Linked Life Data

10859697

Source:http://linkedlifedata.com/resource/pubmed/id/10859697

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-7-20
pubmed:abstractText
Amnesic shellfish poisoning, one of the shellfish poisoning syndromes, is caused by the marine diatom toxin domoic acid (DOM). While in adult rats, mice, monkeys and humans DOM poorly penetrates the blood-brain barrier, DOM has been shown to be very toxic to fetal in newborn mice, because the blood-brain barrier is incomplete during neurodevelopment. This fact may explain why neonates show a higher sensitivity to neurotoxins like DOM as compared to adult animals. Mechanistic studies on DOM's neurotoxicity have mainly concentrated on the investigation of DOM's effect on neuronal tissue. Recent studies have shown that glia is also involved in DOM's neurotoxicity to the adult as well as the developing nervous system. The scientific literature strongly supports the hypothesis that the microglia may play a critical role in mediating DOM's neurotoxic effects. However, the effect of DOM on microglia has not been systematically investigated. The literature supporting our hypothesis is presented and discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0306-9877
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Harcourt Publishers Ltd.
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
837-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The marine toxin domoic acid may affect the developing brain by activation of neonatal brain microglia and subsequent neurotoxic mediator generation.
pubmed:affiliation
Department of Pharmacology, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois, USA. amayer@midwestern.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't