Annual cycle of the chromaffin cells of Triturus cristatus

Abstract

Morphology of the chromaffin cells of Triturus cristatus during a complete annual cycle has been investigated. General ultrastructural characteristics are similar for all chromaffin cells, including numerous small mitochondria, well-developed Golgi apparatus and rough endoplasmic reticulum with short cisternae. The primary difference among cells is the type of the chromaffin granules they posses. These are of two kinds: adrenalin (A) and noradrenalin granules (NA). Both types are simultaneously present in the chromaffin cells but with different ratios during the year. During December-January and May-August, NA granules largely prevail, while in September-November and February-April, A and NA granules are present in about equal quantities. The total quantity of catecholamine granules, however, is relatively constant throughout the year. These findings suggest that T. cristatus has a single type of chromaffin cell, the granule content of which varies according to different functional states. The catecholamines are apparently discharged by exocytosis.

Effects of noradrenaline administration on the interrenal gland of the newt, Triturus carnifex: Evidence of intra‐adrenal paracrine interactions

“…2A) and July (Fig. 2B) have the general ultrastructural features previously described (Laforgia and Capaldo, 1991): a large nucleus with some heterochromatin close to the nuclear membrane, an endoplasmic reticulum made up of vesicles and short cisternae forming smooth (SER) or rough (RER) endoplasmic reticulum, numerous rounded or elongated mitochondria, and a well-developed Golgi apparatus. Noradrenalin granules are of variable shape and have a very electron-dense core, sometimes not separated from the limiting membrane.…”

“…Triturus carnifex has a single type of chromaffin cell, having an annual cycle with seasonal variations in the noradrenaline/adrenaline granule ratio within the cells. In the periods of the year characterized by extreme temperatures (winter or summer), there is a strong prevalence of NA granules; in the milder periods (autumn or spring), A and NA granules are present in the cells in almost equal quantities (Laforgia and Capaldo, 1991). The chromaffin cells in March ( Fig.…”

“…The interrenal gland of this species has a marked degree of intermingling between steroidogenic and chromaffin cells that may represent the morpholog-ical background for such paracrine interactions. In an earlier report (Capaldo et al, 2002), we showed that in vivo acetylcholine administration directly influenced the chromaffin cells, eliciting NA or A secretion, according to the period in the chromaffin cell functional cycle (Laforgia and Capaldo, 1991), and indirectly influenced the steroidogenic cells via the chromaffin cells. We suggested that Ach-induced NA release enhanced, whereas Ach-induced A release inhibited, aldosterone secretion from steroidogenic cells.…”

Effects of ACTH and corticosteroids on phenylethanoIamine‐N‐methyltransferase (PNMT) expression as determined by immunocytochemical localization in the adrenal gland of the lizardPodarcis sicula

“…The other classes of vertebrates behave differently: in amphibians PNMT is independent of the level of corticosteroids (Dupont et al, 1911;Laforgia & Capaldo, 1991), while in reptiles it is under the control of steroids secreted by the adrenal cortex (Laforgia & Varano, 1978b;Laforgia et al, 1982).…”

Effects of adrenaline administration on the interrenal gland of the newt, Triturus carnifex: Evidence of intraadrenal paracrine interactions

“…In a previous study (unpubl. data), we showed that in vivo acetylcholine (Ach) administration directly influenced the chromaffin cells, eliciting noradrenaline or adrenaline secretion, according to the period in the chromaffin cell functional cycle (Laforgia and Capaldo, 1991), and indirectly influenced the steroidogenic cells via the chromaffin cells. We suggested that Ach-induced noradrenaline secretion enhanced, whereas Ach-induced adrenaline secretion inhibited aldosterone release from steroidogenic cells.…”