Systemic administration of @entity3390 produces an abnormally persistent latent inhibition which is reversed by @entity1088 but not XXXX .

@entity1088 @entity9178 @entity71 @entity1457 @entity2526 @entity161 @entity143 @entity1767 @entity35 @entity3390
RATIONALE: @entity9178 ( @entity9178 ) refers to retarded conditioning to a stimulus as a consequence of its inconsequential pre-exposure, and disrupted @entity9178 in the @entity35 is considered to model an @entity71 in @entity161 . Blockade of @entity143 receptor transmission, which produces behavioral effects potentially relevant to @entity161 symptomatology in several animal models, has been reported to spare @entity9178 . OBJECTIVES: To show that systemic administration of the non-competitive @entity143 antagonist @entity3390 will lead to an abnormally persistent @entity9178 which will emerge under conditions that disrupt @entity9178 in controls, and that this will be reversed by the atypical neuroleptic @entity1088 but not by the typical neuroleptic @entity1767 , as found for other @entity143 antagonist-induced models. METHODS: @entity9178 was measured in a thirst-motivated conditioned emotional response (CER) procedure by comparing suppression of drinking in response to a tone in @entity35 which previously received 0 (non-pre-exposed) or 40 tone exposures (pre-exposed) followed by two (experiment 1) or five (experiments 2-5) tone - foot @entity1457 . RESULTS: @entity3390 at doses of 0.1 and 0.2 mg/kg reduced conditioned suppression while no effect on suppression was seen at the 0.05 mg/kg dose. At the latter dose, intact @entity9178 was seen with parameters that produced @entity9178 in controls (40 pre-exposures and two conditioning trials). Raising the number of conditioning trials to five disrupted @entity9178 in control @entity35 , but @entity3390 -treated @entity35 continued to show @entity9178 , and this abnormally persistent @entity9178 was due to the action of @entity3390 in the conditioning stage. @entity3390 -induced @entity9178 was unaffected by both @entity1767 (0.1 mg/kg) and @entity1088 (5 mg/kg) administered in conditioning, and was reversed by @entity1088 but not by @entity1767 administered in pre-exposure. CONCLUSION: @entity3390 -induced perseveration of @entity9178 is consistent with other reports of perseverative behaviors, suggested to be particularly relevant to negative symptoms of @entity161 , following @entity143 receptor blockade. We suggest that @entity9178 may model impaired attentional set shifting associated with negative symptoms of @entity161 . Moreover, the finding that the action of @entity3390 on @entity9178 and the action of @entity1088 are exerted in different stages of the @entity9178 procedure suggests that the @entity3390 -based @entity9178 model may provide a unique screening tool for the identification of novel antipsychotic compounds, whereby the @entity161 -mimicking @entity2526 is drug-induced, but the detection of the antipsychotic action is not dependent on the mechanism of action of the pro-psychotic drug.
