The present experiments tested the effects of conventional (dorsal aspirati
on and electrolytic) and excitotoxic (N-methyl-D-aspartate [NMDA]) hippocam
pal lesions and fimbria-fornix (FF) transection on prepulse inhibition (PPI
) of startle response and on open-field activity. Activity was increased by
FF transection and by conventional but not excitotoxic hippocampal lesions
; complete NMDA lesion increased amphetamine-induced activity. Whereas dors
al hippocampal aspiration lesion disrupted PPI, the phenomenon was not affe
cted by dorsal hippocampal electrolytic lesion, partial or complete excitot
oxic (NMDA) hippocampal lesions, or complete FF transection, which interrup
ted the cholinergic input to the hippocampus as well as the hippocampal-sub
icular input to the nucleus accumbens. Systemic apomorphine disrupted PPI i
n both FF-transected rats and their controls. It is suggested that the hipp
ocampus is essential for PPI disruption rather than for PPI expression.