Stimulatory Action (stimulatory + action)

Distribution by Scientific Domains


Selected Abstracts


Evidence for a Stimulatory Action of Melanin-Concentrating Hormone on Luteinising Hormone Release Involving MCH1 and Melanocortin-5 Receptors

JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2006
J. F. Murray
Abstract The present series of studies aimed to further our understanding of the role of melanin-concentrating hormone (MCH) neurones in the central regulation of luteinising hormone (LH) release in the female rat. LH release was stimulated when MCH was injected bilaterally into the rostral preoptic area (rPOA) or medial preoptic area (mPOA), but not when injected into the zona incerta (ZI), of oestrogen-primed ovariectomised rats. In rats that were steroid-primed to generate a surge-like release of LH, MCH administration into the ZI blocked this rise in LH release: no such effect occurred when MCH was injected into the rPOA or mPOA. In vitro, MCH stimulated gonadotrophin-releasing hormone (GnRH) release from hypothalamic explants. Double-label immunohistochemistry showed GnRH-immunoreactive neurones in the vicinity of and intermingled with immunoreactive MCH processes. MCH is the endogenous ligand of the MCH type 1 receptor (MCH1-R). Previously, we have shown a role for melanocortin-5 receptors (MC5-R) in the stimulatory action of MCH, so we next investigated the involvement of both MCH1-R and/or MC5-R in mediating the actions of MCH on GnRH and hence LH release. The stimulatory action of MCH in the rPOA was inhibited by administration of antagonists for either MCH1-R or MC5-R. However, in the mPOA, the action of MCH was blocked only by the MC5-R antagonist. LH release was stimulated by an agonist for MC5-R injected into the rPOA or mPOA; this was blocked by the MC5-R antagonist but not the MCH1-R antagonist. These results indicate that both MCH1-R and MC5-R are involved in the central control of LH release by MCH. [source]


Stimulatory action of mitemcinal (GM-611), an acid-resistant non-peptide motilin receptor agonist, on colonic motor activity and defecation: spontaneous and mitemcinal-induced giant migrating contractions during defecation in dogs

NEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2009
T. Hirabayashi
Abstract, The aim of this study was to characterize giant migrating contractions (GMCs) during spontaneous defecation in dogs and to investigate the effect of mitemcinal (an orally active and highly acid-resistant motilin receptor agonist) on colonic motility to assess the possibility of using it for the treatment of colonic motility disorders. To assess colonic motility, strain-gauge force transducers were implanted on the gastrointestinal tract of five dogs, and the behaviour of the dogs was monitored with a noctovision-video camera system. The effect of mitemcinal (0, 3, 10 or 30 mg per dog) and sennoside (300 mg per dog) on colonic motility was assessed 24 h after oral administration. During a 39-day period, the starting point of most of the 140 GMCs was between the transverse colon and the descending colon, but some variation was observed. In the daytime, the GMCs originated from somewhat more proximal positions than at night. Mitemcinal caused an increase in the GMC-index (integration of contractile amplitude and duration) and proximal translocation of the GMC starting point, but did not cause an increase in the number of defecations 12 h after administration. Sennoside, however, caused a significant increase in the number of defecations, an increase in the GMC-index, and prolongation of the duration of GMCs. The GMC starting point in the canine colon varied during spontaneous defecation. Mitemcinal was a potent prokinetic drug to mimic a spontaneous defecation compared with sennoside. Mitemcinal evacuates more intestinal luminal contents during the defecation than does sennoside. [source]


Female Estrogen Receptor ,,/, Mice Are Partially Protected Against Age-Related Trabecular Bone Loss

