Linked Life Data

16903859

Source:http://linkedlifedata.com/resource/pubmed/id/16903859

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-8-14
pubmed:abstractText
Evidence suggests that neurotrophins are essential for the survival and phenotypic maintenance of cholinergic basal forebrain (BF) neurons. We evaluated the pattern of programmed cell death in the BF of the rat during development and after ablations of the cerebral cortex, a major target area and source of neurotrophins for BF neurons. We identified dying cells using the TUNEL (terminal deoxynucleotidyl-transferase-mediated dUTP-biotin nick end labelling) method and confirmed their apoptotic morphology with electron microscopy. Moreover, we demonstrated the expression of the apoptotic marker active caspase-3 in cells with features of apoptosis. TUNEL(+) cells were present in the developing BF during the first two postnatal weeks. Their frequency peaked at postnatal day (P)1 and at P5. TUNEL used in conjunction with immunofluorescence for neuronal nuclear protein (NeuN) showed that, at both peak stages, the majority of apoptotic cells were neurons. Extensive lesions of the cerebral cortex at different ages (P0, P7 and P14) did not induce significant changes in the frequency of apoptotic BF neurons. However, they resulted in alterations in the morphological phenotype of choline acetyltransferase (ChAT)-immunoreactive neurons in the BF, and a reduction in their number which was inversely proportional to the age at which the lesions were performed. We suggest that: (i) apoptosis is temporally coordinated with the morphological and neurochemical differentiation of BF neurons and the establishment of connections with their target areas; and (ii) cortical ablations do not affect the survival of BF neurons, but they influence the phenotype of cholinergic BF neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
573-85
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16903859-Acetylcholine, pubmed-meshheading:16903859-Aging, pubmed-meshheading:16903859-Animals, pubmed-meshheading:16903859-Animals, Newborn, pubmed-meshheading:16903859-Apoptosis, pubmed-meshheading:16903859-Basal Nucleus of Meynert, pubmed-meshheading:16903859-Caspase 3, pubmed-meshheading:16903859-Caspases, pubmed-meshheading:16903859-Cerebral Cortex, pubmed-meshheading:16903859-Choline O-Acetyltransferase, pubmed-meshheading:16903859-Denervation, pubmed-meshheading:16903859-Immunohistochemistry, pubmed-meshheading:16903859-In Situ Nick-End Labeling, pubmed-meshheading:16903859-Microscopy, Electron, Transmission, pubmed-meshheading:16903859-Nerve Degeneration, pubmed-meshheading:16903859-Nerve Tissue Proteins, pubmed-meshheading:16903859-Neural Pathways, pubmed-meshheading:16903859-Neurons, pubmed-meshheading:16903859-Nuclear Proteins, pubmed-meshheading:16903859-Phenotype, pubmed-meshheading:16903859-Rats, pubmed-meshheading:16903859-Rats, Wistar
pubmed:year
2006
pubmed:articleTitle
Apoptosis in the rat basal forebrain during development and following lesions of connections.
pubmed:affiliation
Department of Anatomy and Histology, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't