Details
| Originalsprache | Englisch |
|---|---|
| Seiten (von - bis) | 127-36 |
| Seitenumfang | 10 |
| Fachzeitschrift | The journal of membrane biology |
| Jahrgang | 139 |
| Ausgabenummer | 2 |
| Publikationsstatus | Veröffentlicht - Apr. 1994 |
Abstract
Cholecystokinin-octapeptide (CCK-OP) induces a time- and dose-dependent decrease of gap junctional conductance in isolated pairs of pancreatic acinar cells. In double whole-cell experiments, the time course could be described by the latency and the half-life time (t1/2) of cell-to-cell uncoupling. The latency shows a biphasic dependence on [CCK-OP] with a minimum of about 50 sec at 10(-9) M CCK-OP. In the presence of vasoactive intestinal peptide (VIP), the biphasic relationship is shifted to lower CCK-OP concentrations. The increase of latency at high concentrations of CCK-OP (> 10(-9) M) was blocked by addition of a VIP-antagonist. t1/2 decreases monophasically with increasing [CCK-OP]. Addition of GTP gamma S to the pipette solution suppresses the [CCK-OP] dependence of the latency and potentiates the uncoupling phase. The kinetic data are discussed in terms of CCK binding to receptors of high and low affinity. Evidence is presented that secretion and cell-to-cell coupling are not related by an all-or-none process, but that for physiological CCK-OP concentrations, gap junctional uncoupling follows secretion.
Zitieren
- Standard
- Harvard
- Apa
- Vancouver
- BibTex
- RIS
in: The journal of membrane biology, Jahrgang 139, Nr. 2, 04.1994, S. 127-36.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Regulation of gap junctional coupling in isolated pancreatic acinar cell pairs by cholecystokinin-octapeptide, vasoactive intestinal peptide (VIP) and a VIP-antagonist
AU - Ngezahayo, A
AU - Kolb, H A
PY - 1994/4
Y1 - 1994/4
N2 - Cholecystokinin-octapeptide (CCK-OP) induces a time- and dose-dependent decrease of gap junctional conductance in isolated pairs of pancreatic acinar cells. In double whole-cell experiments, the time course could be described by the latency and the half-life time (t1/2) of cell-to-cell uncoupling. The latency shows a biphasic dependence on [CCK-OP] with a minimum of about 50 sec at 10(-9) M CCK-OP. In the presence of vasoactive intestinal peptide (VIP), the biphasic relationship is shifted to lower CCK-OP concentrations. The increase of latency at high concentrations of CCK-OP (> 10(-9) M) was blocked by addition of a VIP-antagonist. t1/2 decreases monophasically with increasing [CCK-OP]. Addition of GTP gamma S to the pipette solution suppresses the [CCK-OP] dependence of the latency and potentiates the uncoupling phase. The kinetic data are discussed in terms of CCK binding to receptors of high and low affinity. Evidence is presented that secretion and cell-to-cell coupling are not related by an all-or-none process, but that for physiological CCK-OP concentrations, gap junctional uncoupling follows secretion.
AB - Cholecystokinin-octapeptide (CCK-OP) induces a time- and dose-dependent decrease of gap junctional conductance in isolated pairs of pancreatic acinar cells. In double whole-cell experiments, the time course could be described by the latency and the half-life time (t1/2) of cell-to-cell uncoupling. The latency shows a biphasic dependence on [CCK-OP] with a minimum of about 50 sec at 10(-9) M CCK-OP. In the presence of vasoactive intestinal peptide (VIP), the biphasic relationship is shifted to lower CCK-OP concentrations. The increase of latency at high concentrations of CCK-OP (> 10(-9) M) was blocked by addition of a VIP-antagonist. t1/2 decreases monophasically with increasing [CCK-OP]. Addition of GTP gamma S to the pipette solution suppresses the [CCK-OP] dependence of the latency and potentiates the uncoupling phase. The kinetic data are discussed in terms of CCK binding to receptors of high and low affinity. Evidence is presented that secretion and cell-to-cell coupling are not related by an all-or-none process, but that for physiological CCK-OP concentrations, gap junctional uncoupling follows secretion.
KW - Amylases/metabolism
KW - Animals
KW - Cell Communication/drug effects
KW - Electrophysiology
KW - Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
KW - Guanosine Diphosphate/analogs & derivatives
KW - Intercellular Junctions/drug effects
KW - Male
KW - Mice
KW - Pancreas/drug effects
KW - Signal Transduction
KW - Sincalide/pharmacology
KW - Thionucleotides/pharmacology
KW - Vasoactive Intestinal Peptide/pharmacology
U2 - 10.1007/BF00232431
DO - 10.1007/BF00232431
M3 - Article
C2 - 7520502
VL - 139
SP - 127
EP - 136
JO - The journal of membrane biology
JF - The journal of membrane biology
SN - 0022-2631
IS - 2
ER -