous system and its link to disease remain unclear.
Purpose of the Study:
- To investigate the role of VRK2 in the central nervous system using a zebrafish model.
- To explore the behavioral and neurochemical consequences of VRK2 deficiency.
Main Methods:
- Evaluation of vrk2-deficient (vrk2-/-) zebrafish.
- Behavioral analysis including aggression and social preference tests.
- Measurement of brain neurotransmitter content (GABA) and neuronal morphology.
Main Results:
- Female vrk2-/- zebrafish exhibited significantly aggressive behavior and altered social preferences compared to wild-type (vrk2+/+) controls.
- vrk2-/- zebrafish displayed lower gamma-aminobutyric acid (GABA) levels in the brain.
- A higher density of neuronal dendrites was observed in the brains of vrk2-/- zebrafish.
Conclusions:
- Female vrk2-/- zebrafish serve as a relevant model for studying malbehavior, including aggression and social interaction deficits.
- The observed behavioral changes in VRK2-deficient zebrafish are associated with reduced brain GABAergic function.
- These findings highlight VRK2's potential role in regulating brain function and behavior relevant to neuropsychiatric disorders.
