Biomedical subjects

V Montel

Publications and source records attributed to V Montel.

26 records · Page 2Linked to original sources

PubMed1997

Proteasome and myogenesis.

In this report, we examine the involvement of the ubiquitin-proteasome pathway during fusion and differentiation of myoblast primary cell cultures. Up-regulation of proteasome was observed at the maximum fusion rate and was preceded by an increase of unidentified ubiquitin-conjugates. Cell permeable proteasome inhibitors prevent fusion as do antisense oligodesoxyribonucleotides targetted to three proteasome subunits. Identical results were obtained using E3 ubiquitin-ligases dipeptide inhibitor. Involvement of the ubiquitin-proteasome pathway in the regulation of myogenic factors was hypothesized.

Animals↗

PubMed1997

Effect of bovine serum albumin on the calcium release channel of sarcoplasmic reticulum from rabbit skeletal muscle.

The effect of bovine serum albumin (BSA) on the activity of the calcium release channel of the sarcoplasmic reticulum from rabbit skeletal muscle was investigated using both tension recording from skinned fibres and electrophysiological recording of unitary channel currents from planar lipid membranes. BSA had no effect on the Ca2+ affinity of the contractile proteins, elicited no tension per se in Ca(2+)-loaded skinned fibres, but potentiated caffeine-induced tension. Maximum potentiation was observed with 0.05-0.5% BSA. BSA (0.1%) had no detectable effect on the basal activity of the Ca(2+)-release channel incorporated in lipid bilayer. However, channel stimulation elicited by either caffeine (2 mM) or ATP (60 microM) was further enhanced by BSA (0.1%), as indicated by significant increases in Po, the open probability of the channel. These results suggest that BSA can modulate the response of the skeletal muscle SR Ca(2+)-release channel to different activators such as caffeine and ATP.

Adenosine Triphosphate↗

PubMed1996

Hypothalamic metabolism of neurotransmitters (serotonin, norepinephrine, dopamine) and NPY, and gonadal and adrenal activities, during the early postnatal period in the rat.

It is noteworthy that in the rat the early postnatal life is marked by an activation of both the corticostimulating function of the adenohypophysis in neonates of both sexes and of the gonadostimulating function mainly in males. In order to specify if such neuroendocrine variations are temporally correlated with changes in the hypothalamic metabolism of neurotransmitters, the hypothalamic metabolism of serotonin (5 HT), norepinephrine (NE), and dopamine (DA) and the hypothalamic content of neuropeptide Y (NPY) have been investigated in newborn rats of both sexes, delivered at term by cesarean section, as well as changes in the activity of both the hypothalamo-pituitary adrenal axis (HPA) and the hypothalamo-pituitary gonadal axis (HPG). Experimental data suggested that 1) in males a rise in hypothalamic metabolism of 5 HT, NE and DA occurs during the first two hours after delivery, whereas in females, only the metabolism of NE increases. Moreover, the postnatal metabolism of NE was higher in females than in littermate males; 2) NPY content of the hypothalamus, which was at birth significantly higher in males than in females, dropped in the former but not in the latter; 3) in newborn males, an early surge of plasma testosterone occurs, suggesting postnatal activation of the HPG axis; on the other hand, in females, a late and slight increase in plasma estradiol is observed; 4) in early postnatal life, a sex-independent rise in plasma ACTH and adrenal and plasma corticosterone levels suggest a comparable activation of the HPA axis in newborns of both sexes. In conclusion, the early postnatal activation of the corticostimulating function in neonates of both sexes and that of the gonadostimulating function, mainly in males, could be temporally correlated with a rise in the hypothalamic metabolism of two neurotransmitters, 5 HT and NE, and of NPY content. According to our data, a sex-dependent metabolism of neurotransmitters in the hypothalamus is already apparent in early postnatal life.

Adrenal Glands↗

PubMed1996

Effects of prenatal morphine on hypothalamic metabolism of neurotransmitters and gonadal and adrenal activities, during the early postnatal period in the rat.

