Linked Life Data

2575464

Source:http://linkedlifedata.com/resource/pubmed/id/2575464

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-3-8
pubmed:abstractText
Brain development, examined at embryonic day 17, was retarded in murine trisomy 16 (Ts16). Ts16 is considered to serve as a model of the human trisomy 21 (Down's syndrome) by virtue of the presence in the mouse chromosome 16 of a set of genes located in humans in the segment of chromosome 21 that is requisite to produce the phenotypic features of Down's syndrome when present in triplicate. In addition to a reduction in brain size and cortical thickness, we observed a severe reduction throughout the brain in the density of muscarinic receptors, assessed by autoradiographic detection of specifically bound tritiated N-methyl-scopolamine, and by the failure of the development of the differentiated pattern of receptor distribution in the brainstem. The effect of gene dosage was also examined on specific neuronal populations. The distribution of acetylcholine esterase (AChE)-, tyrosine hydroxylase (TH)- and 5-hydroxytryptamine (5-HT)-positive cells in the trisomic brain was similar to that observed in chromosomally balanced littermates. On the other hand, the number of AChE-positive cells was 60-70% of the estimates in littermate controls in regions containing the septum, the vertical and horizontal limbs of the diagonal band and the basal forebrain cholinergic nuclei. Similarly, the number of TH-positive cells was reduced by about 30% in the pons. In contrast, in the trisomic foetuses the number of TH-positive cells in the mesencephalon and the diencephalon was similar to that in littermate controls, while that of 5-HT-positive cells in the mesencephalic nuclei was only slightly affected, if at all. Ts16 results, therefore, in a selective retardation of some neuronal systems, and this may lead to a perturbation of brain development. Furthermore, the systems whose development was retarded selectively are those which in Down's syndrome adults exhibit pronounced deficits of cells that--in case the murine Ts16 is a valid model--may also involve developmental disorders.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0165-3806
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Selective retardation of the development of the basal forebrain cholinergic and pontine catecholaminergic nuclei in the brain of trisomy 16 mouse, an animal model of Down's syndrome.
pubmed:affiliation
Collaborative Centre, National Institute for Medical Research, London, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't