Deviations in brain early serotonergic development as a result of fetal alcohol exposure.

Abstract

Serotonin (5-HT) has specific roles not only as a transmitter but also as a signal for differentiation. We recently found that alcohol drinking during pregnancy resulted in incomplete-neural-tube-fusion which hindered the development of midline cells such as 5-HT neurons in mice. We now report that, at the birth of 5-HT neurons (E11), the 5-HT immunoreative (5-HT-im) neurons are often found missing medial projecting fibers towards ventricle in the Alcohol treated group (ALC) as compared with pair-fed (PF) and Chow-fed groups (Chow) in mice. At E13, there are fewer 5-HT-im neurons in either dorsal or median raphe of ALC as compared with PF or Chow; furthermore, neurite outgrowth and migration of the 5-HT neurons are also compromised with alcohol exposure. We, thus, demonstrated that fetal alcohol exposure compromised 5-HT development as early as at the 5-HT neuron birth. Since 5-HT is a signal for development of many forebrain neurons, the deviation of 5-HT in early life may have consequences on brain development that extend beyond those seen in the 5-HT system.