File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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
KeywordsAcetylcholine
Alzheimer's disease
Physostigmine
Prepulse inhibition
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
2021 Impact Factor: 2.064
2020 SCImago Journal Rankings: 0.782
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.subjectAcetylcholine-
dc.subjectAlzheimer's disease-
dc.subjectPhysostigmine-
dc.subjectPrepulse inhibition-
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
dc.identifier.issnl0014-4819-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats