Linked Life Data

11145976

Source:http://linkedlifedata.com/resource/pubmed/id/11145976

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-1-23
pubmed:abstractText
It has been demonstrated that the endogenous cannabinoid receptor ligand, anandamide, and other N-acylethanolamines (NAEs), accumulate during neuronal injury in vitro, a process that may be linked to the neuroprotective effects of NAEs. The crucial step for generation of NAEs is the synthesis of the corresponding precursors, N-acylethanolamine phospholipids (NAPEs). However, it is unknown whether this key event for NAE formation is regulated differently in the context of insults causing necrotic or apoptotic neuronal death. To address this question, we monitored a range of cortical NAPE species in three infant rat models of in vivo neurodegeneration: (i) necrosis caused by intrastriatal injection of NMDA (25 nmol); (ii) apoptosis induced by systemic administration of the NMDA-receptor antagonist (+)MK-801 (3 x 0.5 mg/kg, i.p.); and (iii) apoptosis following focal necrosis triggered by concussive head trauma. A marked increase of all NAPE species was observed in both hemispheres 4 and 24 h after NMDA-induced injury, with a relatively larger increase in N-stearoyl-containing NAPE species. Thus, the percentage of the anandamide precursor fell from 1.1 to 0.5 mol %. In contrast, administration of (+)MK-801 did not alter cortical NAPE levels. Concussion head trauma resulted in a similar but less pronounced upregulation of NAPE levels at both 4 and 24 h as compared to NMDA injections. Increased levels of NAPE 24 h post-trauma possibly reflect that necrosis is still ongoing at this time point. Consequently, our data suggest that excitotoxic necrotic mechanisms of neurodegeneration, as opposed to apoptotic neurodegeneration, have a profound effect on in vivo NAE precursor homeostasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
39-46
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11145976-Animals, pubmed-meshheading:11145976-Apoptosis, pubmed-meshheading:11145976-Arachidonic Acids, pubmed-meshheading:11145976-Brain Injuries, pubmed-meshheading:11145976-Cerebral Cortex, pubmed-meshheading:11145976-Corpus Striatum, pubmed-meshheading:11145976-Disease Models, Animal, pubmed-meshheading:11145976-Dizocilpine Maleate, pubmed-meshheading:11145976-Ethanolamines, pubmed-meshheading:11145976-Male, pubmed-meshheading:11145976-N-Methylaspartate, pubmed-meshheading:11145976-Necrosis, pubmed-meshheading:11145976-Neurodegenerative Diseases, pubmed-meshheading:11145976-Neurons, pubmed-meshheading:11145976-Phospholipids, pubmed-meshheading:11145976-Polyunsaturated Alkamides, pubmed-meshheading:11145976-Rats, pubmed-meshheading:11145976-Rats, Sprague-Dawley, pubmed-meshheading:11145976-Rats, Wistar, pubmed-meshheading:11145976-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:11145976-Species Specificity, pubmed-meshheading:11145976-Wounds, Nonpenetrating
pubmed:year
2001
pubmed:articleTitle
Accumulation of the anandamide precursor and other N-acylethanolamine phospholipids in infant rat models of in vivo necrotic and apoptotic neuronal death.
pubmed:affiliation
Department of Pharmacology, The Royal Danish School of Pharmacy, Copenhagen, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't