SSRIs like Prozac and Lexapro block the actions of a type of protein called a serotonin transporter, which removes the neurotransmitter serotonin from the signaling space between neurons. Dr. Andrews and her team also studied mice that had been genetically engineered to have a reduction or absence of serotonin transporters in the brain, so they were able to compare the effects of early exposure to antidepressants with the effects of the mice’s permanent reductions in serotonin transporter function.
In humans, genetic reductions in serotonin transporters are thought to be a risk factor for developing anxiety and mood disorders, particularly when combined with stressful life experiences. In fact, in Dr. Andrews’ study, the genetically engineered mice showed more anxiety as adults. “It might be possible that when mothers are treated for depression or anxiety during pregnancy, certain SSRIs taken by the mother may prevent the children from developing the disorders later in their lives,” Dr. Andrews says.
Based on the findings, Dr. Andrews and her team suspect that early exposure to Lexapro might alter the way serotonin neurons innervate brain regions involved in mood and anxiety behavior — a concept they plan to investigate in the future. They also plan to evaluate other SSRIs such as Paxil and Zoloft. “Current antidepressant therapies are ineffective in treating anxiety and depression in large numbers of patients, and advances in predicting individual responses are hindered by difficulties associated with characterizing complex influences of genetic and environmental factors on serotonergic transmission in humans,” the study states. “Highly controlled animal models, such as those studied here, represent avenues by which to identify factors potentially influencing behavioral domains associated with emotion-related disorders.”
“Perinatal vs. Genetic Programming of Serotonin States Associated with Anxiety,”