Article Text

PRENATAL EXPOSURE TO SEROTONIN REUPTAKE INHIBITORS, BUT NOT MATERNAL MOOD, DECREASES NEONATAL S100B LEVELS
  1. J L Pawluski1,
  2. L A M Galea2,
  3. U Brain1,
  4. M Papsdorf1,
  5. T F Oberlander1
  1. 1Department of Pediatrics, University of British Columbia, Vancouver, British Columbia, Canada,
  2. 2Department of Psychology and Brain Research Centre, University of British Columbia, Vancouver, British Columbia, Canada

Abstract

Objectives: The development of the serotonergic system is dependent on serotonin-related astroglial-specific calcium binding protein, S100B. S100B mediates the growth of serotonin neurons and may reflect the developmental integrity of the brain, the effects of early adverse experience and developmental risk. This study was undertaken to determine whether prenatal exposure to serotonin reuptake inhibitor (SRI) antidepressants alters neonatal cord serum S100B levels.

Methods: Maternal depression and anxiety symptoms were assessed during the third trimester (33–36 weeks) using clinician-rated (Hamilton rating scale for anxiety; Hamilton rating scale for depression) and patient-rated measures (Edinburgh postnatal depression scale). Neonatal outcomes including Apgar scores, birth weight, gender and gestational age at birth were determined in 36 prenatally SRI-exposed neonates (230 ± 71 days) and compared with 14 non-exposed neonates. Serum S100B levels were assayed from maternal blood obtained at delivery and cord blood using a S100B ELISA (Biovendor).

Results: S100B levels were significantly lower in prenatally SRI-exposed neonates compared with non-exposed neonates when controlling for lower 5-minute Apgar scores and third trimester maternal mood (p<0.05). In addition, SRI-exposed mothers had significantly elevated maternal serum S100B levels compared with non-exposed mothers (p<0.1).

Conclusions: Prolonged prenatal SRI exposure is associated with lower cord S100B protein levels, even when controlling for depressed/anxious maternal mood. While these findings are consistent with other prenatal exposures that alter central serotonin (alcohol and cocaine), it remains to be determined whether this biomarker reflects altered early serotonergic system function and long-term developmental risk.

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