Key result
Altered DISC1 expression in astrocytes decreased glucose uptake and lactate production, contributing to abnormal affective behaviors and deficient spatial memory in mice that were rescued by systemic L-lactate administration.
Population
Primary mouse astrocytes and transgenic mice with astrocyte-selective expression of dominant-negative…
Comparison
Knockdown of endogenous mouse Disc1 or… vs Control primary astrocytes; control mice…
Design
Preclinical, Mice were randomly allocated to different treatment groups., Data…
Authors
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Astrocytic lactate deficits may drive DISC1 phenotypes in mice; hypothesis-generating for human mood and cognitive disorders.
p-value: p=<0.05
DISC1 regulates lactate production in astrocytes, and its abnormal expression leads to energy supply deficits that may contribute to mood and cognitive disorders.
Jouroukhin et al. (2018) studied Psychiatric disorders (Schizophrenia, depression, bipolar disorder). DISC1 knockdown / DN-DISC1 expression and L-lactate treatment vs. Control astrocytes / vehicle-treated mice was evaluated on Lactate production and behavioral performance (EPM, FST, TFC) (p=<0.05). Altered DISC1 expression in astrocytes decreased glucose uptake and lactate production, contributing to abnormal affective behaviors and deficient spatial memory in mice that were rescued by systemic L-lactate administration.
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