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Ouabain exacerbates botulinum neurotoxin-induced muscle paralysis via progression of muscle atrophy in mice.

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Botulinum neurotoxin serotype A (BoNT/A) inhibits acetylcholine release at the neuromuscular junction in isolated muscles, and ouabain can partially block its effect. However, it is not clear whether ouabain attenuates BoNT/A-induced neuromuscular paralysis in vivo. In this work, we investigated the

Cochlear function after selective spiral ganglion cells degeneration induced by ouabain.

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BACKGROUND Ouabain, a cardiac glycoside that specifically binds to Na/K-ATPase and inhibits its activity, was applied to gerbils to develop a method for studying auditory neuropathy. METHODS Ouabain was applied to the round window of the cochlea in each gerbil by using a piece of gelfoam with 3

Ouabain-induced cochlear degeneration in rat.

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Ouabain, a potent inhibitor of the Na+/K+-ATPase pump, selectively destroys spiral ganglion neurons (SGNs) in gerbils and mice, whereas in guinea pigs it preferentially damages cochlear hair cells. To elucidate the effects of ouabain on the rat inner ear, a species widely used in research, 5 μl of 1

Ouabain-induced cochlear nerve degeneration: synaptic loss and plasticity in a mouse model of auditory neuropathy.

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Ouabain application to the round window can selectively destroy type-I spiral ganglion cells, producing an animal model of auditory neuropathy. To assess the long-term effects of this deafferentation on synaptic organization in the organ of Corti and cochlear nucleus, and to ask whether surviving

Synergistic effect between ouabain and glucocorticoids for the induction of thymic atrophy.

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The present report shows that thymocyte death, induced by glucocorticoids, may be modulated in vivo by ouabain. Young, ten days old, mice injected with 140 mg/kg sodium succcinate of hydrocortisone (HC) intraperitonially (i.p.) displayed, 24 h after the injection, a decrease in thymus size and

Ouabain Does Not Induce Selective Spiral Ganglion Cell Degeneration in Guinea Pigs.

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Round window membrane (RWM) application of ouabain is known to selectively destroy type I spiral ganglion cells (SGCs) in cochleas of several rodent species, while leaving hair cells intact. This protocol has been used in rats and Mongolian gerbils, but observations in the guinea pig are

[Retinal degeneration induced by medical agents. 1. Retinal degeneration induced by ouabain].

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Ouabain binding to chick embryo neuroretina during development in ovo and in monolayer cultures.

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Eight-day-old embryo neuroretinas (NR) were dissociated and cultured as monolayer. [3H]Ouabain binding was investigated during the culture period. [3H]Ouabain binding to NR increases continuously until around the tenth day of culture, but after that it gradually decreased. On the other hand,

Functional and morphological abnormalities induced by ouabain intoxication of the rabbit retina.

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Several researchers have recently used an intravitreal ouabain injection to induce a suitable model of experimental retinopathy and optic neuropathy in various animals. Ouabain administration into the vitreous body of rabbit causes an irreversible degeneration of the retinal layers and consequently

Ischemia-induced alteration of myocardial Na(+)-K(+)-ATPase activity and ouabain binding sites in hypercholesterolemic rabbits.

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The purpose of this study was to explore the effect of ischemia on the Na(+)-K(+)-ATPase activity and ouabain receptor of the myocardial sarcolemma in hypercholesterolemic rabbits. Male New Zealand white rabbits were fed with either standard chow or standard chow supplemented with 0.5% (w/w)

Proliferating cell nuclear antigen involved in the repair process of ouabain-induced brain damage independent of hypertension in rats.

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BACKGROUND Ouabain is a mammalian adrenocortical hormone that is involved in the pathogenesis of hypertension by inhibiting Na-K ATPase activity. It also participates in a variety of kinase-mediated signaling pathways associated with Na-K ATPase. Previous studies have shown that ouabain can cause

Sodium channels contribute to degeneration of dorsal root ganglion neurites induced by mitochondrial dysfunction in an in vitro model of axonal injury.

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Axonal degeneration occurs in multiple neurodegenerative disorders of the central and peripheral nervous system. Although the underlying molecular pathways leading to axonal degeneration are incompletely understood, accumulating evidence suggests contributions of impaired mitochondrial function,

Different ouabain sensitivities of Na+/K(+)-ATPase from Poekilocerus bufonius tissues and a possible physiological cost.

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1. The properties of Na+/K(+)-transporting ATPase in microsomal preparation from mid-gut of the grasshopper, Poekilocerus bufonius, were investigated and compared with the same enzyme from brain and excretory system. 2. Two components of ATPases activity are present in the three tissues studied. 3.

The new targets of ouabain in retinal interneurons of Sprague-Dawley rats.

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Ouabain is both a cardiac glycoside used in therapy of congestive heart failure and an endogenous steroid hormone. It specifically binds to Na(+), K(+)-ATPase (NKA) and blocks its activity. Overdose of ouabain induces retinal damage. In different species ouabain-induced retinal degeneration affects

The effect of ouabain on hearts of cardiomyopathic hamsters: potentiation by isoproterenol.

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The isometric twitch properties of papillary muscles from hearts of 30- to 53-day-old cardiomyopathic hamsters (BIO 14.6) were studied before and after exposure to the cardiac glycoside, ouabain. The diseased tissue was weakly responsive to ouabain (3 to 100 microM), as compared to a more

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