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-meshheading:7738824-Animals,
pubmed-meshheading:7738824-Buffers,
pubmed-meshheading:7738824-Calcium,
pubmed-meshheading:7738824-Calcium Channels,
pubmed-meshheading:7738824-Cytoplasm,
pubmed-meshheading:7738824-Electric Stimulation,
pubmed-meshheading:7738824-Electrophysiology,
pubmed-meshheading:7738824-Fura-2,
pubmed-meshheading:7738824-Kinetics,
pubmed-meshheading:7738824-Male,
pubmed-meshheading:7738824-Nerve Endings,
pubmed-meshheading:7738824-Oxytocin,
pubmed-meshheading:7738824-Patch-Clamp Techniques,
pubmed-meshheading:7738824-Pituitary Gland, Posterior,
pubmed-meshheading:7738824-Rats,
pubmed-meshheading:7738824-Rats, Sprague-Dawley,
pubmed-meshheading:7738824-Vasopressins
|
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
|