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2001
Sara H. Windahl
Abstract Recently, it has been shown that inactivation of estrogen receptor , (ER-,) by gene targeting results in increased cortical bone formation in adolescent female mice. To study the possible involvement of ER-, in the regulation of the mature skeleton, we have extended the analyses to include 1-year-old ER-, knockout mice (ER-,,/,). Male ER-,,/, mice did not express any significant bone phenotypic alterations at this developmental stage. However, the increase in cortical bone parameters seen already in the adolescent female ER-,,/, mice was maintained in the older females. The aged female ER-,,/, mice further exhibited a significantly higher trabecular bone mineral density (BMD) as well as increased bone volume/total volume (BV/TV) compared with wild-type (wt) mice. This was caused by a less pronounced loss of trabecular bone during adulthood in female ER-,,/, mice. The growth plate width was unaltered in the female ER-,,/, mice. Judged by the expression of the osteoclast marker tartrate-resistant acid phosphatase (TRAP) and cathepsin K (cat K; reverse-transcription-polymerase chain reaction [RT-PCR]) as well as the serum levels of C-terminal type I collagen cross-linked peptide, bone resorption appeared unaffected. However, an increase in the messenger RNA (mRNA) expression levels of the osteoblast marker core-binding factor ,1 (Cbfa1) suggested an anabolic effect in bones of old female ER-,,/, mice. In addition, the mRNA expression of ER-, was augmented, indicating a role for ER-, in the development of this phenotype. Taken together, the results show that ER-, is involved in the regulation of trabecular bone during adulthood in female mice and suggest that ER-, acts in a repressive manner, possibly by counteracting the stimulatory action of ER-, on bone formation. [source]


A New Key Neurohormone Controlling Reproduction, Gonadotrophin-Inhibitory Hormone in Birds: Discovery, Progress and Prospects

JOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009
K. Tsutsui
In vertebrates, the neuropeptide control of gonadotrophin secretion is primarily through the stimulatory action of the hypothalamic decapeptide, gonadotrophin-releasing hormone (GnRH). Gonadal sex steroids and inhibin inhibit gonadotrophin secretion via feedback from the gonads, but a hypothalamic neuropeptide inhibiting gonadotrophin secretion was, until recently, unknown in vertebrates. In 2000, we discovered a novel hypothalamic dodecapeptide that directly inhibits gonadotrophin release in quail and termed it gonadotrophin-inhibitory hormone (GnIH). GnIH acts on the pituitary and GnRH neurones in the hypothalamus via a novel G-protein-coupled receptor for GnIH to inhibit gonadal development and maintenance by decreasing gonadotrophin release and synthesis. The pineal hormone melatonin is a key factor controlling GnIH neural function. GnIH occurs in the hypothalamus of several avian species and is considered to be a new key neurohormone inhibiting avian reproduction. Thus, the discovery of GnIH provides novel directions to investigate neuropeptide regulation of reproduction. This review summarises the discovery, progress and prospects of GnIH, a new key neurohormone controlling reproduction. [source]


Evidence for a Stimulatory Action of Melanin-Concentrating Hormone on Luteinising Hormone Release Involving MCH1 and Melanocortin-5 Receptors

JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2006
J. F. Murray
Abstract The present series of studies aimed to further our understanding of the role of melanin-concentrating hormone (MCH) neurones in the central regulation of luteinising hormone (LH) release in the female rat. LH release was stimulated when MCH was injected bilaterally into the rostral preoptic area (rPOA) or medial preoptic area (mPOA), but not when injected into the zona incerta (ZI), of oestrogen-primed ovariectomised rats. In rats that were steroid-primed to generate a surge-like release of LH, MCH administration into the ZI blocked this rise in LH release: no such effect occurred when MCH was injected into the rPOA or mPOA. In vitro, MCH stimulated gonadotrophin-releasing hormone (GnRH) release from hypothalamic explants. Double-label immunohistochemistry showed GnRH-immunoreactive neurones in the vicinity of and intermingled with immunoreactive MCH processes. MCH is the endogenous ligand of the MCH type 1 receptor (MCH1-R). Previously, we have shown a role for melanocortin-5 receptors (MC5-R) in the stimulatory action of MCH, so we next investigated the involvement of both MCH1-R and/or MC5-R in mediating the actions of MCH on GnRH and hence LH release. The stimulatory action of MCH in the rPOA was inhibited by administration of antagonists for either MCH1-R or MC5-R. However, in the mPOA, the action of MCH was blocked only by the MC5-R antagonist. LH release was stimulated by an agonist for MC5-R injected into the rPOA or mPOA; this was blocked by the MC5-R antagonist but not the MCH1-R antagonist. These results indicate that both MCH1-R and MC5-R are involved in the central control of LH release by MCH. [source]


Novel bromomelatonin derivatives suppress osteoclastic activity and increase osteoblastic activity: implications for the treatment of bone diseases