It is noteworthy that exposure to opiates during fetal development results in permanent changes in adults related to morphological, behavioral and biochemical measures; however little is known concerning the effects of such drugs in early postnatal life. We investigated in newborn rats the effects of prenatal morphine-exposure on both-the hypothalamic metabolism of norepinephrine (NE), serotonin (5 HT) and neuropeptide Y (NPY)-the activity of the hypothalamo-pituitary gonadal and adrenal axes. In a previous study performed in newborns of untreated mothers, we reported some sex-dependent changes in the metabolism of NE, 5 HT and NPY in the hypothalamus and an early activation of the gonadostimulating function and of the corticostimulating one. In control newborns from saline-treated mothers, a slight increase in the hypothalamic metabolism of NE (males) and 5 HT (males and females) was observed and it was comparable in both sexes. On the other hand, the hypothalamic content of NPY was unaffected in early postnatal period in newborn males as well as in females. These changes observed on hypothalamic metabolisms are temporally correlated with the early postnatal activation of the corticostimulating function in neonates of both sexes and that of the gonadostimulating one, mainly in males. Prenatal morphine exposure altered the hypothalamic metabolism of 5 HT which was increased mainly in newborn females but did not affect either the metabolism of NE or the NPY content of the hypothalamus. The more drastic effect of the prenatal morphine treatment is the atrophy and hypoactivity of the adrenals in newborns of both sexes at birth time and during the early postnatal period. In contrast morphine did not impair postnatal surge of the plasma testosterone level in male pups as well as late and slight increase of plasma estradiol in female ones.

Adrenal Glands↗

PubMed1994

In vitro steroidogenic effects of neuropeptide Y (NPY1-36), Y1 and Y2 receptor agonists (Leu31-Pro34 NPY, NPY18-36) and peptide YY (PYY) on rat adrenal capsule/zona glomerulosa.

The effects of neuropeptide Y (NPY1-36), of two analogs (Leu31-Pro34 NPY and NPY18-36) and of Peptide YY (PYY) on aldosterone and corticosterone secretions by freshly isolated rat adrenal capsule/zona glomerulosa preparations were investigated in vitro. NPY-related peptides (NPY1-36, Leu31-Pro34 NPY, NPY18-36), but not PYY, induced a dose-dependent release of aldosterone at concentrations ranging from 10(-8) to 10(-6) M. All the investigated peptides failed to significantly affect corticosterone secretion in concentrations ranging from 10(-10) to 10(-6) M (NPY1-36, NPY18-36), 10(-11) to 10(-6) M (Leu31-Pro34 NPY) or 10(-9) to 10(-6) M (PYY). Aldosterone secretion by this preparation of isolated adrenal capsule/zona glomerulosa was also significantly stimulated by high potassium levels (55 mEq) or by angiotensin II (AII) in concentrations ranging from 10(-8) to 10(-6) M. Moreover, NPY and Y1 or Y2 receptor agonists were positive aldosterone releasing agents as potent as AII. The present data support the existence of: (1) NPY binding sites of the Y3-like subtype, on rat adrenal capsule/zona glomerulosa. (2) A stimulatory effect of NPY on aldosterone production. So that the NPYergic innervation of the rat adrenal capsule/zona glomerulosa could be implicated in the multifactorial control of aldosterone production.

Aldosterone↗

PubMed1994

Neuropeptide Y (NPY)- and vasoactive intestinal peptide (VIP)-induced aldosterone secretion by rat capsule/glomerular zone could be mediated by catecholamines via beta 1 adrenergic receptors.

The effects of two Neuropeptide Y (NPY) analogs (Y1- and Y2-type) and vasoactive intestinal peptide (VIP) on both catecholamine (adrenaline and noradrenaline) release and aldosterone production by rat adrenal capsule/glomerular zone, have been investigated in vitro. The adrenal capsule/glomerular zones, collected from adult male rats, were incubated in a medium (Krebs-Ringer bicarbonate buffer supplemented with glucose and bovine serum albumin) containing or not one of the following synthetic peptides: human Leu31,Pro34-NPY (an agonist of the Y1-type receptors), human/porcine NPY18-36 (an agonist of the Y2-type receptors) and VIP at the concentration of 10(-7) M, associated or not with 10(-7) M atenolol (a beta 1 adrenergic antagonist) or ICI-118,551 hydrochloride (a beta 2 adrenergic antagonist). The two NPY analogs as well as the VIP stimulated the release of catecholamines and of aldosterone. The beta 1 adrenergic antagonist, but not the beta 2 one, which failed to affect basal aldosterone production when given alone, prevented NPY18-36-, Leu31,Pro34-NPY- or VlP-induced aldosterone secretion. Present data support the hypothesis that adrenaline and/or noradrenaline could mediate the effects of both NPY and VIP on aldosterone secretion via beta 1 adrenergic receptors; alternatively, the steroidogenic effect of NPY or VIP could be related to direct interaction between NPY- or VIP-specific binding sites, present on the capsule/glomerular zone of the rat adrenal cortex, and beta 1 adrenergic receptors. Then the NPYergic, VIPergic and catecholaminergic innervation of the adrenal cortex, previously characterized by immunohistochemistry, may be a potent stimulatory element in the nervous control of the aldosterone secretion.

