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Lian-sheng Zhao

2 papers in the library · publishing 2021-2022

Papers

Chronic lithium treatment ameliorates ketamine-induced mania-like behavior via the PI3K-AKT signaling pathway

Zoological Research November 18, 2022 Rongjun Ni, Tianhao Gao, Yi-Yan Wang et al.

Chronic lithium exposure reduces mania-like behavior and c-Fos expression in the medial prefrontal cortex of adult male mice treated with ketamine. Transcriptome sequencing of the prefrontal cortex shows that lithium inactivates the PI3K-AKT signaling pathway. Inhibiting AKT signaling with MK2206 or knocking down AKT in the mPFC reverses ketamine-induced mania, while activating AKT with SC79 promotes mania in low-dose ketamine-treated mice. Inhibiting PI3K with LY294002 also reverses mania, but inhibiting mTOR with rapamycin has no effect. Lithium may therefore ameliorate ketamine-induced mania via the PI3K-AKT pathway, suggesting a novel target for bipolar disorder treatment.

Chronic lithium exposure attenuates ketamine-induced mania-like behavior and c-Fos expression in the forebrain of mice.

Pharmacology, Biochemistry and Behavior January 12, 2021 Tianhao Gao, Rongjun Ni, Shasha Liu et al.

Pretreatment with lithium moderates the effects of a single dose of ketamine on mania-like behavior and c-Fos expression in the mouse forebrain. Ketamine increased movement and induced higher c-Fos expression in several forebrain regions, including the lateral septal nucleus, hypothalamus, amygdala, and hippocampus. Chronic lithium treatment attenuated the ketamine-induced increase in movement and inhibited the rise in c-Fos-immunoreactive neurons in the dentate gyrus, CA1, dorsal and ventral subiculum, and amygdaloid nuclei. These findings may help understand mania episodes related to ketamine treatment for major depressive disorder and bipolar disorder.