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gamma aminobutyric acid/atrophie
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Seite 1 von 376 Ergebnisse
gamma-Aminobutyric acid system in developing and degenerating mouse retina.
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Freeze-dried sections (14 microns thick) of retinal layers were prepared from mice with retinal degeneration (C3H strain) and control mice (C57BL strain). The weighed sections (2-30 ng dry weight) were analyzed using our microassay methods. In the control retina, gamma-aminobutyric acid (GABA)
Gamma-aminobutyric acid specifically inhibits progression of tubular fibrosis and atrophy in nephrectomized rats.
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Gamma-aminobutyric acid (GABA) was administered orally to rats for 60 d after excision of five-sixths of their kidney volume. A decrease in renal function parameters was observed in these nephrectomized rats. However, the administration of GABA ameliorated renal dysfunction, and a longer
Overexpression of gamma-aminobutyric acid transporter subtype I leads to cognitive deterioration in transgenic mice.
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OBJECTIVE
To explore the physiological role of gamma-aminobutyric acid transporter subtype I (GAT1) in cognition.
METHODS
Transgenic mice were produced by pronuclei microinjection method. Integration of transgene was identified by Southern-blot and PCR analysis in various generations. Level of GAT1
Multilevel transneuronal degeneration after brain damage. Behavioral events and effects of anticonvulsant gamma-aminobutyric acid-related drugs.
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Recent morphologic and behavioral studies of the effects of gamma-aminobutyric acid agents on transsynaptic degeneration after cortical and striatal damage are reviewed and discussed. Following unilateral lesions of the anteromedial cortex, mild atrophy appears in the ipsilateral striatum and
Enhanced γ-aminobutyric acid accumulation, alleviated componential deterioration and technofunctionality loss of germinated wheat by hypoxia stress.
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Germination is an effective biofortification strategy to enhance micronutrients of staple grains. The current study targeted at comparing the effects of normoxia and hypoxia on γ-aminobutyric acid (GABA) content and the componential changes underlying the technofunctionality of germinated wheat.
Exposure to glyphosate- and/or Mn/Zn-ethylene-bis-dithiocarbamate-containing pesticides leads to degeneration of γ-aminobutyric acid and dopamine neurons in Caenorhabditis elegans.
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Previous studies demonstrate a positive correlation between pesticide usage and Parkinson's disease (PD), which preferentially targets dopaminergic (DAergic) neurons. In order to examine the potential relationship between two common pesticides and specific neurodegeneration, we chronically (24 h) or
PACAP-mediated neuroprotection of neurochemically identified cell types in MSG-induced retinal degeneration.
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Pituitary adenylate cyclase-activating polypeptide (PACAP) is neuroprotective in animal models of different brain pathologies and injuries, including cerebral ischemia, Parkinson's disease, and different types of retinal degenerations. We have previously shown that PACAP is protective against
Evaluation of the protective effects of PACAP with cell-specific markers in ischemia-induced retinal degeneration.
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Pituitary adenylate cyclase activating polypeptide (PACAP) is a neurotrophic and neuroprotective peptide that has been shown to exert protective effects in different neuronal injuries, such as traumatic brain injury, models of neurodegenerative diseases and cerebral ischemia. We have provided
Cerebellar atrophy in human and murine succinic semialdehyde dehydrogenase deficiency.
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Human succinic semialdehyde dehydrogenase deficiency, an autosomal recessive disorder of γ-aminobutyric acid (GABA) catabolism, was modeled by a murine model sharing the phenotype of ataxia and seizures. Magnetic resonance imaging (MRI) with volumetry was obtained on 7 patients versus controls, and
Computational molecular phenotyping of retinal sheet transplants to rats with retinal degeneration.
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Retinal progenitor sheet transplants have been shown to extend neuronal processes into a degenerating host retina and to restore visual responses in the brain. The aim of this study was to identify cells involved in transplant signals to retinal degenerate hosts using computational molecular
Afferent fibers from the septum terminate on gamma-aminobutyric acid (GABA-) interneurons and granule cells in the area dentata of the rat.
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Interneurons in the area dentata of the rat were immunostained with an antibody to gamma-aminobutyric acid. After septal lesions, degenerating terminals were found in asymmetric synaptic contact with granule cell somata and dendritic elements of immunoreactive and nonreactive cells in the
Gamma-aminobutyric acid(B) autoreceptors in substantia nigra and neostriatum of the weaver mutant mouse.
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The weaver mutation causes cell loss in the center of the substantia nigra, pars compacta. We compared the depression of gamma-aminobutyric acid (GABA)(A) synaptic currents by the GABA(B) agonist R-baclofen in pars compacta neurons of weaver mice which were largely spared from cell degeneration and
Effect of milacemide, a glycinamide derivative, on the rat brain gamma-aminobutyric acid system.
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Milacemide (CP 1552 S, 2-n-pentylaminoacetamide), a drug with anti-epileptic potency, increases the gamma-aminobutyric acid (GABA) content specifically in the substantia nigra of rat brain. The effect is dose-related from 25 to 100 mg/kg p.o. The time course shows that at 100 mg/kg p.o. after 2, 3
Decreased CSF concentrations of homovanillic acid and gamma-aminobutyric acid in Alzheimer's disease. Age- or disease-related modifications?
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Fifteen patients, 48 to 72 years old, with Alzheimer's disease were studied. Clinical status was assessed by neurologic and neuropsychologic examinations and psychometric testing. Patients were divided into two groups on the basis of clinical assessment: group 1, little mental deterioration, and
Alterations in the gamma-aminobutyric acid-gated chloride channel following transient forebrain ischemia in the gerbil.
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The role of inhibitory neurotransmission in selective neuronal degeneration after transient forebrain ischemia was studied by binding of t-[35S]butylbicyclophosphorothionate ([35S]TBPS) to the gamma-aminobutyric acid (GABA)-gated chloride channel and measurement of GABAA receptor function in
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