Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-10-23
pubmed:abstractText
Systemic administration of the mitochondrial toxin 3-nitropropionic acid (3NP) to rats produces striatal lesions that mimic some aspects of pathology in Huntington's disease (HD). To evaluate whether 3NP-induced lesions cause sensorimotor gating deficits observed in HD, we measured prepulse inhibition (PPI) of the acoustic startle reflex after systemic administration of 3NP (10, 15, or 20 mg/kg) to 5-month-old rats. PPI, the reduction of startle magnitude by a weak auditory prestimulus, is significantly reduced in patients with HD. Two daily injections of 3NP produced gross histologic evidence of striatal lesions in some rats and significantly reduced PPI. Striatal lesions also significantly disrupted amphetamine-induced stereotypy, another index of dorsal striatal function. 3NP thus reproduces a specific objective and quantifiable gating deficit found in patients with HD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
231
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Mitochondrial toxin 3-nitropropionic acid produces startle reflex abnormalities and striatal damage in rats that model some features of Huntington's disease.
pubmed:affiliation
Department of Psychiatry, UCSD School of Medicine, La Jolla, CA 92093-0804, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't