Identification and localization of steroid-binding and nonsteroid-binding forms of the glucocorticoid receptor in the mouse P1798 lymphosarcoma

Rowan, Brian G.; Ip, Margot M.

doi:10.1016/0960-0760(94)00193-p

Cited by 4 publications

(2 citation statements)

References 46 publications

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“…The REMstage was more inhibited than the NREM stage and disappeared completely in some animals (Table 3). Spectral analysis of electrical activity on corticograms and hippocampograms during that period revealed severe disturbances of the hippocampal 0 rhythm, as evidenced by enhanced slow-wave component of this rhythm (4-7 Hz) and reduced fast-wave component (8)(9)(10)(11)(12). Twenty-four hour afcer MPTP administration, the NREM stage tended to increase, while the proportion of wakefulness in the sleep-wake cycle decreased, but both still differed from their control levels; the proportion of REM episodes remained low (Table 3).…”

Section: Resultsmentioning

confidence: 99%

Abnormal sleep pattern and impaired learning capacity in rats with MPTP-induced Parkinsonian syndrome

et al. 1996

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Rats with the Parkinsonian syndrome induced by systemic injection of the neurotoxin 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) develop extrapyramidal disorders (oligokinesia, tremor, and rigidity) which depend on the dose and duration of action of MPTP. At 15 and 30 mg/kg MPTP impairs the learning of the conditioned passive avoidance response, shortens both stages of sleep, particularly the paradoxical (REM) stage, and prolongs the period of wakefulness. The mnestic function disturbance is not associated with extrapyramidal disorders, since it develops in their absence. In MPTP-treated rats memory and sleep disorders are interrelated. Key Words: extrapyramidal disorders; Parkinsonian syndrome; sleep patternIn addition to extrapyramidal symptoms (tremor, oligokinesia, and rigidity) and characteristic autonomic disturbances, patients with parkinsonism have impaired intellectual and mnestic functions and develop sleep disorders [5][6][7][8]. The causes of these abnormalities and their relation to pathogenesis and therapy of Parkinson's disease so far remain unclear. The Parkinsonian syndrome has Laboratory of Psychopharmacology, Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow been modeled with the use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin which damages dopaminergic neurons of the striatum thus inducing extrapyramidal disturbances [2,9]. Chronic administration of MPTP in low doses to monkeys impairs the learning of Conditioned responses, the effect being reversed by dopaminergic agonists [10].In this study we examined mnestic functions and sleep disorders in rats with the Parkinsonian syndrome induced by MPTP.

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Section: Resultsmentioning

confidence: 99%

Abnormal sleep pattern and impaired learning capacity in rats with MPTP-induced Parkinsonian syndrome

et al. 1996

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“…Molecular targets of steroid hormones are usually located in the cytoplasma membrane. The following trigger mechanisms of nongenomic effect of steroid hormones have been demonstrated: 1) stimulation of Na+/K+-ATPase in the kidney tubular epithelium [12,13]; 2) activation of rapid calcium entry by progesterone, testosterone, and lc~,25-dihydroxyvitamin D 3 [3-5,9,14]; 3) modification of the metabolism of second messengers in normal and transformed cells [6,7,11]; 4) modulation of the activity of neuronal Cl-channels coupled to GABA Areceptors [8]. The nongenomic effects of steroid hormones are characterized by latency, duration of their action (within 30 min), and tolerance to the blockers of RNA and protein syntheses.…”

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confidence: 99%

Human platelets as the object of investigation of the molecular mechanisms underlying nongenomic effects of glucocorticoid hormones

1996

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The effect of hydrocortisone (100 nM-10 gM) on the major biochemical parameters of platelet activity (intracellular free calcium concentration, thromboxane B 2 content, and baseline and stimulated levels of cAMP and cGMP) is examined. The results obtained indicate that the inhibitory effect of glucocorticoids on platelet aggregation is mediated by activation of the adenylate cyclase system and suppression of the calcium response. Presumably, neither guanylate cyclase nor phospholipase A2-dependent systems are the targets of nongenomic actions of glucocorticoid hormones. Platelets can serve as a convenient tool for the investigation of nongenomic effects of glucocorticoid hormones. Key Words: hydrocortisone; calcium; cGMP; cAMP; thromboxane; inhibitors and activators of plateletsNongenomic effects contribute considerably to the physiological and pharmacological activity of steroid hormones. Molecular targets of steroid hormones are usually located in the cytoplasma membrane. The following trigger mechanisms of nongenomic effect of steroid hormones have been demonstrated: 1) stimulation of Na+/K+-ATPase in the kidney tubular epithelium [12,13]; 2) activation of rapid calcium entry by progesterone, testosterone, and lc~,25-dihydroxyvitamin D 3 [3-5,9,14]; 3) modification of the metabolism of second messengers in normal and transformed cells [6,7,11]; 4) modulation of the activity of neuronal Cl-channels coupled to GABA Areceptors [8]. The nongenomic effects of steroid hormones are characterized by latency, duration of their action (within 30 min), and tolerance to the blockers of RNA and protein syntheses. Steroids induce a membranotropic effect without penetrating the plasma Department of Pharmacology and Radiobiology, Russian State Medical University, Moscow membrane, which has been used to distinguish between genomic (mediated by intracellular receptors) and nongenomic effects. For example, the membrane stage in the action of steroid hormones can be identified with the use of these hormones immobilized on a high-molecular-weight carrier [1]. Anuclear ceils (erythrocytes and platelets) provide another approach to the investigation of the mechanisms underlying the membrane-mediated effects of steroids.The aim of the present study was to develop a theoretical and experimental basis for the evaluation of the nongenomic effect of the glucocorticoid hydrocortisone (cortisol) on platelet activity. MATERIALS AND METHODSThe procedures of platelet isolation, loading with the fluorescent probe Fura 2-AM, and calculation of the intracellular free calcium content were described elsewhere [2]. The content of cAMP, cGMP, and thromboxane B 2 was measured by the radioligand

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Agonist-free transformation of the glucocorticoid receptor in human B-lymphoma cells

Berg

Smets

Rooij

1996

The Journal of Steroid Biochemistry and Molecular Biology

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Identification and localization of steroid-binding and nonsteroid-binding forms of the glucocorticoid receptor in the mouse P1798 lymphosarcoma

Cited by 4 publications

References 46 publications

Abnormal sleep pattern and impaired learning capacity in rats with MPTP-induced Parkinsonian syndrome

Abnormal sleep pattern and impaired learning capacity in rats with MPTP-induced Parkinsonian syndrome

Human platelets as the object of investigation of the molecular mechanisms underlying nongenomic effects of glucocorticoid hormones

Agonist-free transformation of the glucocorticoid receptor in human B-lymphoma cells

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