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Gábor Laskay

Bio: Gábor Laskay is an academic researcher from University of Szeged. The author has contributed to research in topics: Osmotic shock & Membrane potential. The author has an hindex of 9, co-authored 14 publications receiving 652 citations.

Papers
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Journal ArticleDOI
TL;DR: In this article, the authors report correlative in vitro and in vivo evidence that an excitotoxic cascade mediates Abeta neurotoxicity in the rat magnocellular nucleus basalis (MBN).
Abstract: Whereas a cardinal role for beta-amyloid protein (Abeta) has been postulated as a major trigger of neuronal injury in Alzheimer's disease, the pathogenic mechanism by which Abeta deranges nerve cells remains largely elusive. Here we report correlative in vitro and in vivo evidence that an excitotoxic cascade mediates Abeta neurotoxicity in the rat magnocellular nucleus basalis (MBN). In vitro application of Abeta to astrocytes elicits rapid depolarization of astroglial membranes with a concomitant inhibition of glutamate uptake. In vivo Abeta infusion by way of microdialysis in the MBN revealed peak extracellular concentrations of excitatory amino acid neurotransmitters within 20-30 min. Abeta-triggered extracellular elevation of excitatory amino acids coincided with a significantly enhanced intracellular accumulation of Ca2+ in the Abeta injection area, as was demonstrated by 45Ca2+ autoradiography. In consequence of these acute processes delayed cell death in the MBN and persistent loss of cholinergic fibre projections to the neocortex appear as early as 3 days following the Abeta-induced toxic insult. Such a sequence of Abeta toxicity was effectively antagonized by the N-methyl-D-aspartate (NMDA) receptor ligand dizocilpine maleate (MK-801). Moreover, Abeta toxicity in the MBN decreases with advancing age that may be associated with the age-related loss of NMDA receptor expression in rats. In summary, the present results indicate that Abeta compromises neurons of the rat MBN via an excitotoxic pathway including astroglial depolarization, extracellular glutamate accumulation, NMDA receptor activation and an intracellular Ca2+ overload leading to cell death.

265 citations

Journal ArticleDOI
TL;DR: It is concluded that rapeseed tolerates Cu excess better than Indian mustard, reflecting serious oxidative stress in B. juncea.

120 citations

Journal ArticleDOI
TL;DR: The most recent literature about the responses of sorghum to the most important abiotic stresses: nutrient deficiency, aluminium stress, drought, high salinity, waterlogging or temperature stress the plants have to cope with during cultivation are summarized.
Abstract: Sorghum [(Sorghum bicolor L.) Moench] is a highly productive crop plant, which can be used for alternative energy resource, human food, livestock feed or industrial purposes. The biomass of sorghum can be utilized as solid fuel via thermochemical routes or as a carbohydrate substrate via fermentation processes. The plant has a great adaptation potential to drought, high salinity and high temperature, which are important characteristics of genotypes growing in extreme environments. However, the climate change in the 21st century may bring about new challenges in the cultivated areas. In this review, we summarize the most recent literature about the responses of sorghum to the most important abiotic stresses: nutrient deficiency, aluminium stress, drought, high salinity, waterlogging or temperature stress the plants have to cope with during cultivation. The advanced molecular and system biological tools provide new opportunities for breeders to select stress-tolerant and high-yielding cultivars.

119 citations

Journal ArticleDOI
TL;DR: A novel pentapeptide LPYFD-amide, an analog of Soto's LPFFD, significantly decreased neurite degeneration, tau aggregation, and cell viability reduction induced by Abeta 1-42, indicating that Abeta might induce neurodegeneration even at an early stage of Abeta-cell contact.

66 citations

Journal ArticleDOI
TL;DR: It was found that the fast activation of the ABA biosynthesis in the roots generated an enhanced ABA pool in the shoot, which brought about a faster closure of the stomata upon increasing osmotic stress and, as a result, the plants could maintain ψw in the tissues close to the control level.

57 citations


Cited by
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Journal ArticleDOI
25 Jun 2009-Neuron
TL;DR: It is concluded that soluble Abeta oligomers perturb synaptic plasticity by altering glutamate recycling at the synapse and promoting synapse depression.

