K. Muneoka et al., PRENATAL DEXAMETHASONE EXPOSURE ALTERS BRAIN MONOAMINE METABOLISM ANDADRENOCORTICAL-RESPONSE IN RAT OFFSPRING, American journal of physiology. Regulatory, integrative and comparative physiology, 42(5), 1997, pp. 1669-1675
In this study, it has been clearly demonstrated that prenatal dexameth
asone treatment (Dex; 0.05 mg/kg on gestational days 17, 18, and 19) r
esulted in the significant reductions of 5-hydroxytryptamine (5-HT) tu
rnover in four brain regions, including the neocortex, hippocampus, hy
pothalamus, and midbrain + pons-medulla (M+P-M) but not in the striatu
m in the offspring at 3 and 14 wk of life, as well as dopamine turnove
r in the hypothalamus. [H-3]paroxetine binding densities were increase
d in the hypothalamus and M+P-M at 14 wk of life, which corresponded t
o increased 5-HT contents in both regions. On the other hand, signific
antly lower norepinephrine contents in the neocortex and hippocampus w
ere observed in the Dex group compared with the control group at 14 wk
of life. In addition, the exposure to new environmental condition ele
vated blood corticosterone levels and enhanced behavioral activities t
o a greater extent in the Dex group than in controls at 7 wk of life,
suggesting that elevated glucocorticoid levels during the pregnancy mi
micked prenatal mild stress, producing developmental alterations in br
ain monoamine metabolism, endocrine response, and behavior in adult of
fspring.