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fear conditioning learning (UGO Basile S.R.L)

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UGO Basile S.R.L fear conditioning learning
Fear Conditioning Learning, supplied by UGO Basile S.R.L, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/learning/Fear+Conditioning+for+Observational+Learning/pmc03976746-40-28-10
Average 92 stars, based on 1 article reviews

fear conditioning learning - by Bioz Stars, 2026-10

92/100 stars

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Mouse Assay:

Article Title: A decrease in NR2B expression mediated by DNA hypermethylation induces perioperative neurocognitive disorder in aged mice
Article Snippet: All data were recorded with a camera and analyzed blindly with Smart Video Tracking Software (Panlab; Harvard Apparatus). .. Mice were subjected to the hippocampus‐dependent contextual fear conditioning test using the Ugo Basile Fear Conditioning System (Ugo Basile Srl) as described previously. ..

Isolation:

Article Title: Effects of repeated anodal transcranial direct current stimulation on auditory fear extinction in C57BL/6J mice.
Article Snippet: .. Auditory fear conditioning and fear extinction were carried out in a fear conditioning apparatus containing a test box (17 cmwidth x 17 cm length x 24 cm height) placed in a soundproof chamber (Isolation Cubicle 46000-590, Ugo Basile). ..

other:

Article Title: GluA3 autoantibodies induce alterations in dendritic spine and behavior in mice.
Article Snippet: Fear conditioning took place in a standard conditioning chamber (Ugo Basile).

Article Title: Lysosomal TPCN (two pore segment channel) inhibition ameliorates beta-amyloid pathology and mitigates memory impairment in Alzheimer disease.
Article Snippet: Impairment of the macroautophagy/autophagy-lysosomal pathway (ALP) can lead to amyloid plaque accumulation in Alzheimer disease (AD); however, the underlying mechanism remains unresolved.. This study revealed a mechanism of ALP impairment mediated by gain-of-function of lysosomal TPCN2/TPC2 (two pore segment channel 2) and suggests a molecular target for AD intervention.. Using mutant PSEN1/PS1 (presenilin 1)-expressing human neuroblastoma SH-SY5Y and familial AD fibroblasts collected from human patients, we showed lysosomal pH was increased in AD cells due to exaggerated TPCN2-mediated calcium (Ca) release which increases lysosomal pH and compromises ALP degradation.