| pubmed-article:9751781 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C1420841 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C2698300 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C1153410 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
| pubmed-article:9751781 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:9751781 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:9751781 | pubmed:dateCreated | 1998-10-22 | lld:pubmed |
| pubmed-article:9751781 | pubmed:abstractText | In comparison to the well characterized role of the principal subunit of voltage-gated Ca2+ channels, the pore-forming, antagonist-binding alpha1 subunit, considerably less is understood about how beta subunits contribute to neuronal Ca2+ channel function. We studied the role of the Ca2+ channel beta3 subunit, the major Ca2+ channel beta subunit in neurons, by using a gene-targeting strategy. The beta3 deficient (beta3-/-) animals were indistinguishable from the wild type (wt) with no gross morphological or histological differences. However, in sympathetic beta3-/- neurons, the L- and N-type current was significantly reduced relative to wt. Voltage-dependent activation of P/Q-type Ca2+ channels was described by two Boltzmann components with different voltage dependence, analogous to the "reluctant" and "willing" states reported for N-type channels. The absence of the beta3 subunit was associated with a hyperpolarizing shift of the "reluctant" component of activation. Norepinephrine inhibited wt and beta3-/- neurons similarly but the voltage sensitive component was greater for N-type than P/Q-type Ca2+ channels. The reduction in the expression of N-type Ca2+ channels in the beta3-/- mice may be expected to impair Ca2+ entry and therefore synaptic transmission in these animals. This effect may be reversed, at least in part, by the increase in the proportion of P/Q channels activated at less depolarized voltage levels. | lld:pubmed |
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| pubmed-article:9751781 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9751781 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751781 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9751781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751781 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9751781 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9751781 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:9751781 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:SmithS MSM | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:TsienR WRW | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:ShinH SHS | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:ChiuSS | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:LeeS BSB | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:SchellerR HRH | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:KimH LHL | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:NamkungYY | lld:pubmed |
| pubmed-article:9751781 | pubmed:author | pubmed-author:SkrypnykN VNV | lld:pubmed |
| pubmed-article:9751781 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9751781 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:9751781 | pubmed:volume | 95 | lld:pubmed |
| pubmed-article:9751781 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9751781 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9751781 | pubmed:pagination | 12010-5 | lld:pubmed |
| pubmed-article:9751781 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
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| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:meshHeading | pubmed-meshheading:9751781-... | lld:pubmed |
| pubmed-article:9751781 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9751781 | pubmed:articleTitle | Targeted disruption of the Ca2+ channel beta3 subunit reduces N- and L-type Ca2+ channel activity and alters the voltage-dependent activation of P/Q-type Ca2+ channels in neurons. | lld:pubmed |
| pubmed-article:9751781 | pubmed:affiliation | Department of Life Science, Pohang University of Science and Technology, San-31, Hyoja-Dong, Pohang, 790-784, Republic of Korea. | lld:pubmed |
| pubmed-article:9751781 | pubmed:publicationType | Journal Article | lld:pubmed |
