Summary: Exposure to antidepressants during the first few weeks of pregnancy has long term implications for sensory processing in the offspring.
Source: SfN
Exposure to antidepressants during pregnancy and the first weeks of life can alter sensory processing well into adulthood, according to research in mice recently published in eNeuro.
Physicians are increasingly prescribing a common antidepressant to their pregnant patients, even though the effect on the fetus isn’t fully known. A working theory of depression implicates the neurotransmitter serotonin because many depressed patients experience relief when prescribed selective serotonin reuptake inhibitors (SSRIs). Whatever its role in depression, serotonin is critical for healthy brain development and function.
While previous research has shown changes in behavior and brain structure with prenatal and early life exposure to SSRIs, Rahn et al. explored changes in brain activity. After exposing mice to the SSRI fluoxetine during gestation and the first two weeks after birth, the team deployed optical imaging to examine the mouse brains exposed to fluoxetine and compare them to control mice. In the resting state, the brains of both sets of mice were nearly identical. When their front paws were stimulated, the fluoxetine-exposed mice displayed abnormal brain activity in sensory areas.
The effect was observed during adulthood in mice, suggesting this developmental exposure to SSRIs causes long-term changes to sensory processing.
Source:
SfN
Media Contacts:
Calli McMurray – SfN
Image Source:
The image is credited to Rahn et al., eNeuro 2019.
Original Research: Close access
“Maternal Fluoxetine Exposure Alters Cortical Hemodynamic and Calcium Response of Offspring to Somatosensory Stimuli”. Rachel M. Rahn, Susan E. Maloney, Lindsey M. Brier, Joseph D. Dougherty and Joseph P. Culver.
eNeuro doi:10.1523/ENEURO.0238-19.2019.
Abstract
Maternal Fluoxetine Exposure Alters Cortical Hemodynamic and Calcium Response of Offspring to Somatosensory Stimuli
Epidemiological studies have found an increased incidence of neurodevelopmental disorders in populations prenatally exposed to selective serotonin reuptake inhibitors (SSRIs). Optical imaging provides a minimally invasive way to determine if perinatal SSRI exposure has long-term effects on cortical function. Herein we probed the functional neuroimaging effects of perinatal SSRI exposure in a fluoxetine-exposed (FLX) mouse model. While resting-state homotopic contralateral functional connectivity was unperturbed, the evoked cortical response to forepaw stimulation was altered in FLX mice. The stimulated cortex showed decreased activity for FLX versus controls, by both hemodynamic responses (oxyhemoglobin [HbO2]) and neuronal calcium responses (Thy1-GCaMP6f fluorescence). Significant alterations in both cortical HbO2 and calcium response amplitude were seen in the cortex ipsilateral to the stimulated paw in FLX as compared to controls. The cortical regions of largest difference in activation between FLX and VEH also were consistent between HbO2 and calcium contrasts at the end of stimulation. Taken together, these results suggest a global loss of response signal amplitude in FLX versus controls. These findings indicate that perinatal SSRI exposure has long-term consequences on somatosensory cortical responses.
Significance Statement
Use of selective serotonin reuptake inhibitors (SSRIs) by pregnant women has increased in the past decades, raising questions regarding the long-term effects of SSRI usage during pregnancy on offspring. In order to isolate the effect of perinatal SSRI exposure from genetic variables or a maternal psychiatric diagnosis, we used in vivo functional neuroimaging to examine adult cortical function both at rest and in response to a somatosensory input in a mouse model of perinatal SSRI exposure. Our mouse model displayed no global disruption of brain function at rest when compared to controls, while its cortical response to a somatosensory stimulus was reduced, as measured by both hemodynamics and excitatory calcium signaling.
