Declan 

Present treatment of neuropsychiatric diseases, such as anxiety and depression, often targets the neurotransmitters dopamine and serotonin. Frequent treatment resistance warrants the advent of novel therapies that could benefit patients. Prior research suggests the deletion of Nsun2—a tRNA methyltransferase—results in complex behavioral changes relating to anxiety and depression, yet it is unclear whether those changes are a consequence of an increase in amino acid supply or altered tRNAs. This study focused on the amino acid glycine and replicated the phenotype found in mice lacking Nsun2 by deleting GLDC to disrupt the glycine cleavage system, which regulates glycine. One goal of this study was to determine if the direct increase in glycine, brought on by the ablation of the glycine cleavage system, is sufficient to see behavioral changes in escape motivation. Cre-lox recombination—a DNA cleavage system derived from a bacteriophage—was used to breed a mouse line with a compromised glycine cleavage system. After confirming increased glycine levels with fluorometric assays, the mice were subject to the forced swim test, and the results were analyzed to find the effect on behavioral despair. GLDC knockout mice, which had higher glycine levels, exhibited less behavioral despair than the control group. This directly links glycine metabolism to lower behavioral despair, providing the possibility of a new depression treatment that targets amino acids. Although these findings first need to be corroborated, the changes elicited by GLDC KO give reason for further research as it’s relevant to neuropsychiatric diseases.