TY - JOUR
T1 - Differential involvement of the shell and core subterritories of the nucleus accumbens in latent inhibition and amphetamine-induced activity
AU - Weiner, I.
AU - Gal, G.
AU - Rawlins, J. N.P.
AU - Feldon, J.
N1 - Funding Information:
This research was supported by a grant from the Ministry of Science and The Arts of Israel, and the Commission of the European Community.
PY - 1996/11
Y1 - 1996/11
N2 - Latent inhibition (LI) consists of retardation in conditioning to a stimulus as a consequence of its prior non-reinforced preexposure. In view of findings that LI is disrupted in acute schizophrenic patients and evidence from animal experiments pointing to the involvement of the mesolimbic dopamine (DA) system in this phenomenon, the present study investigated the effects of electrolytic lesions to the shell and core subterritories of the nucleus accumbens on LI in rats (Expt. 1). LI was indexed by the amount of suppression of drinking in the presence of a tone that was either pre-exposed or not prior to its pairing with reinforcement (a foot shock). Expt. 2 tested the effects of the DA antagonist, haloperidol, on LI in shell- and core-lesioned animals. Expt. 3 tested the effects of shell and core lesions on spontaneous and amphetamine-induced locomotion. In Expt. 1, LI, i.e., lower suppression of drinking in the pre-exposed as compared to the non-pre-exposed animals, was obtained in the sham-operated condition. Core and shell lesions produced distinct effects on LI. Animals with core lesions developed LI, but exhibited an overall lower suppression of drinking in comparison to the sham-operated animals. In contrast, shell lesions led to a disappearance of LI. Expt. 2 replicated the differential effects of shell and core lesions on LI, although in this experiment, core lesion did not attenuate suppression of drinking. Haloperidol prevented shell-induced abolition of LI. In Expt. 3, shell- but not core-lesioned animals were more active than sham controls following amphetamine administration. These results provide evidence for functional differences between the shell and core subregions, as well as for the involvement of the mesolimbic DA system in LI.
AB - Latent inhibition (LI) consists of retardation in conditioning to a stimulus as a consequence of its prior non-reinforced preexposure. In view of findings that LI is disrupted in acute schizophrenic patients and evidence from animal experiments pointing to the involvement of the mesolimbic dopamine (DA) system in this phenomenon, the present study investigated the effects of electrolytic lesions to the shell and core subterritories of the nucleus accumbens on LI in rats (Expt. 1). LI was indexed by the amount of suppression of drinking in the presence of a tone that was either pre-exposed or not prior to its pairing with reinforcement (a foot shock). Expt. 2 tested the effects of the DA antagonist, haloperidol, on LI in shell- and core-lesioned animals. Expt. 3 tested the effects of shell and core lesions on spontaneous and amphetamine-induced locomotion. In Expt. 1, LI, i.e., lower suppression of drinking in the pre-exposed as compared to the non-pre-exposed animals, was obtained in the sham-operated condition. Core and shell lesions produced distinct effects on LI. Animals with core lesions developed LI, but exhibited an overall lower suppression of drinking in comparison to the sham-operated animals. In contrast, shell lesions led to a disappearance of LI. Expt. 2 replicated the differential effects of shell and core lesions on LI, although in this experiment, core lesion did not attenuate suppression of drinking. Haloperidol prevented shell-induced abolition of LI. In Expt. 3, shell- but not core-lesioned animals were more active than sham controls following amphetamine administration. These results provide evidence for functional differences between the shell and core subregions, as well as for the involvement of the mesolimbic DA system in LI.
KW - activity
KW - core
KW - latent inhibition
KW - nucleus accumbens
KW - rat
KW - shell
UR - http://www.scopus.com/inward/record.url?scp=0030297527&partnerID=8YFLogxK
U2 - 10.1016/S0166-4328(96)00051-4
DO - 10.1016/S0166-4328(96)00051-4
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AN - SCOPUS:0030297527
SN - 0166-4328
VL - 81
SP - 123
EP - 133
JO - Behavioural Brain Research
JF - Behavioural Brain Research
IS - 1-2
ER -