Linked Life Data

3373181

Source:http://linkedlifedata.com/resource/pubmed/id/3373181

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-6-24
pubmed:abstractText
We examined the effects of extracellular and intracellular pH changes on the influx of radioactive 45Ca, the concentration of ionized Ca (pCai) as monitored with the Ca-sensitive fluorescent indicator fura-2, and the efflux of dopamine in presynaptic nerve endings (synaptosomes) isolated from rat brain corpora striata and preloaded with [3H]dopamine. Cytosolic pH (pHi) was monitored by loading the synaptosomes with the H+-sensitive fluorescent indicator 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) (see Nachshen, D. A., and P. Drapeau, 1988, Journal of General Physiology, 91:289-303). An abrupt decrease of the pH of the external medium, from 7.4 to 5.5, produced a slow decrease of pHi (over a 5-min period) from an initial value of 7.2 to a steady state level of approximately 5.8. When 20 mM acetate was present in acidic media, pHi dropped as fast as could be measured (within 2 s) to a level similar to that reached (more slowly) in the absence of acetate. It was therefore possible to lower pHi over short time periods to different levels depending on whether or not acetate was present upon extracellular acidification. Extracellular acidification to pH 5.5 (in the absence of acetate) had no significant effect on pCai and dopamine release over a 30-s period (pHi = 6.4). Acidification in the presence of acetate lowered pHi to 5.8 without affecting pCai, but dopamine efflux increased approximately 20-fold. This increase in basal dopamine release was also observed in the absence of extracellular Ca. Thus, intraterminal, but not extracellular, acidification could stimulate the efflux of dopamine in a Ca-independent manner. The high Q10 (3.6) of acid-stimulated dopamine efflux in the presence of nomifensine (which blocks the dopamine carrier) was consistent with an activation of vesicular dopamine release by H+. When synaptosomes were both depolarized for 2 s in high-K (77.5 mM) solutions and acidified (in the absence of acetate), there was a parallel block of 45Ca entry and evoked dopamine release (50% block at pH 6.0 with 0.2 mM external Ca). When acetate was included in the acidic media to further reduce pHi, Ca entry remained blocked, but evoked dopamine release was increased. Therefore, extracellular, but not cytosolic, acidification inhibited the release of dopamine by blocking voltage-gated Ca channels. The stimulation by cytosolic acidification of both basal and evoked dopamine release suggests that vesicular release in resting and depolarized synaptosomes was directly activated by cytoplasmic H+.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-10822500, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-11340, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-13884962, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-14946732, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-241848, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-2580977, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-3373180, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-358784, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-4020707, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-4152974, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-4295698, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-45400, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-49421, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6129628, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6141561, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6326601, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6330284, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6434728, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6704432, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6815204, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-6834103, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-701355, http://linkedlifedata.com/resource/pubmed/commentcorrection/3373181-7117549
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1295
pubmed:author
pubmed:issnType
Print
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
305-15
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Effects of lowering extracellular and cytosolic pH on calcium fluxes, cytosolic calcium levels, and transmitter release in presynaptic nerve terminals isolated from rat brain.
pubmed:affiliation
Neurosciences Unit, Montreal General Hospital Research Institute, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't