Source:http://linkedlifedata.com/resource/pubmed/id/11007898
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
19
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pubmed:dateCreated |
2000-10-13
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pubmed:abstractText |
Ca(2+) signaling is important in many fundamental neuronal processes including neurotransmission, synaptic plasticity, neuronal development, and gene expression. In cerebellar Purkinje neurons, Ca(2+) signaling has been studied primarily in the dendritic region where increases in local Ca(2+) have been shown to occur with both synaptic events and spontaneous electrical activity involving P-type voltage-gated Ca(2+) channels (VGCCs), the predominant VGCC expressed by Purkinje neurons. Here we show that Ca(2+) signaling is also a prominent feature of immature Purkinje neurons at developmental stages that precede expression of dendritic structure and involves L-type rather than P-type VGCCs. Immature Purkinje neurons acutely dissociated from postnatal day 4-7 rat pups exhibit spontaneous cytoplasmic Ca(2+) oscillations. The Ca(2+) oscillations require entry of extracellular Ca(2+), are blocked by tetrodotoxin, are communicated to the nucleus, and correlate closely with patterns of endogenously generated spontaneous and evoked electrical activity recorded in the neurons. Immunocytochemistry showed that L-, N-, and P/Q-types of VGCCs are present on the somata of the Purkinje neurons at this age. However, only the L-type VGCC antagonist nimodipine effectively antagonized the Ca(2+) oscillations; inhibitors of P/Q and N-type VGCCs were relatively ineffective. Release of Ca(2+) from intracellular Ca(2+) stores significantly amplified the Ca(2+) signals of external origin. These results show that a somatic signaling pathway that generates intracellular Ca(2+) oscillations and involves L-type VGCCs and intracellular Ca(2+) stores plays a prominent role in the Ca(2+) dynamics of early developing Purkinje neurons and may play an important role in communicating developmental cues to the nucleus.
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pubmed:grant | |
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,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Glial Fibrillary Acidic Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1529-2401
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7394-403
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11007898-Action Potentials,
pubmed-meshheading:11007898-Animals,
pubmed-meshheading:11007898-Calcium,
pubmed-meshheading:11007898-Calcium Channel Blockers,
pubmed-meshheading:11007898-Calcium Channels, L-Type,
pubmed-meshheading:11007898-Calcium Signaling,
pubmed-meshheading:11007898-Cell Nucleus,
pubmed-meshheading:11007898-Cells, Cultured,
pubmed-meshheading:11007898-Cerebellum,
pubmed-meshheading:11007898-Cytoplasm,
pubmed-meshheading:11007898-Glial Fibrillary Acidic Protein,
pubmed-meshheading:11007898-Patch-Clamp Techniques,
pubmed-meshheading:11007898-Purkinje Cells,
pubmed-meshheading:11007898-Rats,
pubmed-meshheading:11007898-Sodium Channel Blockers,
pubmed-meshheading:11007898-gamma-Aminobutyric Acid
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pubmed:year |
2000
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pubmed:articleTitle |
L-Type calcium channels mediate calcium oscillations in early postnatal Purkinje neurons.
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pubmed:affiliation |
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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