This study investigated whether prenatal exposure to cocaine alters re
flex excitability in adulthood. Pregnant rats received 30 or 60 mg/kg/
day cocaine HCl i.g. during gestational days 8-22. Vehicle treated con
trol rats were pair-fed/watered to rats receiving 60 mg/kg cocaine. A
non-treated control group was also maintained. At parturition, litters
from all four groups were surrogate fostered and then weaned at 21 da
ys of age. In adulthood, rats were tested in an acoustic startle respo
nse (ASR) apparatus for 120 trials using a 116 dB signal on 2 consecut
ive days. On Day 2: subjects received a single injection of d-amphetam
ine sulfate s.c. (1.0 mg/kg) just prior to testing. ASR amplitude and
latency were recorded. For average amplitude, significant effects for
prenatal treatment were observed. Cocaine-exposed female rats demonstr
ated decreased ASR amplitude compared to offspring of pair-fed control
s during both the initial test Session and following amphetamine admin
istration as well. Overall, amphetamine increased startle. For latency
, there were no significant treatment effects or effects of amphetamin
e administration. However, preplanned comparisons indicated that prena
tal cocaine exposure interacted with trial block. Therefore, these dat
a indicate that prenatal cocaine decreased startle amplitude in adults
, primarily in females, and that startle-elicited amphetamine response
s were dampened as well. The effects on latency indicate that amphetam
ine does not alter reaction times in prenatal cocaine exposed rats whi
le it does in controls.