Linked Life Data

19828725

Source:http://linkedlifedata.com/resource/pubmed/id/19828725

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-12-7
pubmed:abstractText
Neurons may initiate behavior or store information by translating prior activity into a lengthy change in excitability. For example, brief input to the bag cell neurons of Aplysia results in an approximate 30-min afterdischarge that induces reproduction. Similarly, momentary stimulation of cultured bag cells neurons evokes a prolonged depolarization lasting many minutes. Contributing to this is a voltage-independent cation current activated by Ca(2+) entering during the stimulus. However, the cation current is relatively short-lived, and we hypothesized that a second, voltage-dependent persistent current sustains the prolonged depolarization. In bag cell neurons, the inward voltage-dependent current is carried by Ca(2+); thus we tested for persistent Ca(2+) current in primary culture under voltage clamp. The observed current activated between -40 and -50 mV exhibited a very slow decay, presented a similar magnitude regardless of stimulus duration (10-60 s), and, like the rapid Ca(2+) current, was enhanced when Ba(2+) was the permeant ion. The rapid and persistent Ca(2+) current, but not the cation current, were Ni(2+) sensitive. Consistent with the persistent current contributing to the response, Ni(2+) reduced the amplitude of a prolonged depolarization evoked under current clamp. Finally, protein kinase C activation enhanced the rapid and persistent Ca(2+) current as well as increased the prolonged depolarization when elicited by an action potential-independent stimulus. Thus the prolonged depolarization arises from Ca(2+) influx triggering a cation current, followed by voltage-dependent activation of a persistent Ca(2+) current and is subject to modulation. Such synergy between currents may represent a common means of achieving activity-dependent changes to excitability.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1522-1598
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3753-65
pubmed:meshHeading
pubmed-meshheading:19828725-Animals, pubmed-meshheading:19828725-Aplysia, pubmed-meshheading:19828725-Biophysical Phenomena, pubmed-meshheading:19828725-Biophysics, pubmed-meshheading:19828725-Calcium, pubmed-meshheading:19828725-Calcium Channel Blockers, pubmed-meshheading:19828725-Calcium Signaling, pubmed-meshheading:19828725-Cells, Cultured, pubmed-meshheading:19828725-Electric Stimulation, pubmed-meshheading:19828725-Ion Channel Gating, pubmed-meshheading:19828725-Ions, pubmed-meshheading:19828725-Membrane Potentials, pubmed-meshheading:19828725-Neurons, pubmed-meshheading:19828725-Nickel, pubmed-meshheading:19828725-Patch-Clamp Techniques, pubmed-meshheading:19828725-Potassium Channel Blockers, pubmed-meshheading:19828725-Tetradecanoylphorbol Acetate, pubmed-meshheading:19828725-Tetraethylammonium
pubmed:year
2009
pubmed:articleTitle
Persistent Ca2+ current contributes to a prolonged depolarization in Aplysia bag cell neurons.
pubmed:affiliation
Department of Physiology, Queen's University, Kingston, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't