The goal of these studies was to determine whether neonatal viral exposure
leads to a deficit in information processing in adulthood, To accomplish th
is, rats were infected neonatally with rat cytomegalovirus, and acoustic st
artle responses were measured when rats were 120 days old, Acoustic startle
was elicited by using a 118-decibel (dB) white noise alone or after a prep
ulse 10 dB above background (65 dB); responses were measured after an injec
tion of saline or the dopamine agonist apomorphine, Response amplitudes aft
er the pulse alone were not significantly altered by either viral exposure
or apomorphine, Responses of animals exposed to the prepulse before the pul
se were approximately 10% of that after the pulse alone and did not differ
between control or virus-exposed animals injected with saline, Animals inje
cted with apomorphine exhibited a greater startle response than animals inj
ected with saline, and control and virus-exposed rats injected with apomorp
hine differed in the magnitude of their responses. Apomorphine attenuated r
esponses after the prepulse, and virus-exposed animals exhibited more than
twice the attenuation than non-virus-exposed animals, Analysis of prepulse
inhibition, calculated from the acoustic startle data, indicated that altho
ugh viral exposure alone did not significantly affect information processin
g, when virus-injected rats were exposed to apomorphine, a significant 38%
decrease in prepulse inhibition was apparent. Findings demonstrate that rat
s infected neonatally with rat cytomegalovirus exhibit a deficit in sensori
motor gating upon dopamine stimulation, supporting a possible link between
viral infection and schizophrenia. (C) 1999 Wiley-Liss, Inc.