JOURNAL OF PINEAL RESEARCH, Issue 3 2008
Nobuo Suzuki
Abstract:, The teleost scale is a calcified tissue that contains osteoclasts, osteoblasts, and bone matrix, all of which are similar to those found in mammalian membrane bone. Using the goldfish scale, we recently developed a new in vitro assay system and previously demonstrated that melatonin suppressed both osteoclastic and osteoblastic activities in this assay system. In mammals, 2-bromomelatonin possesses a higher affinity for the melatonin receptor than does melatonin. Using a newly developed synthetic method, we synthesized 2-bromomelatonin, 2,4,6-tribromomelatonin and novel bromomelatonin derivatives (1-allyl-2,4,6-tribromomelatonin, 1-propargyl-2,4,6-tribromomelatonin, 1-benzyl-2,4,6-tribromomelatonin, and 2,4,6,7-tetrabromomelatonin) and then examined the effects of these chemicals on osteoclasts and osteoblasts. All bromomelatonin derivatives, as well as melatonin, had an inhibitory action on osteoclasts. In particular, 1-benzyl-2,4,6-tribromomelatonin (benzyl-tribromomelatonin) possessed a stronger activity than melatonin. At an in vitro concentration of 10,10 m, benzyl-tribromomelatonin still suppressed osteoclastic activity after 6 hr of incubation. In reference to osteoblasts, all bromomelatonin derivatives had a stimulatory action, although melatonin inhibited osteoblastic activity. In addition, estrogen receptor mRNA expression (an osteoblastic marker) was increased in benzyl-tribromomelatonin (10,7 m)-treated scales. Taken together, the present results strongly suggest that these novel melatonin derivatives have significant potential for use as beneficial drug for bone diseases such as osteoporosis. [source]


STEROID EFFECTS ON THE GENE EXPRESSION OF PERIPHERAL MYELIN PROTEINS

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002
RC Melcangi
The present article summarizes recent observations obtained in our laboratory which clearly indicate that sex steroids exert relevant effects on the peripheral nervous system. In particular, the following important points have emerged: (1) Steroids exert stimulatory actions on the synthesis of the proteins proper of the peripheral myelin (e.g., glycoprotein Po and peripheral myelin protein 22) in vivo and on the Schwann cells in culture; (2) in many cases the actions of hormonal steroids are not due to their native molecular forms but rather to their metabolites (e.g., dihydroprogesterone and tetrahydroprogesterone in the case of progesterone; dihydrotestosterone and 5 alpha-androstane-3 alpha,17 beta -diol in the case of testosterone); (3) the mechanism of action of the various steroidal molecules may involve both classical (progesterone and androgen receptors) and nonclassical steroid receptors (GABA, receptor); and finally, (4) the stimulatory action of steroid hormones on the proteins of the peripheral myelin might have clinical significance in cases in which the rebuilding of myelin is needed (e.g., aging, peripheral injury, demyelinating diseases, and iabetic neuropathy). [source]


Central nervous system stimulatory action from the root extract of Plumbago zeylanica in rats

PHYTOTHERAPY RESEARCH, Issue 2 2001
C. P. Bopaiah
Abstract The effects of a 50% ethanol extract of the root of Plumbago zeylanica (P. zeylanica) were investigated on locomotor behaviour and central dopaminergic activity in rats. The effects on the ambulatory behaviour were assessed along with the levels of dopamine (DA) and its metabolite homovanillic acid (HVA) in the striatum after a single oral dose (100, 200 and 300,mg/kg body weight) of the extract. The extract significantly increased the spontaneous motility in animals. The ambulatory and rotatory behaviour in the treated groups were higher than in the control group (p,<,0.05). There were marked differences in the ambulatory behaviour between 100 and 300,mg/kg, indicating that the responses were stimulatory and dose-dependent. The stereotypic behaviour which is characteristic of a dopamine agonist showed biphasic effects. However, there was no significant difference between the groups (p,>,0.05). The results showed that the extract of the root of P. zeylanica specifically enhanced the spontaneous ambulatory activity without inducing stereotypic behaviour. The neurochemical estimations revealed elevated levels of DA and HVA in striatum compared with the control rats (p,<,0.01). The levels were higher for the 100,mg/kg treated group than the other groups. The levels declined by increasing the dosage of the extract to 200,mg/kg and 300,mg/kg, however, these levels remained higher than the control group. The relationship between motor activity and levels of dopamine are not parallel. These behavioural and biochemical results indicated stimulatory properties of the extract of the root of P. zeylanica, which may be mediated by dopaminergic mechanisms in the rat brain. Copyright 2001 John Wiley & Sons, Ltd. [source]


