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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-9-25
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pubmed:abstractText |
Entry of calcium ions into the neuron is a triggering signal for initiation of several processes which may lead to modification of synaptic connectivity. The developmental changes of voltage-dependent L-type calcium channel (VDLCC) were studied using [3H]PN 200 110 nifedipine displaceable binding in the barrel cortex of mice, a model structure for studying cortical plasticity. In vitro binding autoradiography was used to examine quantitatively the pattern of [3H]PN 200 110 binding to brains of animals aged from 3 to 70 days. The binding values in the somatosensory cortex rose two-fold in the period examined, reaching a plateau in the 4th postnatal week. The laminar pattern of binding changed during development, with the locus of heaviest labeling shifting from layer IV to II/III in the third postnatal week and thin bands of labeling developing in layers IV and VI. A very faint barrel-like pattern of labeling in the barrel field was observed. Neither this pattern nor the binding values were altered by unilateral neonatal removal of all vibrissal follicles. Saturation studies of binding to crude synaptosomal fractions of cerebral cortex of mice aged 3, 15, 28 and 70 days revealed the presence of a single binding site, with Bmax increasing from 48.7 +/- 5.1 fmol/mg protein at postnatal day 3 to 191.7 +/- 9.6 fmol/mg protein at day 70. No developmental changes in KD values were found. No correlation was found between the critical period for cytoarchitectonic plasticity of the barrels and the time when high values of VDLCC binding were observed.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Dihydropyridines,
http://linkedlifedata.com/resource/pubmed/chemical/Isradipine,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0165-3806
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
67
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
293-300
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1324806-Aging,
pubmed-meshheading:1324806-Animals,
pubmed-meshheading:1324806-Autoradiography,
pubmed-meshheading:1324806-Binding, Competitive,
pubmed-meshheading:1324806-Calcium Channel Blockers,
pubmed-meshheading:1324806-Calcium Channels,
pubmed-meshheading:1324806-Dihydropyridines,
pubmed-meshheading:1324806-Isradipine,
pubmed-meshheading:1324806-Kinetics,
pubmed-meshheading:1324806-Mice,
pubmed-meshheading:1324806-Neuronal Plasticity,
pubmed-meshheading:1324806-Nifedipine,
pubmed-meshheading:1324806-Somatosensory Cortex,
pubmed-meshheading:1324806-Tritium,
pubmed-meshheading:1324806-Vibrissae
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pubmed:year |
1992
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pubmed:articleTitle |
Voltage-dependent L-type calcium channels in the development and plasticity of mouse barrel cortex.
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pubmed:affiliation |
Department of Neurophysiology, Nencki Institute, Warsaw, Poland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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