ORIGINAL ARTICLE Anna Capaldo Æ Flaminia Gay Æ Maria De Falco Francesca Virgilio Æ Vincenza Laforgia Lorenzo Varano The adrenal gland of newt Triturus carnifex (Amphibia, Urodela) following in vivo betamethasone administration Accepted: 23 March 2006 / Published online: 22 April 2006 Ó Springer-Verlag 2006 Abstract The response of the adrenal gland of Triturus carnifex to betamethasone administration was studied; the effects were evaluated by examination of the ultra- structural morphological features of the tissues as well as the serum levels of aldosterone, corticosterone, norepi- nephrine and epinephrine. In March and June, beta- methasone significantly decreased the serum levels of aldosterone and corticosterone and the lipid droplet content in the steroidogenic cells. Moreover, betameth- asone influenced the chromaffin tissue, enhancing in March (when the chromaffin cells produce norepineph- rine and epinephrine in almost equal quantities) epi- nephrine serum levels and the numeric ratio between norepinephrine and epinephrine granules in the chro- maffin cells. In June, (when the chromaffin cells contain almost exclusively norepinephrine granules) betametha- sone administration raised norepinephrine serum levels, whereas a decrease in the numeric ratio between nor- epinephrine and epinephrine granules in the chromaffin cells was found. Finally, betamethasone administration did not evoke in June any increase in the mean number of epinephrine granules in the chromaffin cells and/or in epinephrine serum levels, as would be expected if phenyletanolamine-N-methyl transferase (PNMT) en- zyme, converting norepinephrine into epinephrine, were activated by corticosteroids. The results of this study showed that betamethasone decreased aldosterone and corticosterone serum levels and enhanced catecholamine serum concentrations. Moreover, the present results suggest that a stimulatory role of glucocorticoids on PNMT enzyme may be ruled out. Keywords Adrenal gland Æ Aldosterone Æ Catecholamines Æ Corticosterone Æ Ultrastructure Introduction In Amphibia, as in other Vertebrates (Nussdorfer 1996; Bornstein et al. 1997; Manojlovic´ Stojanoski et al. 2006), corticosteroids suppress ACTH secretion. Cor- ticosterone or aldosterone administration was shown to depress overall synthesis of both corticosteroids, sug- gesting that these steroids do not specifically inhibit their own synthesis, but they both have negative feed- back relationships with pituitary ACTH (Dupont et al. 1976; Hanke 1978). Studies concerning the effects of corticosteroid administration on the adrenal gland activity were performed prevalently within the Anura, whereas data are few for Urodela or Gymnophiona (Thurmond et al. 1986; Kloas and Hanke 1990; Gupta and Hanke 1994; Kloas et al. 1997). In anurans glu- cocorticoid administration was found to cause regres- sion of interrenal cells and reduction in interrenal 3-b- hydroxysteroid dehydrogenase, catalyzing the oxidation of pregnenolone to progesterone (Hanke 1978; Mas- ood-Hussain and Saidapur 1984). However, cortico- sterone has been shown to have also a direct inhibitory effect on adrenal steroid secretion (Netchitailo et al. 1991). In contrast, the effects of corticosteroids produced by steroidogenic inter-renal cells on chromaffin tissue in amphibians are less understood (Kloas and Hanke 1992; Kloas et al. 1997). In mammals, glucocorticoids modulate catecholamine synthesis, storage and secre- tion; moreover, they have been implicated in chro- maffin cell differentiation (Bornstein et al. 1997; Hodel 2001; Hiwatashi et al. 2002; Yonekubo et al. 2003; Laborie et al. 2003; Carrasco-Serrano and Criado 2004; Crivellato et al. 2006). The activity of the enzyme phenyletanolamine-N-methyl transferase (PNMT), converting norepinephrine (NE) into epinephrine (E), in mammals and other species of Vertebrates, is stimulated A. Capaldo (&) Æ F. Gay Æ M. De Falco Æ F. Virgilio V. Laforgia Æ L. Varano Department of Biological Sciences, Section of Evolutive and Comparative Biology, University of Naples ‘‘Federico II’’, Via Mezzocannone 8, 80134 Naples, Italy E-mail: nevotta16@libero.it Tel.: +39-081-2535173 Fax: +39-081-2535035 Anat Embryol (2006) 211: 577–584 DOI 10.1007/s00429-006-0096-y