| pubmed-article:11978831 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11978831 | lifeskim:mentions | umls-concept:C0085140 | lld:lifeskim |
| pubmed-article:11978831 | lifeskim:mentions | umls-concept:C0021516 | lld:lifeskim |
| pubmed-article:11978831 | lifeskim:mentions | umls-concept:C1821244 | lld:lifeskim |
| pubmed-article:11978831 | lifeskim:mentions | umls-concept:C0068563 | lld:lifeskim |
| pubmed-article:11978831 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:11978831 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:11978831 | pubmed:dateCreated | 2002-4-29 | lld:pubmed |
| pubmed-article:11978831 | pubmed:abstractText | Serotonergic (5-HT) axons from the raphe nuclei are among the earliest afferents to innervate the developing forebrain. The present study examined whether GAP-43, a growth-associated protein expressed on growing 5-HT axons, is necessary for normal 5-HT axonal outgrowth and terminal arborization during the perinatal period. We found a nearly complete failure of 5-HT immunoreactive axons to innervate the cortex and hippocampus in GAP-43-null (GAP43-/-) mice. Abnormal ingrowth of 5-HT axons was apparent on postnatal day 0 (P0); quantitative analysis of P7 brains revealed significant reductions in the density of 5-HT axons in the cortex and hippocampus of GAP43-/- mice relative to wild-type (WT) controls. In contrast, 5-HT axon density was normal in the striatum, septum, and amygdala and dramatically higher than normal in the thalamus of GAP43-/- mice. Concentrations of serotonin and its metabolite, 5-hydroxyindolacetic acid, and norepinephrine were decreased markedly in the anterior and posterior cerebrum but increased in the brainstem of GAP43-/- mice. Cell loss could not account for these abnormalities, because unbiased stereological analysis showed no significant difference in the number of 5-HT dorsal raphe neurons in P7 GAP43-/- versus WT mice. The aberrant 5-HT innervation pattern persisted at P21, indicating a long-term alteration of 5-HT projections to forebrain in the absence of GAP-43. In heterozygotes, the density and morphology of 5-HT axons was intermediate between WT and homozygous GAP43-/- mice. These results suggest that GAP-43 is a key regulator in normal pathfinding and arborization of 5-HT axons during early brain development. | lld:pubmed |
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| pubmed-article:11978831 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11978831 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11978831 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11978831 | pubmed:month | May | lld:pubmed |
| pubmed-article:11978831 | pubmed:issn | 1529-2401 | lld:pubmed |
| pubmed-article:11978831 | pubmed:author | pubmed-author:DonovanStacy... | lld:pubmed |
| pubmed-article:11978831 | pubmed:author | pubmed-author:MamounasLaura... | lld:pubmed |
| pubmed-article:11978831 | pubmed:author | pubmed-author:AndrewsAnne... | lld:pubmed |
| pubmed-article:11978831 | pubmed:author | pubmed-author:BlueMary EME | lld:pubmed |
| pubmed-article:11978831 | pubmed:author | pubmed-author:McCaslandJame... | lld:pubmed |
| pubmed-article:11978831 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11978831 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11978831 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:11978831 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11978831 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11978831 | pubmed:pagination | 3543-52 | lld:pubmed |
| pubmed-article:11978831 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11978831 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11978831 | pubmed:articleTitle | GAP-43 is critical for normal development of the serotonergic innervation in forebrain. | lld:pubmed |
| pubmed-article:11978831 | pubmed:affiliation | Department of Cell and Developmental Biology, State University of New York Upstate Medical University, Syracuse, New York 13210, USA. | lld:pubmed |
| pubmed-article:11978831 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11978831 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11978831 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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