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Investigator Lynette C. Daws, Ph.D., and colleagues at the University of Texas Health Science Center at San Antonio, have found a mechanism that may explain why antidepressant treatments fail to work for a large percentage of people suffering from depression and other related disorders.
Reporting in the December Proceedings of the National Academy of Sciences, the authors state: “Mood disorders cause much suffering and are the single greatest cause of lost productivity worldwide. Although multiple medications, along with behavioral therapies, have proven effective for some individuals, millions of people lack an effective therapeutic option.”
A genetic defect in the serotonin transport protein 5-HTT, which transports the neurotransmitter serotonin in the brain, is believed to elevate the risk for multiple disorders, including anxiety, alcoholism and major depression. A class of antidepressant medications called SSRIs (selective serotonin reuptake inhibitors) works by increasing the level of serotonin available to bind to its receptor. When antidepressants fail to work, Dr. Daws and team hypothesized that it is due to the expression of other genes that inactivate the receptor; that an alternate transporter, organic transporter type 3 (OCT3), is upregulated in brains with defective 5-HTT expression, and may thus prevent the neurochemical events necessary for therapeutic benefit.
The researchers bred mice genetically engineered to mimic the 5-HTT defect. They demonstrated that blocking OCT3 had an antidepressant effect on the animals. Dr. Daws has stated that having a potential new brain target to boost serotonin levels might translate into better treatment for depression.
(This study was adapted from Proceedings of the National Academy of Sciences.)
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