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  • 1
    Electronic Resource
    Electronic Resource
    Interactions Between the Glutamate and Glycine Recognition Sites of the N-Methyl-d-Aspartate Receptor from Rat Brain, as Revealed from Radioligand Binding Studies (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The N-methyl-d-aspartate (NMDA) receptor possesses two distinct amino acid recognition sites, one for glutamate and one for glycine, which appear to be allosterically linked. Using rat cortex/hippocampus P2 membranes we have investigated the effect of glutamate recognition site ligands on [3H]glycine (agonist) and (±)4-trans-2-car-boxy-5,7-dichloro-4-[3H]phenylaminocarbonylamino-1,2,3,4-tetrahydroquinoline ([3H]l-689,560; antagonist) binding to the glycine site and the effect of glycine recognition site ligands on l-[3H]glutamate (agonist), dl-3-(2-carboxypiperazin-4-yl)-[3H]propyl-1 -phosphonate ([3H]-CPP; “C-7” antagonist), and cis-4-phosphonomethyl-2-[3H]piperidine carboxylate ([3H]CGS-19755; “C-5” antagonist) binding to the glutamate site. “C-7” glutamate site antagonists partially inhibited [3H]l-689,560 binding but had no effect on [3H]glycine binding, whereas “C-5” antagonists partially inhibited the binding of both radioligands. Glycine, d-serine, and d-cycloserine partially inhibited [3H]CGS-19755 binding but had little effect on l-[3H]-glutamate or [3H]CPP binding, whereas the partial agonists (+)-3-amino-1-hydroxypyrrolid-2-one [(+)-HA-966], 3R-(+)cis-4-methyl-HA-966 (l-687,414), and 1-amino-1-carboxycyclobutane all enhanced [3H]CPP binding but had no effect on [3H]CGS-19755 binding, and (+)-HA-966 and l-687,414 inhibited l-[3H]glutamate binding. The association and dissociation rates of [3H]l-689,560 binding were decreased by CPP and d-2-amino-5-phosphonopentanoic acid (“C-5”). Saturation analysis of [3H]l-689,560 binding carried out at equilibrium showed that CPP had little effect on the affinity or number of [3H]l-689,560 binding sites. These results indicate that complex interactions occur between the glutamate and glycine recognition sites on the NMDA receptor. In addition, mechanisms other than allosterism may underlie some effects, and the possibility of a steric interaction between CPP and [3H]l-689,560 is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb13397.x
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  • 2
    Electronic Resource
    Electronic Resource
    Attenuation and augmentation of ischaemia-related neuronal death by tumour necrosis factor-α in vitro (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Upregulation of the pro-inflammatory cytokine tumour necrosis factor-α (TNF) occurs rapidly in the brain following ischaemia, although it is unclear whether this represents a neurotoxic or neuroprotective response. We have investigated whether TNF has different actions in the pre- and postischaemic periods in a tissue culture model of cerebral ischaemia. Organotypic hippocampal slice cultures were prepared from 8–10-day-old rats and maintained in vitro for 14 days. Neuronal damage was induced by either 1 h oxygen–glucose deprivation or 3 h exposure to NMDA or the superoxide generator duroquinone, and assessed after 24 h by propidium iodide fluorescence. TNF pretreatment was neuroprotective against both oxygen–glucose deprivation and duroquinone. This effect was associated with an activation of the transcription factor NFκB and upregulation of manganese superoxide dismutase, and was prevented by a free radical scavenger. When addition of TNF was delayed until the postinsult period, an exacerbation of neurotoxicity occurred, which was also prevented by a free radical scavenger. The actions of TNF are determined by whether TNF is present before or after an ischaemia-related insult. Both actions are mediated through the production of free radicals, and the response to TNF is determined by whether a cell is metabolically competent to respond by synthesis of antioxidant defences.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2000.00273.x
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  • 3
    Electronic Resource
    Electronic Resource
    Potential signalling pathways underlying corticotrophin-releasing hormone-mediated neuroprotection from excitotoxicity in rat hippocampus (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neurochemistry 80 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In several neurological disorders including cerebral ischaemia, glutamate has been implicated as a neurotoxic agent in the mechanisms leading to neuronal cell death. The role of corticotrophin-releasing hormone (CRH), the 41-amino acid peptide, which activates the HPA axis in response to stressful stimuli, remains controversial. In this study, we report that CRH in low physiological concentrations (2 pm), prevented glutamate-induced neurotoxicity via receptor-mediated mechanisms when administered to organotypic hippocampal cultures both during and after the glutamate-induced insult. Detailed investigations on the mechanisms mediating this neuroprotective effect showed that activation of the adenylate cyclase pathway and induction of MAP kinase phosphorylation mediate the CRH action. In addition we showed that CRH can inhibit the phosphorylation of JNK/SAPK by glutamate. Most importantly, we showed that CRH can afford neuroprotection against neurotoxicity up to 12 h following the insult, suggesting that CRH is acting at a late stage in the neuronal death cycle, and this might be important in the development of novel neuroprotective agents in order to improve neuronal survival following the insult.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0022-3042.2001.00712.x
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    Paper (German National Licenses)
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