PMID- 9763629
OWN - NLM
STAT- MEDLINE
DCOM- 19981229
LR  - 20190512
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 512 ( Pt 2)
IP  - Pt 2
DP  - 1998 Oct 15
TI  - alpha-adrenergic stimulation of cytosolic Ca2+ oscillations and exocytosis in 
      identified rat corticotrophs.
PG  - 385-93
AB  - 1. The patch clamp technique was used in conjunction with a fluorescent Ca2+ 
      indicator (indo-1, or indo-1FF) to measure simultaneously cytosolic Ca2+ 
      concentration ([Ca2+]i), ionic current and changes in membrane capacitance in 
      single rat corticotrophs identified with the reverse haemolytic plaque assay. 2. 
      Application of the adrenocorticotropin (ACTH) secretagogue noradrenaline (NA; 
      norepinephrine), triggered [Ca2+]i oscillation in corticotrophs via 
      alpha-adrenergic receptors and the guanosine trisphosphate (GTP) binding 
      protein-coupled phosphoinositide pathway. 3. Simultaneous measurement of [Ca2+]i 
      and capacitance shows that exocytosis was triggered during the first cycle of 
      NA-induced [Ca2+]i oscillation and the mean increase in cell membrane surface 
      area was 1.4 +/- 0.3 % (n = 6). 4. When Ca2+ was directly released from the 
      inositol 1,4, 5 trisphosphate (IP3)-sensitive store via flash photolysis of caged 
      IP3, the mean increase in cell surface area was 1.5 +/- 0.5 % (n = 6). Thus, 
      NA-stimulated ACTH secretion in rat corticotrophs is closely coupled to 
      intracellular Ca2+ release. 5. Large and rapid elevation of [Ca2+]i (>15 microM) 
      via flash photolysis of caged Ca2+ triggered two phases of exocytosis: a rapid 
      exocytic burst that was complete in approximately 100 ms and a slow burst that 
      continued for many seconds. 6. The rapid exocytic burst reflected the exhaustion 
      of a pool of readily releasable granules and, on average, increased the cell 
      surface by 2.8 +/- 0.1 % (n = 14). 7. We suggest that the relatively weak 
      exocytic response in corticotrophs during intracellular Ca2+ release may be 
      partially attributed to a smaller pool of readily releasable granules.
FAU - Tse, A
AU  - Tse A
AD  - Department of Pharmacology, 9-70 Medical Science Building, University of Alberta, 
      Edmonton, Alberta, Canada T6G 2H7. Amy.Tse@U.Alberta.ca
FAU - Tse, F W
AU  - Tse FW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - SY7Q814VUP (Calcium)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Adrenergic alpha-Agonists/*pharmacology
MH  - Adrenocorticotropic Hormone/metabolism
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Signaling/drug effects/physiology
MH  - Cytosol/drug effects/*metabolism/radiation effects
MH  - Electric Stimulation
MH  - Electrophysiology
MH  - Exocytosis/*drug effects/radiation effects
MH  - GTP-Binding Proteins/metabolism
MH  - In Vitro Techniques
MH  - Inositol 1,4,5-Trisphosphate/metabolism
MH  - Male
MH  - Membrane Potentials/physiology
MH  - Norepinephrine/pharmacology
MH  - Patch-Clamp Techniques
MH  - Photolysis
MH  - Pituitary Gland/cytology/drug effects/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
PMC - PMC2231208
EDAT- 1998/10/09 00:00
MHDA- 1998/10/09 00:01
PMCR- 1999/10/15
CRDT- 1998/10/09 00:00
PHST- 1998/10/09 00:00 [pubmed]
PHST- 1998/10/09 00:01 [medline]
PHST- 1998/10/09 00:00 [entrez]
PHST- 1999/10/15 00:00 [pmc-release]
AID - 10.1111/j.1469-7793.1998.385be.x [doi]
PST - ppublish
SO  - J Physiol. 1998 Oct 15;512 ( Pt 2)(Pt 2):385-93. doi: 
      10.1111/j.1469-7793.1998.385be.x.