Linked Life Data

9426309

Source:http://linkedlifedata.com/resource/pubmed/id/9426309

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-3-23
pubmed:abstractText
The ion Ca2+ has been shown to play an important role in a wide variety of cellular functions, one of them being related to cell differentiation in which nerve growth factor (NGF) is involved. Chromaffin cells obtained from adrenals of 2- to 3-day-old rats were cultured for 7 days. During this time, these cells were subjected to the application of either NGF or extremely low frequency magnetic fields (ELF MF). Since this induced cell differentiation toward neuronal-like cells, the mechanism by which this occurred was studied. When the L-Ca2+ channel blocker nifedipine was applied simultaneously with ELF MF, this differentiation did not take place, but it did when an N-Ca2+ channel blocker was used. In contrast, none of the Ca2+ channel blockers prevented differentiation in the presence of NGF. In addition, Bay K-8644, an L-Ca2+ channel agonist, increased both the percentage of differentiated cells and neurite length in the presence of ELF MF. This effect was much weaker in the presence of NGF. [3H]-noradrenaline release was reduced by nifedipine, suggesting an important role for L-Ca2+ channels in neurotransmitter release. Total high voltage Ca2+ currents were significantly increased in ELF MF-treated cells with NGF, but these currents in ELF MF-treated cells were more sensitive to nifedipine. Amperometric analysis of catecholamine release revealed that the KCl-induced activity of cells stimulated to differentiate by ELF MF is highly sensitive to L-type Ca2+ channel blockers. A possible mechanism to explain the way in which the application of magnetic fields can induce differentation of chromaffin cells into neuronal-like cells is proposed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0302-766X
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
217-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9426309-3-Pyridinecarboxylic acid..., pubmed-meshheading:9426309-Adrenal Medulla, pubmed-meshheading:9426309-Animals, pubmed-meshheading:9426309-Calcium, pubmed-meshheading:9426309-Calcium Channel Blockers, pubmed-meshheading:9426309-Calcium Channels, pubmed-meshheading:9426309-Calcium Channels, L-Type, pubmed-meshheading:9426309-Cells, Cultured, pubmed-meshheading:9426309-Chromaffin Cells, pubmed-meshheading:9426309-Electromagnetic Fields, pubmed-meshheading:9426309-Ion Channel Gating, pubmed-meshheading:9426309-Mollusk Venoms, pubmed-meshheading:9426309-Nerve Growth Factors, pubmed-meshheading:9426309-Neurites, pubmed-meshheading:9426309-Nifedipine, pubmed-meshheading:9426309-Norepinephrine, pubmed-meshheading:9426309-Potassium Chloride, pubmed-meshheading:9426309-Rats, pubmed-meshheading:9426309-Rats, Wistar
pubmed:year
1998
pubmed:articleTitle
The role of voltage-gated Ca2+ channels in neurite growth of cultured chromaffin cells induced by extremely low frequency (ELF) magnetic field stimulation.
pubmed:affiliation
Depto. de Fisiología, Facultad de Medicina, Facultad de Medicina, Universidad Nacional Autónoma de México, Apdo. Postal 70-250, 04510 Mexico City, Mexico D.F.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't