Morphological effects of somatostatin on rat somatotrophs previously activated by growth hormone-releasing factor

Abstract

Correlative morphological and physiological analysis was carried out in order to clarify the role of somatostatin in the inhibition of the secretion of growth hormone (GH) from somatotrophs of the rat anterior pituitary gland in vivo. Transmission electron microscopy combined with immunogold labelling showed an increased number of exocytotic GH-containing secretory granules in somatotrophs fixed between 2 and 10 min after injection of GH-releasing factor (GRF). Injection of GRF also induced the appearance of immunopositive material in cisternae of the Golgi apparatus, many coated vesicles and multivesicular bodies. Microtubules were observed more frequently throughout the cytoplasm, particularly in and near the Golgi region. At 2 and 10 min after injection of somatostatin (SRIF), both the number of exocytotic figures in the somatotrophs previously stimulated by GRF and the amount of radioimmunoassayable GH in the plasma were clearly decreased. Undulation of the plasma membrane (PM) induced by GRF rapidly disappeared, and the number of granules just beneath the plasma membrane was significantly reduced. After injection of SRIF, parallel bundles of microfilaments were often observed in the space between the granules and the plasma membrane. SRIF did not cause a noticeable decrease in the amount of immunopositive material, coated vesicles and multivesicular bodies in the Golgi areas or any significant changes in the distribution of microtubules. SRIF therefore appears to inhibit hormone release mainly at the level of the plasma membrane, probably through changes in the distribution of microfilaments.

Immunocytochemical and Immunoelectron-Microscopic Study of Somatotrophs in ICR and Nonobese Diabetic Mice

“…The relationship between morphological heterogeneity and functional heterogeneity of GH cells remains to be clarified. In the rat GH cells no obvious relationship was detected between the degreee of response to GH-releasing hormone and the different type of GH cells [Shimada et al, 1990].…”

Morphometric and Functional Changes of Rat Pituitary Somatotropes and Lactotropes after Central Administration of Somatostatin

“…By contrast, only a few studies have investigated morphological features of somatotropes during inhibition or stimulation of GH secretion [20,21]. Shimada et al [21] suggest that inhibition of GH release by SRIH involves a change in distribution of microfilaments rather than microtubules. These authors found microfilament bundles running parallel to the plasmalemma in the space between granules at 2 and 5 min after injection of SRIH.…”

“…A number of physiological and biochemical studies in vivo and in vitro have been performed to examine the role of both somatostatins on the mechanism of GH secretion [4,15,18,19]. By contrast, only a few studies have investigated morphological features of somatotropes during inhibition or stimulation of GH secretion [20,21]. Shimada et al [21] suggest that inhibition of GH release by SRIH involves a change in distribution of microfilaments rather than microtubules.…”

Somatostatin system: molecular mechanisms regulating anterior pituitary hormones

“…Although it remains to be determined whether SRIF regulates pituitary Ca 2C levels independently of K C channels, GH release correlates with both frequency and amplitude of calcium oscillations, while calcium channel blockers and SRIF acutely suppress Ca 2C extrusion (Holl et al 1988). SRIF treatment resulted in Ca 2C -dependent redistribution of cytoplasmic microfilaments, without affecting intracellular somatotroph GH content (Shimada et al 1990), in addition to reduced association of exocytosis-associated RAB3B and SNARE proteins (Matsuno et al 2003 Adenylate cyclase/cAMP/PKA signalling SRIF inhibits pituitary adenylate cyclase/cAMP/PKA signaling, thereby inhibiting pituitary hormone synthesis and cell growth. SRIF inhibits cAMP production and ACTH secretion induced by CRH, forskolin, isoproterenol, vasoactive intestinal polypeptide (VIP), and cholera toxin in AtT-20 cells (Heisler et al 1982).…”