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Exploration of the Neuronal Subtype Specificity of an Ethanol Responsive Gene: Glycogen Synthase Kinase 3 Beta (Gsk3b)
Dalton Huey, Depts. of Bioinformatics, Biology & Chemistry, A. van der Vaart, G. M. Harris, and M. F. Miles, with Dr. Sarah Golding, Dept. of Biology
Previous work done in our laboratory revealed that Glycogen Synthase Kinase 3 Beta (Gsk3b) functions as a hub gene in a network of genes regulated by acute ethanol in the medial prefrontal cortex (mPFC) across a mouse genetic panel. Adult mice treated with acute ethanol showed increased phosphorylation of GSK3B on the Ser9 residue in prefrontal cortex. Subsequent viral-mediated overexpression of Gsk3bin mouse mPFC caused an increase in ethanol consumption and pharmacological inhibition of GSK3B decreased ethanol consumption. However, it is unknown what neuron subtypes are driving this change in behavior. Here, we provide evidence that deletion of Gsk3bin Camk2a+ glutamatergic neurons of the mPFC results in a decrease in ethanol consumption in both continuous and intermittent access drinking paradigms. Furthermore, we have recently designed and validated a plasmid for Cre-dependent overexpression of Gsk3b, along with a Cre-dependent reporter as a control. These plasmids are planned for use in conjunction with different Cre drivers for viral-mediated expression in any cell type. Dissection of the neural circuitry of this ethanol responsive pathway can lead to a better assessment of Gsk3bas a potential target for the treatment of alcohol use disorders. Work supported by grants R01A027581 and P50AA022537 to MFM.
Sarah Golding, Ph.D.
Virginia Commonwealth University. Undergraduate Research Opportunities Program
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