Linked Life Data

6102527

Source:http://linkedlifedata.com/resource/pubmed/id/6102527

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1980-6-27
pubmed:abstractText
Since the intracellular concentrations of Na+ and Ca2+ are relatively low and the cell's ability to actively expel or sequester these ions is limited, prolonged, high-frequency impulse activity at many crustacean axon terminals can result in significant increases in [Na+]i and [Ca2+]i. These changes parallel increases in transmitter output and may persist for several seconds (short-term facilitation, or STF) or even for many hours (long-term facilitations, or LTF). These two phenomena appear to be qualitatively distinct processes. The unique properties of LTF include: 1) the need for Na+ (but not Ca2+) in the extracellular media; 2) long decay times (from minutes to hours); 3) acceleration of devolpment and retardation of decay under conditions that inhibit the membrane Na+-K+ pump, e.g., cardiac glycosides, low [K+]o. The subcellular mechanism(s) linking Na+ accumulation to increased transmitter release are unknown but may involve alterations in [Ca2+]i, either through release from intracellular stores or through increased membrane conductance. Sodium-induced modifications in transmitter synthesis, storage, or availability may also be involved. Long-term functional changes in synaptic efficacy like LTF may provide important clues to more general questions of nervous system plasticity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-9446
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1524-6
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Intracellular sodium accumulation and transmitter release at crustacean neuromuscular junctions.
pubmed:publicationType
Journal Article