2008NeuroendocrinologyRequires access

Immunoreactive Delta Sleep-Inducing Peptide Secretion from Mouse Dissociated, Anterior Pituitary Cells: Regulation by Corticotropin-Releasing Factor and Arginine Vasopressin

Anders Bjartell, María G. Castro, Rolf Ekman, F. Sundler, Erik Widerlöv, Y. Peng Loh

Open publisher page 15 citations

Abstract

Immunoreactive delta sleep-inducing peptide (IR-DSIP) has previously been localized to the ACTH/MSH cells of the human and porcine pituitary gland. In the present report, the distribution of IR-DSIP in the mouse pituitary gland was examined by immunocytochemistry. In this species, IR-DSIP was found to be co-localized with thyroid-stimulating hormone (TSH) in anterior pituitary thyrotrophs and was also present in nerve fibers in the posterior and intermediate lobes. The effect of synthetic DSIP on IR-ACTH release from dissociated mouse anterior pituitary cells was also studied. DSIP (greater than or equal to 10(-9) M) inhibited both basal and CRF-induced IR-ACTH release from these cells. In addition, the effect of synthetic rat corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on IR-DSIP secretion was investigated. CRF and AVP at concentrations of 10(-11)-10(-7)M inhibited release of IR-DSIP from mouse anterior pituitary cells by 63%. When CRF and AVP (10(-10)-10(-7) M) were given concomitantly, the maximal inhibition of IR-DSIP release was observed at a concentration of 10(-8)M of CRF and AVP. However, these two peptides when given together showed no additive effect on IR-DSIP secretion. These findings suggest that during CRF induction of ACTH secretion from anterior pituitary corticotrophs, CRF may also act simultaneously to inhibit DSIP secretion from the thyrotrophs.

About this research paper

What this paper is about

Immunoreactive delta sleep-inducing peptide (IR-DSIP) has previously been localized to the ACTH/MSH cells of the human and porcine pituitary gland. In the present report, the distribution of IR-DSIP in the mouse pituitary gland was examined by immunocytochemistry. In this species, IR-DSIP was found to be co-localized with thyroid-stimulating hormone (TSH) in anterior pituitary thyrotrophs and was also present in nerve fibers in the posterior and intermediate lobes. The effect of synthetic DSIP on IR-ACTH release from dissociated mouse anterior pituitary cells was also studied. DSIP (greater than or equal to 10(-9) M) inhibited both basal and CRF-induced IR-ACTH release from these cells. In addition, the effect of synthetic rat corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on IR-DSIP secretion was investigated. CRF and AVP at concentrations of 10(-11)-10(-7)M inhibited release of IR-DSIP from mouse anterior pituitary cells by 63%. When CRF and AVP (10(-10)-10(-7) M) were given concomitantly, the maximal inhibition of IR-DSIP release was observed at a concentration of 10(-8)M of CRF and AVP. However, these two peptides when given together showed no additive effect on IR-DSIP secretion. These findings suggest that during CRF induction of ACTH secretion from anterior pituitary corticotrophs, CRF may also act simultaneously to inhibit DSIP secretion from the thyrotrophs.

Why it matters

OpenAlex reports 15 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Immunoreactive delta sleep-inducing peptide (IR-DSIP) has previously been localized to the ACTH/MSH cells of the human and porcine pituitary gland. In the present report, the distribution of IR-DSIP in the mouse pituitary gland was examined by immunocytochemistry. In this species, IR-DSIP was found to be co-localized with thyroid-stimulating hormone (TSH) in anterior pituitary thyrotrophs and was also present in nerve fibers in the posterior and intermediate lobes. The effect of synthetic DSIP on IR-ACTH release from dissociated mouse anterior pituitary cells was also studied. DSIP (greater than or equal to 10(-9) M) inhibited both basal and CRF-induced IR-ACTH release from these cells. In addition, the effect of synthetic rat corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) on IR-DSIP secretion was investigated. CRF and AVP at concentrations of 10(-11)-10(-7)M inhibited release of IR-DSIP from mouse anterior pituitary cells by 63%. When CRF and AVP (10(-10)-10(-7) M) were given concomitantly, the maximal inhibition of IR-DSIP release was observed at a concentration of 10(-8)M of CRF and AVP. However, these two peptides when given together showed no additive effect on IR-DSIP secretion. These findings suggest that during CRF induction of ACTH secretion from anterior pituitary corticotrophs, CRF may also act simultaneously to inhibit DSIP secretion from the thyrotrophs.

Key concepts: Internal medicine, Endocrinology, Anterior pituitary, Vasopressin, Corticotropic cell, Thyrotropic cell, Pituitary gland, Hypothalamus

Related papers

Back to paper searchBrowse research topicsOriginal source
Immunoreactive Delta Sleep-Inducing Peptide Secretion from Mouse Dissociated, Anterior Pituitary Cells: Regulation by Corticotropin-Releasing Factor and Arginine Vasopressin — Research Paper | ScholarLens