Linked Life Data

10869803

Source:http://linkedlifedata.com/resource/pubmed/id/10869803

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-8-24
pubmed:abstractText
Although mutations in amyloid precursor protein (APP) are known to be involved in the development of Alzheimer's disease in some individuals, the role of this protein in normal brain function is poorly understood. We have reported previously that in APP-null mice long-term potentiation (LTP) in the CA1 region of the hippocampus is present but its magnitude is reduced compared to wild-type littermate controls. In the present study, we have confirmed this deficit using a different theta burst induction protocol. Significantly, however, we find that this deficit is no longer apparent when LTP experiments are performed following blockade of gamma-aminobutyric acid(A) receptors. These results suggest that the LTP process per se is not altered by the absence of APP. The deficit may therefore be an indirect consequence of other changes in the hippocampus that occur in the APP-null animal.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Similar levels of long-term potentiation in amyloid precursor protein -null and wild-type mice in the CA1 region of picrotoxin treated slices.
pubmed:affiliation
MRC Centre for Synaptic Plasticity and Department of Anatomy, University of Bristol, UK. s.m.fitzjohn@bris.ac.uk
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't