Linked Life Data

16472930

Source:http://linkedlifedata.com/resource/pubmed/id/16472930

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-5-5
pubmed:abstractText
The uncrossed retinotectal projection of rats undergoes extensive axonal elimination and subsequent growth of axonal arbors in topographically appropriate territories within the first two/three postnatal weeks. Nitric oxide has been implicated in development and stabilization of synapses in the retinotectal pathway since blockade of nitric oxide synthesis disrupts the normal pattern of retinal innervation in subcortical nuclei. The present work investigated the role of arachidonic acid pathway in the development and maintenance of ipsilateral retinotectal axons. We also investigated the role of this retrograde messenger in the modulation of plasticity that follows retinal lesions in the opposite eye. Pigmented rats received systemic treatment with quinacrine, a phospholipase A2 inhibitor, indomethacin, a cyclooxygenase inhibitor, nordihydroguaiaretic acid, a 5-lipoxygenase inhibitor or vehicle during 4-8 days at various postnatal ages. Rats given a unilateral temporal retinal lesion were treated with either quinacrine or vehicle during the same period. For anterograde tracing of ipsilateral retinal projections, animals received intraocular injections of horseradish peroxidase. Before the third postnatal week no difference was observed in the laminar or topographic organization of the ipsilateral retinotectal projection between vehicle and treated rats in either normal or lesion conditions. After the third postnatal week, however, systemic blockade of phospholipase A2 or 5-lipoxygenase, but not cyclooxygenase induced sprouting of uncrossed axons throughout the collicular visual layers in unoperated rats. In retinal lesion groups, phospholipase A2 blockade increased the sprouting of uncrossed intact axons to the collicular surface in the same period. The results suggest that arachidonic acid or lipoxygenase metabolites play a role in the maintenance of the retinotectal synapses after the critical period and that the blockade of the arachidonic acid pathway induces reactive sprouting of retinal axons late in development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
139
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
979-89
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16472930-Animals, pubmed-meshheading:16472930-Animals, Newborn, pubmed-meshheading:16472930-Arachidonic Acid, pubmed-meshheading:16472930-Enzyme Inhibitors, pubmed-meshheading:16472930-Immunohistochemistry, pubmed-meshheading:16472930-Indomethacin, pubmed-meshheading:16472930-Lipoxygenase Inhibitors, pubmed-meshheading:16472930-Neuronal Plasticity, pubmed-meshheading:16472930-Nordihydroguaiaretic Acid, pubmed-meshheading:16472930-Phospholipases A, pubmed-meshheading:16472930-Phospholipases A2, pubmed-meshheading:16472930-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:16472930-Quinacrine, pubmed-meshheading:16472930-Rats, pubmed-meshheading:16472930-Retina, pubmed-meshheading:16472930-Signal Transduction, pubmed-meshheading:16472930-Synapses, pubmed-meshheading:16472930-Synaptic Transmission, pubmed-meshheading:16472930-Visual Pathways
pubmed:year
2006
pubmed:articleTitle
Blockade of arachidonic acid pathway induces sprouting in the adult but not in the neonatal uncrossed retinotectal projection.
pubmed:affiliation
Instituto de Biofísica Carlos Chagas Filho, UFRJ, Rio de Janeiro, RJ, Brazil.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't