Mechanism of insulin action on glucose metabolism in ruminants

ANIMAL SCIENCE JOURNAL, Issue 6 2002
Shin-ichi SASAKI
ABSTRACT This review presents a brief overview on the mechanism of insulin action on glucose metabolism at the molecular basis in ruminants. For ruminants, an exact mechanism of insulin on glucose metabolism is still rudimentary, but it is clear that originally, if not all, the mechanism of insulin action in ruminants was the same as in other species. Like non-ruminants, the insulin-sensitive glucose transporter GLUT 4 is thought to be a key-protein in the control of glucose uptake and metabolism in ruminants, and insulin regulates glucose transport by stimulating the translocation of GLUT 4 from an intracellular membrane pool to the plasma membrane in adipocytes and muscles. Moreover, insulin-induced GLUT 4 translocation is activated through the common intracellular signaling pathway of insulin phosphatidylinositol 3-kinase (PI3-kinase) signaling pathway rather than the mitogen activated protein kinase (MAP kinase)-dependent signaling pathway. However, GLUT 4 mRNA and protein, and insulin-induced GLUT 4 translocation on adipocytes and muscles in ruminants are lower than those in rodents and human subjects. Furthermore, insulin-induced PI3-kinase activation is reduced concomitantly with the lower content of insulin receptor substrate-1 (IRS-1) in ruminants. In spite of normal status, a resistance to the stimulatory action of insulin on glucose metabolism in ruminants as compared to non-ruminants may be due to, at least in part, the lower content of GLUT 4 and the lower capacity of insulin signal transduction, resulting to the lower glucose transport activity. [source]


STEROID EFFECTS ON THE GENE EXPRESSION OF PERIPHERAL MYELIN PROTEINS

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002
RC Melcangi
The present article summarizes recent observations obtained in our laboratory which clearly indicate that sex steroids exert relevant effects on the peripheral nervous system. In particular, the following important points have emerged: (1) Steroids exert stimulatory actions on the synthesis of the proteins proper of the peripheral myelin (e.g., glycoprotein Po and peripheral myelin protein 22) in vivo and on the Schwann cells in culture; (2) in many cases the actions of hormonal steroids are not due to their native molecular forms but rather to their metabolites (e.g., dihydroprogesterone and tetrahydroprogesterone in the case of progesterone; dihydrotestosterone and 5 alpha-androstane-3 alpha,17 beta -diol in the case of testosterone); (3) the mechanism of action of the various steroidal molecules may involve both classical (progesterone and androgen receptors) and nonclassical steroid receptors (GABA, receptor); and finally, (4) the stimulatory action of steroid hormones on the proteins of the peripheral myelin might have clinical significance in cases in which the rebuilding of myelin is needed (e.g., aging, peripheral injury, demyelinating diseases, and iabetic neuropathy). [source]


Obestatin , a ghrelin-associated peptide that does not hold its promise to suppress food intake and motility

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2007
G. Gourcerol
Abstract, Ghrelin is a gut peptide well established to induce prokinetic and appetite stimulatory actions. Obestatin is a novel 23-amino acid peptide derived from the processing of the ghrelin gene. The peptide name was in keeping with its initially reported actions to suppress food intake and digestive motility and to antagonize ghrelin's stimulatory effect through interaction with the orphan GPR-39 receptor. However, subsequently, these findings have been questioned because obestatin actions to reduce food intake and to inhibit gastrointestinal (GI) motility in vivo and in vitro have not been reproduced by several groups. Furthermore, while GPR-39 appears to be involved in gut motor functions, convergent reports showed that obestatin is not the cognate ligand for this receptor. In light of recent controversy over the effects of obestatin, the present findings from De Smet et al. provides additional evidence that obestatin does not influence food intake and GI motility in vivo and in vitro. Taken together, existing reports curtail the initial promise that obestatin is a new regulator of appetite and digestive motility. Therefore, it is proposed to rename obestatin as ghrelin-associated peptide. [source]