Abstract
Perinatal alcohol exposure (AE) has multiple detrimental effects on cognitive and various behavioral outcomes, but little is known about its impact on the autonomic functions. In a rat model of fetal alcohol spectrum disorders (FASD), we investigated neurochemical and neuroanatomical alterations in two brainstem nuclei, the hypoglossal nucleus (XIIn) and the dorsal nucleus of the vagus nerve (Xdn). One group of male Sprague-Dawley rats (n=6) received 2.625 g/kg ethanol intragastrically twice daily on postnatal days (PD) 4-9, a period equivalent to the third trimester of human pregnancy, and another group (n=6) was sham-intubated. On PD 18-19, the rats were perfused and medullary sections were immunohistochemically processed for choline acetyltransferase (ChAT) or two aminergic receptors that mediate excitatory drive to motoneurons, α&sub1;-adrenergic (α&sub1;-R) and serotonin 2A (5-HT(2A)-R), and c-Fos. Based on ChAT labeling, AE rats had reduced numbers of motoneurons in the ventral XIIn (XIIn-v; 35.4±1.3 motoneurons per side and section vs. 40.0±1.2, p=0.022), but not in the dorsal XIIn or Xdn. Consistent with ChAT data, both the numbers of α&sub1;-R-labeled motoneurons in the XIIn-v and the area of the XIIn-v measured using 5-HT(2A)-R staining were significantly smaller in AE rats (19.7±1.5 vs. 25.0±1.4, p=0.031 and 0.063 mm² ±0.002 vs. 0.074±0.002, p=0.002, respectively). Concurrently, both 5-HT(2A)-R and c-Fos staining tended to be higher in AE rats, suggesting an increased activation. Thus, postnatal AE causes motoneuronal loss in the XIIn-v. This may compromise upper airway control and contribute to increased risk of upper airway obstructions and sudden infant death in FASD victims.