Effect with time of a norepinephrine synthesis inhibitor (U-14,624) on hypothalamic catecholamine and plasma gonadotrophin concentrations in the ovariectomized rat

Kohn, Sarah; Morgan, W. W.; Carrillo, Alberto J.

doi:10.1530/jrf.0.0660185

Cited by 2 publications

(2 citation statements)

References 11 publications

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“…The purpose of the present study was to con firm and extend our preliminary observations of a sex dif ference in acute bromocriptine-induced increases in JH-E: binding in hypothalamus and pituitary of the rat [19][20][21][22]75]. We chose to do this both by again giving the DA agonist bromocriptine [9,15] to provide exogenous DA stimulation and, in a separate study, by administering an inhibitor of norepinephrine (NE) synthesis to increase endogenous DA levels and release [16,36,64]. We then compared JH-E' binding in male and female rats in vivo after such drug treatments.…”

mentioning

confidence: 99%

Sex Differences in [<sup>3</sup>H]-Estradiol Binding in Brain and Pituitary after Acute Dopaminergic Treatment

Gietzen¹,

Woolley²

1986

Neuroendocrinology

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Responses to estrogen differ between the sexes, yet sex differences in specific binding of estradiol (E2) to its receptor are not observed consistently. Dopaminergic treatment has been shown to increase binding of ³H-E₂ in selected brain areas and anterior pituitary in the female rat, and the dopaminergic system is sexually differentiated. In order to determine whether or not dopaminergic stimulation might induce sex differences in ³H-E₂ binding, male and female gonadectomized-adrenalectomized rats were pretreated either with bromocriptine, a dopamine agonist, or with diethyldithiocarbamate (DDC), an inhibitor of dopamine β-hydroxylase. DDC was used in order to increase endogenous release of dopamine. After such acute dopaminergic treatment, specific binding of ³H-E₂ in nuclear and extranuclear fractions of 6 brain areas and pituitary in vivo was determined 1 h after intravenous injection of Η-E₂ (1 µg/kg body weight). Administration of either bromocriptine or DDC increased specific ³H-E₂ binding to nuclear and extranuclear fractions of basal hypothalamus and anterior pituitary from female but not from male rats, thus inducing sex differences in binding in these two tissues. Bromocriptine also increased specific binding in the pineal in females. Total binding was increased in a crude membrane fraction (P₂) from pituitary of female but not of male rats after administration of DDC, but the percent of extranuclear specific binding found in the P₂ fraction was decreased after DDC in both males and females. The findings suggest that dopaminergic stimulation may induce sex differences in ³H-E2 binding by increasing binding in some brain areas and anterior pituitary in females but not in males.

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confidence: 99%

Sex Differences in [<sup>3</sup>H]-Estradiol Binding in Brain and Pituitary after Acute Dopaminergic Treatment

Gietzen¹,

Woolley²

1986

Neuroendocrinology

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“…Our findings are consistent with some other reports. For example, Wang et al [ 47 , 48 ] reported that phillyrin showed a protective effect against bone loss in an in vivo model by inhibiting RANKL-induced osteoclast differentiation, but did not affect osteoblast differentiation. Interestingly, phillyrin decreased RANKL expression in an in vivo model of osteolysis.…”

Section: Discussionmentioning

confidence: 99%

N-[2-(4-Acetyl-1-Piperazinyl)Phenyl]-2-(3-Methylphenoxy)Acetamide (NAPMA) Inhibits Osteoclast Differentiation and Protects against Ovariectomy-Induced Osteoporosis

et al. 2020

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Osteoclasts are large, multinucleated cells responsible for bone resorption and are induced in response to the regulatory activity of receptor activator of nuclear factor-kappa B ligand (RANKL). Excessive osteoclast activity causes pathological bone loss and destruction. Many studies have investigated molecules that specifically inhibit osteoclast activity by blocking RANKL signaling or bone resorption. In recent years, we screened compounds from commercial libraries to identify molecules capable of inhibiting RANKL-induced osteoclast differentiation. Consequently, we reported some compounds that are effective at attenuating osteoclast activity. In this study, we found that N-[2-(4-acetyl-1-piperazinyl)phenyl]-2-(3-methylphenoxy)acetamide (NAPMA) significantly inhibited the formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells from bone marrow-derived macrophages in a dose-dependent manner, without cytotoxic effects. NAPMA downregulated the expression of osteoclast-specific markers, such as c-Fos, NFATc1, DC-STAMP, cathepsin K, and MMP-9, at the transcript and protein levels. Accordingly, bone resorption and actin ring formation were decreased in response to NAPMA treatment. Furthermore, we demonstrated the protective effect of NAPMA against ovariectomy-induced bone loss using micro-CT and histological analysis. Collectively, the results showed that NAPMA inhibited osteoclast differentiation and attenuated bone resorption. It is thus a potential drug candidate for the treatment of osteoporosis and other bone diseases associated with excessive bone resorption.

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Effect with time of a norepinephrine synthesis inhibitor (U-14,624) on hypothalamic catecholamine and plasma gonadotrophin concentrations in the ovariectomized rat

Cited by 2 publications

References 11 publications

Sex Differences in [<sup>3</sup>H]-Estradiol Binding in Brain and Pituitary after Acute Dopaminergic Treatment

Sex Differences in [<sup>3</sup>H]-Estradiol Binding in Brain and Pituitary after Acute Dopaminergic Treatment

N-[2-(4-Acetyl-1-Piperazinyl)Phenyl]-2-(3-Methylphenoxy)Acetamide (NAPMA) Inhibits Osteoclast Differentiation and Protects against Ovariectomy-Induced Osteoporosis

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