Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-7-3
pubmed:abstractText
Several studies suggest a pivotal role of amyloid beta (Abeta)(1-42) and nitric oxide (NO) in the pathogenesis of Alzheimer's disease. NO also possess central neuromodulatory properties. To study the soluble Abeta(1-42) effects on dopamine concentrations in rat prefrontal cortex, microdialysis technique was used. We showed that i.c.v. injection or retrodialysis Abeta(1-42) administration reduced basal and K(+)-stimulated dopamine levels, measured 2 and 48 h after peptide administration. Immunofluorescent experiments revealed that after 48 h from i.c.v. injection Abeta(1-42) was no longer detectable in the ventricular space. We then evaluated the role of NO on Abeta(1-42)-induced reduction in dopamine concentrations. Subchronic L-arginine administration decreased basal dopamine levels, measured either 2 h after i.c.v. Abeta(1-42) or on day 2 post-injection, whereas subchronic 7-nitroindazole administration increased basal dopamine concentrations, measured 2 h after i.c.v. Abeta(1-42) injection, and decreased them when measured on day 2 post-Abeta(1-42)-injection. No dopaminergic response activity was observed after K(+) stimulation in all groups. These results suggest that the dopaminergic system seems to be acutely vulnerable to soluble Abeta(1-42) effects. Finally, the opposite role of NO occurring at different phases might be regarded as a possible link between Abeta(1-42)-induced effects and dopaminergic dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
652-63
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Soluble amyloid beta1-42 reduces dopamine levels in rat prefrontal cortex: relationship to nitric oxide.
pubmed:affiliation
Department of Biomedical Sciences, University of Foggia, Foggia, Italy. trabace@unifg.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't