lambda dg4 (Compix Inc)
90
Structured Review
Compix Inc
lambda dg4
Lambda Dg4, supplied by Compix Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lambda+dg-4/lambda+dg4/pm16571773-260-4-19
Average 90 stars, based on 1 article reviews
Lambda Dg4, supplied by Compix Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lambda+dg-4/lambda+dg4/pm16571773-260-4-19
Average 90 stars, based on 1 article reviews
lambda dg4 - by Bioz Stars,
2026-11
90/100 stars
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Microscopy:Article Title: Brain mitochondrial defects amplify intracellular [Ca2+] rise and neurodegeneration but not Ca2+ entry during NMDA receptor activation. Article Snippet: According to the “indirect” excitotoxicity hypothesis, mitochondrial defects increase Ca entry into neurons by rendering NMDA-R hypersensitive to glutamate.. We tested this hypothesis by investigating in the rat striatum and cultured striatal cells how partial mitochondrial complex II inhibition produced by 3-nitropropionic acid (3NP) modifies the toxicity of the NMDA-R agonist quinolinate (QA).. We showed that nontoxic 3NP treatment, leading to partial inhibition of complex II activity, greatly exacerbated striatal degeneration produced by slightly toxic QA treatment through an “all-or-nothing” process. Software:Article Title: Brain mitochondrial defects amplify intracellular [Ca2+] rise and neurodegeneration but not Ca2+ entry during NMDA receptor activation. Article Snippet: According to the “indirect” excitotoxicity hypothesis, mitochondrial defects increase Ca entry into neurons by rendering NMDA-R hypersensitive to glutamate.. We tested this hypothesis by investigating in the rat striatum and cultured striatal cells how partial mitochondrial complex II inhibition produced by 3-nitropropionic acid (3NP) modifies the toxicity of the NMDA-R agonist quinolinate (QA).. We showed that nontoxic 3NP treatment, leading to partial inhibition of complex II activity, greatly exacerbated striatal degeneration produced by slightly toxic QA treatment through an “all-or-nothing” process. Imaging:Article Title: Brain mitochondrial defects amplify intracellular [Ca2+] rise and neurodegeneration but not Ca2+ entry during NMDA receptor activation. Article Snippet: According to the “indirect” excitotoxicity hypothesis, mitochondrial defects increase Ca entry into neurons by rendering NMDA-R hypersensitive to glutamate.. We tested this hypothesis by investigating in the rat striatum and cultured striatal cells how partial mitochondrial complex II inhibition produced by 3-nitropropionic acid (3NP) modifies the toxicity of the NMDA-R agonist quinolinate (QA).. We showed that nontoxic 3NP treatment, leading to partial inhibition of complex II activity, greatly exacerbated striatal degeneration produced by slightly toxic QA treatment through an “all-or-nothing” process. |