Benzodiazepines and steroidogenesis

Whitehouse, B. J.

doi:10.1677/joe.0.1340001

Cited by 14 publications

(3 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This particular histological organization favors cross-talk between the two categories of cells (Yon et al 1994, Lesouhaitier et al 1995. For instance, chromaffin cells of the frog adrenal gland contain serotonin (Delarue et al 1988a), vasotocin (Larcher et al 1989) and vasoactive intestinal polypeptide (Leboulenger et al 1983), which all stimulate corticosteroid secretion (Leboulenger et al 1983, 1984, Delarue et al 1988b, Larcher et al 1989, 1992. The occurrence of immunoreactive ODN in frog adrenochromaffin cells (Lesouhaitier et al 1996) prompted us to investigate the effect of endozepines on adrenocortical cells.…”

Section: Discussionmentioning

confidence: 99%

“…Further studies on the mechanism of action of TTN are required to elucidate the type of receptor responsible for the effect of the peptide on adrenocortical cells. Although exogenous TTN does not act through benzodiazepine receptors, it should be borne in mind that PBR and CBR agonists can modulate corticosteroid secretion (Thomson et al 1992, Whitehouse 1992, Python et al 1993.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of the triakontatetraneuropeptide (TTN) on corticosteroid secretion by the frog adrenal gland

Lesouhaitier

Feuilloley²,

Vaudry³

1998

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Diazepam-binding inhibitor (DBI) was initially isolated from the rat brain as a result of its ability to compete with benzodiazepines for their receptors. Immunohistochemical studies have recently shown the presence of peripheral-type benzodiazepine receptor (PBR)-and DBI-like immunoreactivity in the frog adrenal gland. The aim of the present study was to investigate the effect of two biologically active DBI-derived peptides, the triakontatetraneuropeptide [TTN; ] and the octadecaneuropeptide [ODN; DBI(33-50)], on corticosteroid secretion by frog adrenocortical cells. Exposure of frog adrenal explants to graded concentrations of TTN (3·16 10 8 to 3·16 10 6 M) induced a dose-related increase in corticosterone and aldosterone secretion. In contrast, ODN did not modify corticosteroid output. When repeated pulses of TTN (10 6 M) were administered at 2-h intervals, the response of the adrenal explants to the second dose of TTN was markedly reduced, suggesting the existence of a desensitization phenomenon. Exposure of dispersed adrenal cells to TTN also induced a marked stimulation of corticosteroid secretion, indicating that TTN acts directly on adrenocortical cells. The central-type benzodiazepine receptor (CBR) agonist, clonazepam, did not stimulate corticosteroid secretion and the CBR antagonist, flumazenil, did not block the stimulatory action of TTN. Similarly, the PBR agonist, Ro5-4864, did not mimic the stimulatory effect of TTN and the PBR antagonist, flunitrazepam, did not affect the stimulatory action of TTN. The present study provides the first evidence for a stimulatory effect of TTN on intact adrenocortical cells. The receptor mediating the corticotropic action of TTN is not related to central-or peripheral-type benzodiazepine receptors. Our data suggest that TTN, released by chromaffin cells, may act as a paracrine factor regulating the activity of adrenocortical cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of the triakontatetraneuropeptide (TTN) on corticosteroid secretion by the frog adrenal gland

Lesouhaitier

Feuilloley²,

Vaudry³

1998

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…Although steroidogenic tissues such as the insect prothoracic glands do not respond to hormonal stimulation by cell proliferation, steroidogenesis in some mammalian tissues appears to require the rapid synthesis of relatively short-lived proteins (9), which in turn aid in the transit of cholesterol into the mitochondria for the synthesis of steroids (10,11). In insects, RNA and protein synthesis are required for the full response of the prothoracic glands to PTTH (12)(13)(14)(15)(16).…”

mentioning

confidence: 99%

Molecular Cloning, Developmental Expression, and Phosphorylation of Ribosomal Protein S6 in the Endocrine Gland Responsible for Insect Molting

Song

Gilbert

1997

Journal of Biological Chemistry

View full text Add to dashboard Cite

Phosphorylation of ribosomal protein S6 is requisite for prothoracicotropic hormone (PTTH)-stimulated specific protein synthesis and subsequent ecdysteroidogenesis in the prothoracic glands of the tobacco hornworm, Manduca sexta. To better understand the role of S6 in regulating ecdysteroidogenesis, S6 cDNA was isolated from a Manduca prothoracic gland cDNA library and sequenced. The deduced protein is comprised of 253 amino acids, has a molecular weight of 29,038, and contains four copies of a 10-amino acid motif defining potential DNA-binding sites. This Manduca S6 possesses a consensus recognition sequence for the p70 s6k binding domain as well as six seryl residues at the carboxylterminal sequence of 17 amino acids. Phosphoamino acid analysis revealed that the phosphorylation of Manduca prothoracic gland S6 is limited exclusively to serine residues. Although alterations in the quantity of S6 mRNA throughout the last larval instar and early pupal-adult development were not well correlated with the hemolymph ecdysteroid titer, developmental expression and phosphorylation of S6 were temporally correlated with PTTH release and the hemolymph ecdysteroid titer. These data provide additional evidence that S6 phosphorylation is a critical element in the transduction pathway leading to PTTH-stimulated ecdysteroidogenesis.Insect molting and metamorphosis are elicited by a class of steroid hormones, ecdysteroids, originating in the prothoracic gland (1, 2). These glands are stimulated by a brain neuropeptide, prothoracicotropic hormone (PTTH), 1 that acts via a cascade that includes a Ca 2ϩ /calmodulin-dependent increase in intracellular cAMP, activation of a cAMP-dependent protein kinase, and ultimate phosphorylation of S6, a protein of the ribosomal 40 S subunit (1-4).Previous studies demonstrated that S6 in the prothoracic glands of the tobacco hornworm, Manduca sexta, was phosphorylated at up to five sites under PTTH stimulation (4, 5), a phenomenon typical of S6 phosphorylation in mammals (6).Temporal analysis of PTTH-stimulated S6 phosphorylation showed that phosphorylation and dephosphorylation of S6 closely paralleled the increase and decrease in PTTH-stimulated ecdysteroidogenesis (4). Most importantly, the multiple phosphorylation of S6 was inhibited completely by rapamycin, an inhibitor of S6 phosphorylation (7,8), resulting in the inhibition of PTTH-stimulated specific protein synthesis and subsequent ecdysteroidogenesis (4). These data indicate that S6 phosphorylation is required for both specific protein synthesis and ecdysteroidogenesis in PTTH-stimulated glands.

show abstract

Pharmacology of Sedatives, Hypnotics, and Anxiolytics

Sloan

Wala

1998

Handbook of Substance Abuse

View full text Add to dashboard Cite

Benzodiazepines and steroidogenesis

Cited by 14 publications

References 15 publications

Effect of the triakontatetraneuropeptide (TTN) on corticosteroid secretion by the frog adrenal gland

Effect of the triakontatetraneuropeptide (TTN) on corticosteroid secretion by the frog adrenal gland

Molecular Cloning, Developmental Expression, and Phosphorylation of Ribosomal Protein S6 in the Endocrine Gland Responsible for Insect Molting

Pharmacology of Sedatives, Hypnotics, and Anxiolytics

Contact Info

Product

Resources

About