Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1995-6-5
pubmed:abstractText
1. Electrophysiological measurements of Ca2+ influx using patch clamp methodology were combined with fluorescent monitoring of the free intracellular calcium concentration ([Ca2+]i) to determine mechanisms of Ca2+ regulation in isolated nerve endings from the rat neurohypophysis. 2. Application of step depolarizations under voltage clamp resulted in voltage-dependent calcium influx (ICa) and increase in the [Ca2+]i. The increase in [Ca2+]i was proportional to the time-integrated ICa for low calcium loads but approached an asymptote of [Ca2+]i at large Ca2+ loads. These data indicate the presence of two distinct rapid Ca2+ buffering mechanisms. 3. Dialysis of fura-2, which competes for Ca2+ binding with the endogenous Ca2+ buffers, reduced the amplitude and increased the duration of the step depolarization-evoked Ca2+ transients. More than 99% of Ca2+ influx at low Ca2+ loads is immediately buffered by this endogenous buffer component, which probably consists of intracellular Ca2+ binding proteins. 4. The capacity of the endogenous buffer for binding Ca2+ remained stable during 300 s of dialysis of the nerve endings. These properties indicated that this Ca2+ buffer component was either immobile or of high molecular weight and slowly diffusible. 5. In the presence of large Ca2+ loads a second distinct Ca2+ buffer mechanism was resolved which limited increases in [Ca2+]i to approximately 600 nM. This Ca2+ buffer exhibited high capacity but low affinity for Ca2+ and its presence resulted in a loss of proportionality between the integrated ICa and the increase in [Ca2+]i. This buffering mechanism was sensitive to the mitochondrial Ca2+ uptake inhibitor Ruthenium Red. 6. Basal [Ca2+]i, depolarization-induced changes in [Ca2+]i and recovery of [Ca2+]i to resting levels following an induced increase in [Ca2+]i were unaffected by thapsigargin and cyclopiazonic acid, specific inhibitors of intracellular Ca(2+)-ATPases. Caffeine and ryanodine were also without effect on Ca2+ regulation. 7. Evoked increases in [Ca2+]i, as well as rates of recovery from a Ca2+ load, were unaffected by the extracellular [Na+], suggesting a minimal role for Na(+)-Ca2+ exchange in Ca2+ regulation in these nerve endings. 8. Application of repetitive step depolarizations for a constant period of stimulation resulted in a proportional frequency (up to 40 Hz)-dependent increase in [Ca2+]i. On the other hand, for a constant number of stimuli a reduction in the [Ca2+]i. On the other hand, for a constant number of stimuli a reduction in the [Ca2+]i increase per impulse was observed at higher frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-120951, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1331424, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1357749, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1393151, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1432708, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1432709, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1540689, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1683760, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-181543, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-182956, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-183215, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-1988937, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2157158, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2213592, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2282508, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2348393, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2436546, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2450999, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2451806, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2471780, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2560641, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-2576509, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3178834, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3315032, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3383224, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3469676, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-359758, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3612574, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-4020707, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-4093889, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-4250976, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-4355178, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-4366843, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-6040160, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-6124897, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-6270629, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-6757171, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-6921243, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-702106, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-7504728, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-8107778, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-813768, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-8254513, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-8271200, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-838622, http://linkedlifedata.com/resource/pubmed/commentcorrection/7738824-894260
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
481 ( Pt 2)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-71
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Regulation of intracellular calcium and calcium buffering properties of rat isolated neurohypophysial nerve endings.
pubmed:affiliation
Department of Physiology, University of Michigan, Ann Arbor 48109, USA.
pubmed:publicationType
Journal Article, In Vitro
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