University of Virginia, Charlottesville, Virginia, USA
As mental health conditions become more normalized and widespread, researchers continue to utilize model organisms such as Caenorhabditis elegans to better understand biological mechanisms underlying neurological and neuropsychiatric disorders. Previous studies indicate that mutations to genes coding for insulin signaling can influence the manifestation of Major Depressive Disorder and schizophrenia in human and nematode populations. As such, the effects of altered motivational states should be observed and compared between humans and nematodes. Two assays indicated mutations in the daf-2 gene lead to statistically significant differences in worm survival rate and population growth rate between the ancestral wild type and mutant E1370 C. elegans strains. Worms with the E1370 mutation showed a higher survival rate over a 30-day period and a slower population growth, peak, and decline than the ancestral strain. These findings may indicate how insulin signaling can lead to a lack of motivation in worm and potentially human subjects that can influence broad changes in overall population trends of growth, stabilization, and decline. These chemical and biological adjustments may allow for nematode subjects to conserve energy over extended periods of food deprivation. To gain a comprehensive insight and understanding of the impact of these genetic alterations, future studies should be conducted to observe how changes to other neurotransmitter concentrations and receptors affect survival rate and population growth of C. elegans. In turn, this may allow for conclusions to be drawn as to how genetic mutations influencing neurotransmission and resulting concentrations could explain behavioral shifts in humans.
Abbreviations: MDD – Major Depressive Disorder; IGF-1 – Insulin/Insulin-like Growth Factor 1; MLR – Multiple Linear Regression; GABA – Gamma-Aminobutyric Acid; WT – Wild Type; DMSO – Dimethyl Sulfoxide
Keywords: C. elegans; Major Depressive Disorder; Schizophrenia; Insulin Signaling; Motivation