| pubmed-article:8261139 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C0003577 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C0524955 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C2004454 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C1704711 | lld:lifeskim |
| pubmed-article:8261139 | lifeskim:mentions | umls-concept:C1522240 | lld:lifeskim |
| pubmed-article:8261139 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8261139 | pubmed:dateCreated | 1994-1-27 | lld:pubmed |
| pubmed-article:8261139 | pubmed:abstractText | This study investigates the alterations in the spatiotemporal distribution pattern of the free intracellular Ca2+ concentration ([Ca2+]i) during axotomy and throughout the recovery process of cultured Aplysia neurons, and correlates these alterations with changes in the neurons input resistance and trans-membrane potential. For the experiments, the axons were transected while imaging the changes in [Ca2+]i with fura-2, and monitoring the neurons' resting potential and input resistance (Ri) with an intracellular microelectrode inserted into the cell body. The alterations in the spatiotemporal distribution pattern of [Ca2+]i were essentially the same in the proximal and the distal segments, and occurred in two distinct steps: concomitantly with the rupturing of the axolemma, as evidenced by membrane depolarization and a decrease in the input resistance, [Ca2+]i increased from resting levels of 0.05-0.1 microM to 1-1.5 microM along the entire axon. This is followed by a slower process in which a [Ca2+]i front propagates at a rate of 11-16 microns/s from the point of transection towards the intact ends, elevating [Ca2+]i to 3-18 microM. Following the resealing of the cut end 0.5-2 min post-axotomy, [Ca2+]i recovers in a typical pattern of a retreating front, travelling from the intact ends towards the cut regions. The [Ca2+]i recovers to the control level 7-10 min post-axotomy. In Ca(2+)-free artificial sea water (2.5 mM EGTA) axotomy does not lead to increased [Ca2+]i and a membrane seal is not formed over the cut end. Upon reperfusion with normal artificial sea water, [Ca2+]i is elevated at the tip of the cut axon and a membrane seal is formed. This experiment, together with the observations that injections of Ca2+, Mg2+ and Na+ into intact axons do not induce the release of Ca2+ from intracellular stores, indicates that Ca2+ influx through voltage gated Ca2+ channels and through the cut end are the primary sources of [Ca2+]i following axotomy. However, examination of the spatiotemporal distribution pattern of [Ca2+]i following axotomy and during the recovery process indicates that diffusion is not the dominating process in shaping the [Ca2+]i gradients. Other Ca2+ regulatory mechanisms seem to be very effective in limiting these gradients, thus enabling the neuron to survive the injury. | lld:pubmed |
| pubmed-article:8261139 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8261139 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8261139 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8261139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8261139 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8261139 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8261139 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:8261139 | pubmed:issn | 0953-816X | lld:pubmed |
| pubmed-article:8261139 | pubmed:author | pubmed-author:SpiraM EME | lld:pubmed |
| pubmed-article:8261139 | pubmed:author | pubmed-author:WanM CMC | lld:pubmed |
| pubmed-article:8261139 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8261139 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8261139 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:8261139 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8261139 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8261139 | pubmed:pagination | 657-68 | lld:pubmed |
| pubmed-article:8261139 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:8261139 | pubmed:meshHeading | pubmed-meshheading:8261139-... | lld:pubmed |
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| pubmed-article:8261139 | pubmed:meshHeading | pubmed-meshheading:8261139-... | lld:pubmed |
| pubmed-article:8261139 | pubmed:meshHeading | pubmed-meshheading:8261139-... | lld:pubmed |
| pubmed-article:8261139 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8261139 | pubmed:articleTitle | Spatiotemporal distribution of Ca2+ following axotomy and throughout the recovery process of cultured Aplysia neurons. | lld:pubmed |
| pubmed-article:8261139 | pubmed:affiliation | Department of Neurobiology, Hebrew University of Jerusalem, Israel. | lld:pubmed |
| pubmed-article:8261139 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8261139 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:8261139 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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