Linked Life Data

2598026

Source:http://linkedlifedata.com/resource/pubmed/id/2598026

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-2-6
pubmed:abstractText
Ethylcholine aziridinium ion (AF64) was synthesized from acetylethylcholine mustard hydrochloride and 5 nmol was infused into the third ventricle of rats. Seven days after AF64 treatment, sodium dependent high-affinity choline (HACU) uptake was decreased by 54% in the hypothalamus. The density of hypothalamic (-)-[3H]nicotine binding sites and [alpha-125I]bungarotoxin sites in AF64-treated animals did not differ significantly from controls. A second experiment was performed to elucidate the effect of AF64 treatment on HACU and determine the effect of AF64 on entrained circadian rhythms. Animals were infused with artificial CSF or 5 nmol AF64. Locomotor activity and body temperature were recorded for 3 weeks before and 3 weeks after treatment. Ten of 14 AF64-treated animals showed a decrease in the ratio of dark cycle:light cycle locomotor activity. The decrease in dark-cycle activity was correlated with a disruption of a predominant circadian rhythm. The circadian rhythm (CR) of core body temperature was disrupted only transiently, but the CR of locomotor activity remained disrupted for the duration of the experiment in several AF64-treated animals. HACU was decreased by 48% in animals with disrupted rhythms in comparison with controls but was not significantly decreased in AF64-treated animals with normal dark-cycle activity and circadian activity. These data suggest that the AF64-treated animal may be a good model for studying the role of acetylcholine in maintaining the integrity of certain circadian rhythms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
504
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
238-46
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
AF64 depletes hypothalamic high-affinity choline uptake and disrupts the circadian rhythm of locomotor activity without altering the density of nicotinic acetylcholine receptors.
pubmed:affiliation
Research Division, Boys Town National Institute for Communication Disorders in Children, Omaha, NE 68131.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't