864 citations

Journal ArticleDOI
TL;DR: The molecular basis for memantine efficacy in neurological diseases that are mediated, at least in part, by overactivation of NMDARs, producing excessive Ca2+ influx through the receptor's associated ion channel and consequent free-radical formation is reviewed.
Abstract: Excessive glutamate receptor activity, principally of theN-methyl-D-aspartate (NMDA) subtype, contributes to neuronal damage in a large number of neurologic disorders, including dementia. Until recently, however, NMDA receptor antagonists had all failed in clinical trials. Stuart Lipton reviews the mechanism of action that led to the clinical approval of the first NMDA receptor antagonist, memantine, which has become the newest and one of the best-selling drugs for Alzheimer's disease. Neuroprotective drugs tested in clinical trials, particularly those that block N-methyl-D-aspartate-sensitive glutamate receptors (NMDARs), have failed miserably in large part because of intolerable side effects. However, one such drug, memantine, was recently approved by the European Union and the US FDA for the treatment of dementia following our group's discovery of its clinically tolerated mechanism of action. Here, we review the molecular basis for memantine efficacy in neurological diseases that are mediated, at least in part, by overactivation of NMDARs, producing excessive Ca2+ influx through the receptor's associated ion channel and consequent free-radical formation.

825 citations

Journal ArticleDOI
16 Feb 2015
TL;DR: The results show the need to undertake large-scale analyses, using multidisciplinary approaches, to unravel the consequences of stress on the cell wall and identify the key components that could be targeted to improve biomass production under stress conditions.
Abstract: This review focuses on the responses of the plant cell wall to several abiotic stresses including drought, flooding, heat, cold, salt, heavy metals, light, and air pollutants. The effects of stress on cell wall metabolism are discussed at the physiological (morphogenic), transcriptomic, proteomic and biochemical levels. The analysis of a large set of data shows that the plant response is highly complex. The overall effects of most abiotic stress are often dependent on the plant species, the genotype, the age of the plant, the timing of the stress application, and the intensity of this stress. This shows the difficulty of identifying a common pattern of stress response in cell wall architecture that could enable adaptation and/or resistance to abiotic stress. However, in most cases, two main mechanisms can be highlighted: (i) an increased level in xyloglucan endotransglucosylase/hydrolase (XTH) and expansin proteins, associated with an increase in the degree of rhamnogalacturonan I branching that maintains cell wall plasticity and (ii) an increased cell wall thickening by reinforcement of the secondary wall with hemicellulose and lignin deposition. Taken together, these results show the need to undertake large-scale analyses, using multidisciplinary approaches, to unravel the consequences of stress on the cell wall. This will help identify the key components that could be targeted to improve biomass production under stress conditions.

813 citations

Journal ArticleDOI
TL;DR: This review will initially discuss recent results indicating a link between cholinergic mechanisms and the pathogenic events that characterize AD, notably amyloid-β peptides, and animal models of dementia will be discussed in light of the relationship between basal forebrain cholinerg hypofunction and cognitive impairments in AD.

614 citations

Journal ArticleDOI
TL;DR: Soluble Aβ oligomers at low nanomolar levels present in AD brain increase activation of extrasynaptic NR2B-containing receptors, thereby impairing synaptic plasticity.
Abstract: In Alzheimer's disease (AD), dementia severity correlates strongly with decreased synapse density in hippocampus and cortex. Numerous studies report that hippocampal long-term potentiation (LTP) can be inhibited by soluble oligomers of amyloid β-protein (Aβ), but the synaptic elements that mediate this effect remain unclear. We examined field EPSPs and whole-cell recordings in wild-type mouse hippocampal slices. Soluble Aβ oligomers from three distinct sources (cultured cells, AD cortex, or synthetic peptide) inhibited LTP, and this was prevented by the selective NR2B inhibitors ifenprodil and Ro 25-6981. Soluble Aβ enhanced NR2B-mediated NMDA currents and extrasynaptic responses; these effects were mimicked by the glutamate reuptake inhibitor dl-threo-β-benzyloxyaspartic acid. Downstream, an Aβ-mediated rise in p38 mitogen-activated protein kinase (MAPK) activation was followed by downregulation of cAMP response element-binding protein, and LTP impairment was prevented by inhibitors of p38 MAPK or calpain. Thus, soluble Aβ oligomers at low nanomolar levels present in AD brain increase activation of extrasynaptic NR2B-containing receptors, thereby impairing synaptic plasticity.

564 citations