class=""h4"">Background
Maternal al
cohol use during pregnan
cy
causes a
continuum of long-lasting disabilities in the offspring,
commonly referred to as fetal al
cohol spe
ctrum disorder (FASD). Attention-defi
cit/hypera
ctivity disorder (ADHD) is possibly the most
common behavioral problem in
children with FASD and devising strategies that ameliorate this
condition has great
clini
cal relevan
ce. Studies in rodent models of ADHD and FASD suggest that impairments in the
cAMP signaling
cas
cade
contribute to the hypera
ctivity phenotype. In this work, we investigated whether the
cAMP levels are affe
cted in a long-lasting manner by ethanol exposure during the third trimester equivalent period of human gestation and whether the a
cute administration of the PDE1 inhibitor vinpo
cetine ameliorates the ethanol-indu
ced hypera
ctivity.
class=""h4"">Methods
From postnatal day (P) 2 to P8, Swiss mice either received ethanol (5 g/kg i.p.) or saline every other day. At P30, the animals either received vinpocetine (20 mg/kg or 10 mg/kg i.p.) or vehicle 4 h before being tested in the open field. After the test, frontal cerebral cortices and hippocampi were dissected and collected for assessment of cAMP levels.
class=""h4"">Results
Early alcohol exposure significantly increased locomotor activity in the open field and reduced cAMP levels in the hippocampus. The acute treatment of ethanol-exposed animals with 20 mg/kg of vinpocetine restored both their locomotor activity and cAMP levels to control levels.
class=""h4"">Conclusions
These data lend support to the idea that cAMP signaling system contribute to the hyperactivity induced by developmental alcohol exposure and provide evidence for the potential therapeutic use of vinpocetine in FASD.