Adrenal Glands↗

PubMed1994

Effects of rat corticotrophin-releasing factor, arginine vasopressin and oxytocin on the secretions of adrenocorticotrophic hormone and corticosterone in the fetal rat in late gestation: in vivo and in vitro studies.

The effects of rat corticotrophin-releasing factor (rCRF), arginine vasopressin (AVP) and oxytocin (OT) were investigated in vivo in 21-day-old rat fetuses injected through the umbilical vein and in vitro on perifused anterior pituitary glands from 21-day-old rat fetuses. In vivo, rCRF (1.25 pmol.50 microliter-1.fetus-1), AVP (5 pmol.50 microliter-1.fetus-1) alone and rCRF in association with AVP or oxytocin (12.5 pmol.50 microliter-1.fetus-1) increased plasma adrenocorticotrophic hormone (ACTH) and corticosterone levels only 30 min after the start of injection. During the first 10 min of the sampling period, the injection of these peptides alone or in combination and the injection of saline decreased the plasma ACTH concentration, which was lower than that of uninjected fetuses, but had no effect on the plasma corticosterone concentration. In vitro, the release of ACTH by perifused anterior pituitary glands was increased strongly by rCRF (4 pmol/0.5 ml) but only slightly by AVP (92 pmol/0.5 ml) and oxytocin (198 pmol/0.5 ml). Arginine vasopressin and oxytoxin potentiated the release of ACTH stimulated by rCRF in vitro but not in vivo. Our results suggest that rCRF is the major peptide that controls ACTH secretion in the fetal rat at term. In conclusion, the rise of the ACTH level observed only 30 min after injection of rCRF or AVP suggests the existence of a factor able to inhibit the ACTH response after injection of these peptides. This factor might be elicited by the blood volume expansion.

Adrenocorticotropic Hormone↗

PubMed1992

Effect of rat atrial natriuretic factor on in vivo and in vitro aldosterone and corticosterone secretions in the rat during the perinatal period.

The effect of rat atrial natriuretic factor (rANF) on aldosterone and corticosterone secretion was investigated in vivo in 21-day-old rat fetuses injected intravenously through the umbilical vein and in vitro on isolated adrenal cells from 17-, 19- and 21-day-old fetuses and 1-, 2-, 3- and 4-week-old rats. In vivo, rANF (50 pmol/50 microliters/fetus) inhibited both basal levels and secretion of aldosterone stimulated by adrenocorticotropin hormone (ACTH(1-24), 0.25 pmol/50 microliters/fetus), but not corticosterone secretion. In vitro, the addition of graded concentrations of rANF (0.001, 0.01 and 10 nmol/l) to the incubation medium did not affect the basal aldosterone and corticosterone secretions of fetal and neonatal adrenal cells. ACTH(1-24) (0.1 nmol/l) stimulated productions of both corticosterone and aldosterone by the adrenal cells at all stages studied. The addition of graded concentrations of rANF to the incubation medium containing ACTH(1-24) (0.1 nmol/l) induced a dose-dependent inhibition of aldosterone secretion by the adrenal cells from 21-day-old fetuses and newborn rats. In contrast, no effect was observed on cells from 17- and 19-day-old fetuses. At all stages investigated, the three doses of rANF were unable to affect ACTH-induced corticosterone secretion in vitro. In isolated adrenal cells from 2-week-old rats, rANF (10 nmol/l) inhibited the secretion of aldosterone induced by ACTH(1-24) (0.1 nmol/l), and by different steroids of the aldosterone synthetic pathway (progesterone, 11-deoxycorticosterone, corticosterone, 1 mumol/l for each steroid). These results suggest that rANF is a specific inhibitor of aldosterone synthesis in the perinatal period of the rat and that the inhibitory effect of rANF occurs both during the early and late pathways of aldosteroidogenesis.

Adrenal Glands↗