Linked Life Data

15689567

Source:http://linkedlifedata.com/resource/pubmed/id/15689567

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-2-3
pubmed:abstractText
NMDA receptors (NMDARs) play an important role in the structural maintenance and functional strength of synapses. The causal relationship between these anatomical and functional roles is poorly defined. Using quantitative confocal microscopy, synaptic vesicle immunoreactivity, and differential label of retinal projections, we measured axon volume and synapse density along ipsilateral retinal axons (ipsi axons) sprouting into the superficial visual layers of the superior colliculus (sSC) deafferented by a contralateral retinal lesion (a scotoma) 8 d earlier. When retinal lesions were made at postnatal day 6 (P6), glutamatergic synaptic currents on neurons within the scotoma were significantly reduced. Both ipsi axon sprouting and synapse density were increased by chronic d-AP-5 antagonism of NMDARs. Conversely, ipsi axon sprouting and synapse density were reduced by chronic exposure to the agonist, NMDA, known to functionally depress glutamate transmission in this system. After P11 lesions, however, NMDAR blockade had no effect on sprouting or synapse density. Developmental changes in NMDAR current kinetics could not account for this difference in the structural effects of NMDAR function. Also, synaptic current frequencies within the scotoma were not affected after the P11 lesions. The corticocollicular projection matures during the P11 survival interval and, as indicated by previous work, it is a source of competition for synaptic space and probably of maintained activity in the older sSC. Thus, our results suggest that during early development, NMDAR currents predominantly destabilize nascent synapses. As the neuropil matures, however, competition for synaptic space suppresses axon sprouting and synapse formation regardless of NMDAR function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1291-303
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:15689567-Animals, pubmed-meshheading:15689567-Axons, pubmed-meshheading:15689567-Depression, Chemical, pubmed-meshheading:15689567-Excitatory Amino Acid Agonists, pubmed-meshheading:15689567-Excitatory Amino Acid Antagonists, pubmed-meshheading:15689567-GABA-A Receptor Antagonists, pubmed-meshheading:15689567-Microscopy, Confocal, pubmed-meshheading:15689567-N-Methylaspartate, pubmed-meshheading:15689567-Nerve Regeneration, pubmed-meshheading:15689567-Patch-Clamp Techniques, pubmed-meshheading:15689567-Rats, pubmed-meshheading:15689567-Rats, Sprague-Dawley, pubmed-meshheading:15689567-Receptors, AMPA, pubmed-meshheading:15689567-Receptors, GABA-A, pubmed-meshheading:15689567-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:15689567-Retina, pubmed-meshheading:15689567-Retinal Ganglion Cells, pubmed-meshheading:15689567-Scotoma, pubmed-meshheading:15689567-Single-Blind Method, pubmed-meshheading:15689567-Superior Colliculi, pubmed-meshheading:15689567-Synapses, pubmed-meshheading:15689567-Synaptic Transmission, pubmed-meshheading:15689567-Time Factors, pubmed-meshheading:15689567-Visual Pathways
pubmed:year
2005
pubmed:articleTitle
NMDA receptor currents suppress synapse formation on sprouting axons in vivo.
pubmed:affiliation
McGovern Institute for Brain Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. mcolonne@mit.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural