Early postnatal ethanol administration does not affect prepulse inhibition in rats.

Human prenatal ethanol exposure is associated with relatively widespread cognitive deficits but it is unclear whether general deficits in responsivity to sensory stimuli contribute to or underlie the deficits in later or more complex stages of information processing. The present experiment assessed the effects of early postnatal ethanol administration in rats on prepulse inhibition, with animals tested in adolescence (postnatal day (PD) 35) and early adulthood (PD 70). Animals were assigned to receive ethanol (5.25 g/kg) via intragastric intubation on PD 4-9, sham-intubation, or to a naive control group. Pre-exposure to ethanol did not differentially affect the magnitude of the response to the startle stimulus alone nor did it affect the percent inhibition of the startle response on trials with a prepulse stimulus. Male rats exhibited a greater percent inhibition than female rats on PD 35 at all interstimulus intervals (ISIs) except the shortest, 4 ms. Female rats exhibited a greater percent inhibition than male rats at all ISIs on PD 70. Collectively, these data demonstrate that cognitive deficits associated with early exposure to ethanol may not be attributable to deficits in sensorimotor gating, at least to the extent this construct is measured by prepulse inhibition.