a4b2 nicotinic receptor stimulation of the GABAergic system within the orbitofrontal cortex ameliorates the severe crossmodal object recognition impairment in @entity3652 -treated @entity35 : Implications for XXXX in @entity161 .

@entity2227 @entity1246 @entity71718 @entity1027 @entity18686 @entity73 @entity1239 @entity3652 @entity161 @entity143 @entity35 @entity3390
@entity161 is associated with atypical multisensory integration. @entity35 treated sub-chronically with @entity143 receptor antagonists to model @entity161 are severely impaired on a tactile-to-visual crossmodal object recognition (CMOR) task, and this deficit is reversed by systemic @entity1239 . The current study assessed the receptor specificity of the ameliorative effect of @entity1239 in the CMOR task, as well as the potential for nicotinic receptor (nAChR) interactions with @entity1246 and @entity2227 . Male Long-Evans @entity35 were treated sub-chronically for 10 days with @entity3652 or saline and then tested on the CMOR task after a 10-day washout. Systemic @entity1239 given before the sample phase of the CMOR task reversed the @entity3652 -induced impairment, but this effect was blocked by co-administration of the GABAA receptor antagonist @entity1027 at a dosage that itself did not cause impairment. Pre-sample systemic co-administration of the @entity143 receptor antagonist @entity3390 did not block the remediating effect of @entity1239 in @entity3652 -treated @entity35 . The selective a7 nAChR agonist @entity18686 and a4b2 nAChR agonist @entity71718 were also tested, with only the latter reversing the @entity3652 impairment dose-dependently; @entity1027 also blocked this effect. Similarly, infusions of @entity1239 or @entity71718 into the orbitofrontal cortex (OFC) reversed the CMOR impairment in @entity3652 -treated @entity35 , and systemic @entity1027 blocked the effect of intra-OFC @entity71718 . These results suggest that @entity1239 -induced agonism of a4b2 nAChRs within the OFC ameliorates CMOR deficits in @entity3652 -treated @entity35 via stimulation of the GABAergic system. The findings of this research may have important implications for understanding the nature and potential treatment of @entity73 in @entity161 .
