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Department of Pharmacology and Physiology and the Cancer Center University of Rochester School of Medicine and Dentistry Rochester, New York 14642
These studies examined the importance of
phospholipase Cß (PLCß) in the calcium responses of pituitary
cells using PLCß3 knockout mice. Pituitary tissue from wild-type mice
contained PLCß1 and PLCß3 but not PLCß2 or PLCß4. Both G
q/11
and Gß
can activate PLCß3, whereas only Gq/11 activates
PLCß1 effectively. In knockout mice, PLCß3 was absent, PLCß1 was
not up-regulated, and PLCß2 and PLCß4 were not expressed. Since
somatostatin inhibited influx of extracellular calcium in pituitary
cells from wild-type and PLCß3 knockout mice, the somatostatin signal
pathway was intact. However, somatostatin failed to increase
intracellular calcium in pituitary cells from either wild-type or
knockout mice under a variety of conditions, indicating that it did not
stimulate PLCß3. In contrast, somatostatin increased intracellular
calcium in aortic smooth muscle cells from wild-type mice, although it
evoked no calcium response in cells from PLCß3 knockout animals.
These results show that somatostatin, like other Gi/Go-linked hormones,
can stimulate a calcium transient by activating PLCß3 through
Gß, but this response does not normally occur in pituitary cells.
The densities of Gi and Go, as well as the relative concentrations of
PLCß1 and PLCß3, were similar in cells that responded to
somatostatin with an increase in calcium and pituitary cells. Calcium
responses to 1 nM and 1
µM TRH and GnRH were identical in pituitary
cells from wild-type and PLCß3 knockout mice, as were responses to
other Gq-linked agonists. These results show that in pituitary cells,
PLCß1 is sufficient to transmit signals from Gq-coupled hormones,
whereas PLCß3 is required for the calcium-mobilizing actions of
somatostatin observed in smooth muscle cells.
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