Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1996-11-6
pubmed:abstractText
We examined the effects of chronic NMDA receptor antagonism on the normal postnatal differentiation of calcium- and calmodulin-dependent kinase II (CaM kinase II) in the rat superior colliculus. At postnatal day (P) zero, most CaM kinase II protein, as well as CaM kinase II activity, was detected in the soluble fraction. In vitro phosphorylation of P0 superior colliculus revealed several prominent substrates in both the particulate and soluble fractions. At P19 there was more particulate enzyme than soluble enzyme, and CaM kinase II activity in the particulate fraction was higher than in P0 particulate tissue. Additionally, in vitro phosphorylation of P19 superior colliculus revealed many more CaM kinase II substrates. Chronic NMDA receptor antagonism with 2-amino-5-phosphonovalerate (DL-AP5) caused CaM kinase II to retain many of the characteristics of the enzyme found in P0 untreated superior colliculus. In P19 superior colliculus treated with LD-AP5 from birth, most of the protein was in the soluble fraction, CaM kinase II activity was largely restricted to the soluble fraction, and only a few substrates were observed by in vitro phosphorylation. These effects were not observed in tissue treated with the inactive isomer, L-AP5. These results suggest that synaptic maturation is slowed by antagonism of NMDA receptors during retinotopic map formation.
pubmed:grant
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
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1322-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Chronic NMDA receptor antagonism during retinotopic map formation depresses CaM kinase II differentiation in rat superior colliculus.
pubmed:affiliation
Yale University, Department of Biology, New Haven, CT 06520, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.