B. Pouzet et al., The effects of radiofrequency lesion or transection of the fimbria-fornix on latent inhibition in the rat, NEUROSCIENC, 91(4), 1999, pp. 1355-1368
Latent inhibition consists of a decrement in conditioning to a stimulus as
a result of its prior non-reinforced pre-exposure. Based on evidence pointi
ng to the involvement of the hippocampus and the nucleus accumbens in laten
t inhibition disruption, it has been proposed that latent inhibition depend
s on the integrity of the subicular input to the nucleus accumbens. Since f
ibers originating in the subiculum and destined for the nucleus accumbens r
un through the fimbria-fornix, we assessed the effects of radiofrequency le
sion or transection of the fimbria-fornix, on latent inhibition. The effect
iveness of both lesions was demonstrated by the total disappearance of acet
ylcholinesterase staining in the hippocampus and of retrogradely labeled ce
lls in the hippocampus/subiculum following the injection of the retrograde
tracer biotin-dextran amine into the shell subregion of the nucleus accumbe
ns. Likewise, in accord with previously documented behavioral effects of le
sions to the hippocampus and related structures, both lesions increased spo
ntaneous activity and disrupted performance in Morris water maze, and the r
adiofrequency lesion facilitated the acquisition of two-way active avoidanc
e. In spite of the above, latent inhibition remained unaffected by both fim
bria-fornix lesions, indicating that the critical projections subserving la
tent inhibition are not those traversing the fimbria-fornix from the hippoc
ampus/subiculum to the nucleus accumbens.
The implications of these results for the neural circuitry of latent inhibi
tion and the latent inhibition model of schizophrenia are discussed. (C) 19
99 IBRO. Published by Elsevier Science Ltd.