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Figure 1

(A) Principal intracellular signalling cascades associated to somatostatin receptors in pituitary cells. Somatostatin (or somatostatin analogues) binding to somatostatin receptors inhibits adenylyl cyclase, activates K channels and/or inhibits Ca channels. Phosphotyrosine phosphatases and mitogen-activated protein kinase are modulated as well and along the stimulation of phosphotyrosine phosphatase, may also produce cytostatic actions. More recently, increase in apoptosis via p53 has been shown as well. Most of these effects are mediated by G proteins. (B) Principal signal transduction associated with the activation of dopamine receptors in pituitary cells. Dopamine (or dopamine agonists) binding to pituitary D2 receptors inhibits adenylyl cyclase, phosphatidylinositol metabolism, activates voltage-activated potassium channels and decreases voltage-activated L-type and T-type calcium currents, modulates the activity of phospholipase C, activates the mitogen-activated protein kinase and extracellular signal-regulated kinase pathway. The expression of POU1F1 transcription factor is inhibited by activation of D2 receptors, exerting a negative control on PRL gene expression. Most of these effects are mediated by G proteins. AC, adenylyl cyclase; ER, endoplasmic reticulum; ERK, extracellular signal-regulated kinase; GSK3β, glycogen synthase kinase 3β; MAPK, mitogen-activated protein kinase; Gα, Gβ and Gγ, G-protein subunit; PDPK1, 3-phosphoinositide-dependent protein kinase 1; pHi, intracellular pH; PLC, phospholipase C; PKA, protein kinase A; PTPase, phosphotyrosine phosphatase.

This Article

  1. J Mol Endocrinol vol. 42 no. 5 361-370