Chronic intracerebroventricular exposure to beta-amyloid(1-40) impairs object recognition but does not affect spontaneous locomotor activity or sensorimotor gating in the rat

This study examined the cognitive effects of chronic in vivo exposure to be ta -amyloid(1-40) via the intracerebroventricular route on two distinct par adigms. The first test evaluated a form of early attentional control referr ed to as sensorimotor gating in which an antecedent weak prepulse stimulus modulates the reactivity to a subsequent startle-eliciting stimulus. The se cond test utilized the spontaneous preference for a novel object over that of a familiar one in rats as a measure of object recognition memory. We fou nd that beta -amyloid exposure leads to a severe deficit in the object memo ry test but spares sensorimotor gating. Moreover, unlike the water maze def icit induced by beta -amyloid (Nag et al., in preparation), the deficit on object recognition was resistant to amelioration by systemic physostigmine treatment at a dose of 0.06 mg/kg per day intraperitoneally. The present re sults add to previous reports that beta -amyloid exposure can lead to defic its on hippocampal lesion sensitive tasks, suggesting that dysfunction of t he rhinal cortices in addition to that of the septohippocampal system is im plicated in beta -amyloid-induced behavioral impairments. It therefore lend s support to the hypothesis that beta -amyloid exposure can lead to severe impairment across multiple memory systems.