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

TitleChronic intracerebroventricular exposure to β-amyloid(1-40) impairs object recognition but does not affect spontaneous locomotor activity or sensorimotor gating in the rat
Authors
Issue Date2001
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00221/index.htm
Citation
Experimental Brain Research, 2001, v. 136 n. 1, p. 93-100 How to Cite?
AbstractThis study examined the cognitive effects of chronic in vivo exposure to β-amyloid(1-40) via the intracerebroventricular route on two distinct paradigms. The first test evaluated a form of early attentional control referred to as sensorimotor gating in which an antecedent weak prepulse stimulus modulates the reactivity to a subsequent startle-eliciting stimulus. The second 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 found that β-amyloid exposure leads to a severe deficit in the object memory test but spares sensorimotor gating. Moreover, unlike the water maze deficit induced by β-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 results add to previous reports that β-amyloid exposure can lead to deficits on hippocampal lesion sensitive tasks, suggesting that dysfunction of the rhinal cortices in addition to that of the septohippocampal system is implicated in β-amyloid-induced behavioral impairments. It therefore lends support to the hypothesis that β-amyloid exposure can lead to severe impairment across multiple memory systems.
Persistent Identifierhttp://hdl.handle.net/10722/171692
ISSN
2015 Impact Factor: 2.057
2015 SCImago Journal Rankings: 1.140
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNag, Sen_US
dc.contributor.authorTang, Fen_US
dc.contributor.authorYee, BKen_US
dc.date.accessioned2012-10-30T06:16:24Z-
dc.date.available2012-10-30T06:16:24Z-
dc.date.issued2001en_US
dc.identifier.citationExperimental Brain Research, 2001, v. 136 n. 1, p. 93-100en_US
dc.identifier.issn0014-4819en_US
dc.identifier.urihttp://hdl.handle.net/10722/171692-
dc.description.abstractThis study examined the cognitive effects of chronic in vivo exposure to β-amyloid(1-40) via the intracerebroventricular route on two distinct paradigms. The first test evaluated a form of early attentional control referred to as sensorimotor gating in which an antecedent weak prepulse stimulus modulates the reactivity to a subsequent startle-eliciting stimulus. The second 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 found that β-amyloid exposure leads to a severe deficit in the object memory test but spares sensorimotor gating. Moreover, unlike the water maze deficit induced by β-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 results add to previous reports that β-amyloid exposure can lead to deficits on hippocampal lesion sensitive tasks, suggesting that dysfunction of the rhinal cortices in addition to that of the septohippocampal system is implicated in β-amyloid-induced behavioral impairments. It therefore lends support to the hypothesis that β-amyloid exposure can lead to severe impairment across multiple memory systems.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00221/index.htmen_US
dc.relation.ispartofExperimental Brain Researchen_US
dc.subject.meshAcoustic Stimulation - Methodsen_US
dc.subject.meshAmyloid Beta-Peptides - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCerebral Ventricles - Drug Effects - Physiologyen_US
dc.subject.meshCholinesterase Inhibitors - Pharmacologyen_US
dc.subject.meshEntorhinal Cortex - Drug Effects - Physiologyen_US
dc.subject.meshHippocampus - Drug Effects - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMotor Activity - Drug Effects - Physiologyen_US
dc.subject.meshParathion - Pharmacologyen_US
dc.subject.meshPeptide Fragments - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRecognition (Psychology) - Drug Effects - Physiologyen_US
dc.subject.meshStartle Reaction - Drug Effects - Physiologyen_US
dc.titleChronic intracerebroventricular exposure to β-amyloid(1-40) impairs object recognition but does not affect spontaneous locomotor activity or sensorimotor gating in the raten_US
dc.typeArticleen_US
dc.identifier.emailTang, F:ftang@hkucc.hku.hken_US
dc.identifier.authorityTang, F=rp00327en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s002210000561en_US
dc.identifier.pmid11204417-
dc.identifier.scopuseid_2-s2.0-0035106488en_US
dc.identifier.hkuros71998-
dc.identifier.hkuros58311-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035106488&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume136en_US
dc.identifier.issue1en_US
dc.identifier.spage93en_US
dc.identifier.epage100en_US
dc.identifier.isiWOS:000166225400009-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridNag, S=7103093193en_US
dc.identifier.scopusauthoridTang, F=7201979770en_US
dc.identifier.scopusauthoridYee, BK=7006955693en_US

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