The endozepine ODN stimulates polyphosphoinositide metabolism in rat astrocytes

Patte, Christine; Vaudry, Hubert; Desrues, Laurence; Gandolfo, Pierrick; Strijdveen, I.; Lamacz, Marek; Tonon, Marie‐Christine

doi:10.1016/0014-5793(95)00209-r

Cited by 46 publications

(44 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with this finding, it has been recently shown that, in rat Leydig cells, endozepines stimulate testosterone secretion via a PBRindependent mechanism (Garnier et al 1993). It has also been found that, in rat astrocytes, the endozepine ODN activates a membrane receptor positively coupled to a phospholipase C through a pertussis toxin-sensitive G protein (Patte et al 1995, Lamacz et al 1996, Gandolfo et al 1997. 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.…”

Section: Discussionsupporting

confidence: 58%

“…In addition, DBI acts as an acyl-CoAbinding protein (Knudsen et al 1989), suggesting that it may exert a physiological role as a lipid-transport protein (Mikkelsen & Knudsen 1987). Recent studies conducted in rat astrocytes indicated that endozepines may also activate a membrane receptor positively coupled to a phospholipase C through a pertussis toxin-sensitive G protein (Patte et al 1995, Lamacz et al 1996, Gandolfo et al 1997.…”

Section: Introductionmentioning

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: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

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

“…In addition, it has been shown that several of the effects induced by ODN are mediated via a G-proteincoupled receptor. In particular, in vitro studies have shown that ODN increases intracellular calcium concentration in cultured rat astrocytes through activation of a metabotropic receptor positively coupled to phospholipase C (Patte et al, 1995;Gandolfo et al, 1997). We have previously observed that the inhibitory effect of ODN on feeding behavior is not affected by diazepam, a mixed CBR and PBR agonist (Garcia de Mateos-Verchere et al, 2001).…”

Section: Discussionmentioning

confidence: 98%

“…TTN acts preferentially through peripheral-type benzodiazepine receptors (PBR) located either at the outer mitochondrial membrane or at the plasma membrane level Berkovich et al, 1990;Gandolfo et al, 2001). Finally, ODN can also activate a metabotropic receptor positively coupled to phospholipase C through a pertussis toxin-sensitive G-protein (Patte et al, 1995;Gandolfo et al, 1997). We have previously shown that the anorexigenic effect of ODN was not affected by the mixed CBR/PBR agonist diazepam (Garcia de MateosVerchere et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Characterization of the Receptor Mediating the Anorexigenic Action of the Octadecaneuropeptide: Evidence for an Endozepinergic Tone Regulating Food Intake

Rego

Orta

Leprince

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Peptides of the endozepine family, including diazepam-binding inhibitor, the triakontatetraneuropeptide, and the octadecaneuropeptide (ODN), act through three types of receptors, that is, central-type benzodiazepine receptors (CBR), peripheral-type (mitochondrial) benzodiazepine receptors (PBR) and a metabotropic receptor positively coupled to phospholipase C via a pertussis toxin-sensitive G protein. We have previously reported that ODN exerts a potent anorexigenic effect in rat and we have found that the action of ODN is not affected by the mixed CBR/PBR agonist diazepam. In the present report, we have tested the possible involvement of the metabotropic receptor in the anorexigenic activity of ODN. Intracerebroventricular administration of the C-terminal octapeptide (OP) and its head-to-tail cyclic analog cyclo 1-8 OP (cOP) at a dose of 100 ng mimicked the inhibitory effect of ODN on food intake in fooddeprived mice. The specific CBR antagonist flumazenil and the PBR antagonist PK11195 did not prevent the effect of ODN, OP, and cOP on food consumption. In contrast, the selective metabotropic endozepine receptor antagonist cyclo 1-8 [DLeu 5 ]OP (100-1000 ng; cDLOP) suppressed the anorexigenic effect of ODN, OP, and cOP. At the highest concentration tested (1000 ng), cDLOP provoked by itself a significant increase in food intake. Taken together, the present results indicate that the anorexigenic effect of ODN and OP is mediated through activation of the metabotropic receptor recently characterized in astrocytes. The data also suggest that endogenous ODN, acting via this receptor, exerts an inhibitory tone on feeding behavior.

show abstract

“…Thus, endozepines may interact with central-and peripheral-type benzodiazepine receptors, which are both expressed in the CNS (Costa et al, 1991;Papadopoulos et al, 1992). Concurrently, it has been reported that ODN can also stimulate the activity of astrocytes by interacting with a novel type of receptor pharmacologically and functionally distinct from the classical benzodiazepine receptors (Gandolfo et al, 1997;Patte et al, 1995).…”

Section: Introductionmentioning

confidence: 95%

GABA inhibits endozepine release from cultured rat astrocytes

Patte

Gandolfo

Leprince

et al. 1999

Glia

View full text Add to dashboard Cite

In the mammalian brain, the endogenous ligands for benzodiazepine receptors (also called endozepines) are predominantly synthesized by glial cells. It has recently been reported that rat astrocytes in primary culture release substantial amounts of endozepines. The aim of the present study was to investigate the possible involvement of GABA in the control of endozepine release. Exposure of cultured rat astrocytes to GABA (10−7 to 10−5 M) induced a dose‐related inhibition of endozepine secretion. At higher doses (3 × 10−5 to 10−3 M), the effect of GABA gradually diminished. The inhibitory effect of GABA (10−5 M) was mimicked by the GABAB receptor agonist baclofen (10−5 M). In contrast, the GABAA receptor agonists 3APS and isoguvacine (10−5 M each) did not modify endozepine release. The inhibition of endozepine secretion evoked by GABA and baclofen (10−5 M each) was totally abrogated by the specific GABAB receptor antagonist phaclofen (10−4 M). GABA and baclofen caused a significant inhibition of forskolin‐evoked production of cAMP in astrocytes and this effect was abolished in the presence of phaclofen. In contrast, isoguvacine had no effect on cAMP production. Exposure of astrocytes to dbcAMP induced a time‐ and dose‐dependent stimulation of endozepine release. These data indicate that GABA, acting through GABAB receptors negatively coupled to adenylyl cyclase, inhibits endozepine release from cultured rat astrocytes. The secretion of endozepines thus appears to be a valuable marker to monitor astrocyte activity. GLIA 25:404–411, 1999. © 1999 Wiley‐Liss, Inc.

show abstract

The endozepine ODN stimulates polyphosphoinositide metabolism in rat astrocytes

Cited by 46 publications

References 19 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

Pharmacological Characterization of the Receptor Mediating the Anorexigenic Action of the Octadecaneuropeptide: Evidence for an Endozepinergic Tone Regulating Food Intake

GABA inhibits endozepine release from cultured rat astrocytes

Contact Info

Product

Resources

About