Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-6-4
pubmed:abstractText
At frog neuromuscular junctions immersed in solutions containing 0.5 mM Mn2+, verapamil (40 microM) reduced the increase in miniature end-plate potential (MEPP) frequency produced by tetanic stimulation (50 Hz, 2 min) of the motor nerve to 5% of that in the absence of verapamil. In solutions containing 5 mM Mg2+, verapamil reduced the tetanic increase in MEPP frequency to 8% of that in the absence of verapamil. Verapamil added to solutions containing 0.15 mM Ca2+ decreased the tetanic rise in MEPP frequency to 6% of the control value. In low Ca2+ (nominally Ca2(+)-free) solutions, verapamil decreased the tetanic rise to 70% of the control value. The present results suggest that Mn2+ and Mg2+, as well as Ca2+, enter the nerve terminal through Ca2+ channels during nerve stimulation and promote transmitter release. In addition to its effect on the Ca2+ channel, verapamil at higher concentrations appears to have inhibitory effects on the acetylcholine-gated end-plate channel and on the Na+ channel as suggested by its depressive effects on the amplitudes of MEPPs, end-plate potentials and nerve terminal action potentials.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
510
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
289-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Mn and Mg influxes through Ca channels of motor nerve terminals are prevented by verapamil in frogs.
pubmed:affiliation
Department of Physiology, Kawasaki Medical School, Okayama, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't