Linked Life Data

10188950

Source:http://linkedlifedata.com/resource/pubmed/id/10188950

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-9-8
pubmed:abstractText
Neurotrophic factors are known to promote neuronal survival during development and after acute brain injury. Recent data suggest that some neuropeptides also exhibit neurotrophic activities, as shown for the pituitary adenylate cyclase activating polypeptide, which increases the survival of various neuronal populations in culture. Employing in situ hybridization techniques, we have studied the regulation of messenger RNA for pituitary adenylate cyclase activating polypeptide and its receptor type 1 after a moderate traumatic brain injury to rat brain cortex. We have further compared their messenger RNA expression to that of brain-derived neurotrophic factor and to the amount of cell death occurring in the brain at various times after the brain injury. Levels of brain-derived neurotrophic factor messenger RNA increased rapidly within 2 h after trauma in cortex and hippocampus, and returned to control levels thereafter. The levels of messenger RNA for pituitary adenylate cyclase activating polypeptide also increased with time in the injured brains and reached maximal expression at 72 h, i.e. the end of the observation period. The alterations in pituitary adenylate cyclase activating polypeptide messenger RNA levels were particularly pronounced in the perifocal region and in the ipsilateral dentate gyrus of the brain injury. In contrast, the messenger RNA levels encoding pituitary adenylate cyclase activating polypeptide receptor type 1 first decreased after trauma and were then normalized in the dentate gyrus. There was a large increase in the number of cells labelled for DNA breaks at 12 h post-trauma, indicative of enhanced cell death. The number of labelled cells, however, decreased at later stages concomitant with an increase in the expression of pituitary adenylate cyclase activating polypeptide messenger RNA. Pituitary adenylate cyclase activating polypeptide rescued cortical neurons in cultures against ionomycin-induced cell death, supporting the concept of a neuroprotective effect for the peptide. These results demonstrate a differential regulation of messenger RNA for brain-derived neurotrophic factor and the pituitary adenylate cyclase activating polypeptide and its receptor after brain trauma. The data also suggest that pituitary adenylate cyclase activating polypeptide might have a beneficial effect in brain injury by counteracting neuronal cell death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
235-47
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10188950-Animals, pubmed-meshheading:10188950-Brain, pubmed-meshheading:10188950-Brain Injuries, pubmed-meshheading:10188950-Brain-Derived Neurotrophic Factor, pubmed-meshheading:10188950-Cell Death, pubmed-meshheading:10188950-Disease Models, Animal, pubmed-meshheading:10188950-In Situ Hybridization, pubmed-meshheading:10188950-Male, pubmed-meshheading:10188950-Neurons, pubmed-meshheading:10188950-Neuropeptides, pubmed-meshheading:10188950-Pituitary Adenylate Cyclase-Activating Polypeptide, pubmed-meshheading:10188950-RNA, Messenger, pubmed-meshheading:10188950-Rats, pubmed-meshheading:10188950-Rats, Sprague-Dawley, pubmed-meshheading:10188950-Receptors, Pituitary Adenylate Cyclase-Activating..., pubmed-meshheading:10188950-Receptors, Pituitary Adenylate Cyclase-Activating..., pubmed-meshheading:10188950-Receptors, Pituitary Hormone
pubmed:year
1999
pubmed:articleTitle
Regulation of pituitary adenylate cyclase activating polypeptide and its receptor type 1 after traumatic brain injury: comparison with brain-derived neurotrophic factor and the induction of neuronal cell death.
pubmed:affiliation
Department of Neurosciences, Developmental Neurobiology, Biomedical Center, Uppsala, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't