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

Nerobkova, L. N.; Markina, N. V.; Воронина, Т. А.; Kraineva, V. A.; Garibova, T. L.; Молодавкин, Г. М.; Sharkova, L. M.

doi:10.1007/bf02446577

Cited by 3 publications

(1 citation statement)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Structure 214 is another aminoadamantane derivative that has been studied as an antiparkinsonian agent, e. g., in chemically induced parkinsonism in mice. 381 More recent adamantane derivatives studied in the context of PD are TEMPO-derivatives like 215 382 or the fullerene-derivative 216 . 383 Both compounds have been shown to be active against chemically induced parkinsonism in rodents.…”

Section: Adamantanes Against Diseases Of the Central Nervous Systementioning

confidence: 99%

The Lipophilic Bullet Hits the Targets: Medicinal Chemistry of Adamantane Derivatives

Wanka¹,

Iqbal²,

Schreiner³

2013

Chem. Rev.

580

475

View full text Add to dashboard Cite

Section: Adamantanes Against Diseases Of the Central Nervous Systementioning

confidence: 99%

The Lipophilic Bullet Hits the Targets: Medicinal Chemistry of Adamantane Derivatives

Wanka¹,

Iqbal²,

Schreiner³

2013

Chem. Rev.

580

475

View full text Add to dashboard Cite

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

1996

View full text Add to dashboard Cite

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

show abstract

Transplantation in the nonhuman primate MPTP model of Parkinson's disease: update and perspectives

Wianny

Vezoli

2017

Primate Biol.

View full text Add to dashboard Cite

Abstract. In order to calibrate stem cell exploitation for cellular therapy in neurodegenerative diseases, fundamental and preclinical research in NHP (nonhuman primate) models is crucial. Indeed, it is consensually recognized that it is not possible to directly extrapolate results obtained in rodent models to human patients. A large diversity of neurological pathologies should benefit from cellular therapy based on neural differentiation of stem cells. In the context of this special issue of Primate Biology on NHP stem cells, we describe past and recent advances on cell replacement in the NHP model of Parkinson's disease (PD). From the different grafting procedures to the various cell types transplanted, we review here diverse approaches for cell-replacement therapy and their related therapeutic potential on behavior and function in the NHP model of PD.

show abstract

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

Cited by 3 publications

References 8 publications

The Lipophilic Bullet Hits the Targets: Medicinal Chemistry of Adamantane Derivatives

The Lipophilic Bullet Hits the Targets: Medicinal Chemistry of Adamantane Derivatives

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

Transplantation in the nonhuman primate MPTP model of Parkinson's disease: update and perspectives

Contact Info

Product

Resources

About