FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016475345> ?p ?o ?g. }

• W2016475345 endingPage "212" @default.
• W2016475345 startingPage "199" @default.
• W2016475345 abstract "The aim of this study was to establish a culture system that can serve as a model to study hypoxic-ischemic mechanisms regulating the functional expression of NPY neurons in the perinatal brain. Using an aggregate culture system derived from the rat fetal cortex, we defined the effects of oxygen and glucose deprivation on NPY expression, using BDNF-induced production of NPY as a functional criterion. NPY neurons exhibited a differential susceptibility to oxygen and glucose deprivation. Although the neurons could withstand oxygen deprivation for 16 hr, they were dramatically damaged by 8 hr of glucose deprivation and by 1-4 hr of deprivation of both oxygen and glucose (N+Glu-). One-hour exposure to N+Glu- led to a transient inhibition ( approximately 50%) of NPY production manifesting within 24 hr and recovering by 5 days thereafter, a 2-hr exposure to N+Glu- led to a sustained inhibition (50-75%) manifesting 1-5 days thereafter, and a 4-hr exposure to N+Glu- led to a total irreversible suppression of BDNF-induced production of NPY manifesting within 24 hr and lasting 8 days after re-supply of oxygen and glucose. Moreover, 1-hr exposure to N+Glu- led to a substantial and 4-hr exposure led to a total disappearance of immunostaining for MAP-2 and NPY but not for GFAP; indicating that neurons are the primary cell-type damaged by oxygen-glucose deprivation. Analysis of cell viability (LDH, MTT) indicated that progressive changes in cell integrity take place during the 4-hr exposure to N+Glu- followed by massive cell death 24 hr thereafter. Thus, we defined a culture system that can serve as a model to study mechanisms by which ischemic insult leads to suppression and eventually death of NPY neurons. Importantly, changes in NPY neurons can be integrated into the overall scheme of ischemic injury in the perinatal brain." @default.
• W2016475345 created "2016-06-24" @default.
• W2016475345 creator A5070801908 @default.
• W2016475345 creator A5085980399 @default.
• W2016475345 date "2002-03-28" @default.
• W2016475345 modified "2023-09-25" @default.
• W2016475345 title "Suppression of BDNF-induced expression of neuropeptide Y (NPY) in cortical cultures by oxygen-glucose deprivation: A model system to study ischemic mechanisms in the perinatal brain" @default.
• W2016475345 cites W1483718240 @default.
• W2016475345 cites W1543505880 @default.
• W2016475345 cites W1629179716 @default.
• W2016475345 cites W1899341317 @default.
• W2016475345 cites W1906283391 @default.
• W2016475345 cites W1967548980 @default.
• W2016475345 cites W1968002337 @default.
• W2016475345 cites W1969539885 @default.
• W2016475345 cites W1969990009 @default.
• W2016475345 cites W1971046097 @default.
• W2016475345 cites W1972981050 @default.
• W2016475345 cites W1975823509 @default.
• W2016475345 cites W1976915575 @default.
• W2016475345 cites W1977779461 @default.
• W2016475345 cites W1979899463 @default.
• W2016475345 cites W1988705351 @default.
• W2016475345 cites W1989623506 @default.
• W2016475345 cites W1991909451 @default.
• W2016475345 cites W1993975841 @default.
• W2016475345 cites W2002294810 @default.
• W2016475345 cites W2002615341 @default.
• W2016475345 cites W2004469687 @default.
• W2016475345 cites W2006415061 @default.
• W2016475345 cites W2007562867 @default.
• W2016475345 cites W2007804930 @default.
• W2016475345 cites W2009647277 @default.
• W2016475345 cites W2009950176 @default.
• W2016475345 cites W2010022121 @default.
• W2016475345 cites W2012510307 @default.
• W2016475345 cites W2015556894 @default.
• W2016475345 cites W2017169241 @default.
• W2016475345 cites W2019640290 @default.
• W2016475345 cites W2025421033 @default.
• W2016475345 cites W2027475151 @default.
• W2016475345 cites W2032013354 @default.
• W2016475345 cites W2034382807 @default.
• W2016475345 cites W2035839549 @default.
• W2016475345 cites W2036793658 @default.
• W2016475345 cites W2038790950 @default.
• W2016475345 cites W2039379548 @default.
• W2016475345 cites W2040849685 @default.
• W2016475345 cites W2044431563 @default.
• W2016475345 cites W2045101586 @default.
• W2016475345 cites W2051455962 @default.
• W2016475345 cites W2055278579 @default.
• W2016475345 cites W2058530592 @default.
• W2016475345 cites W2060422151 @default.
• W2016475345 cites W2064110992 @default.
• W2016475345 cites W2065878236 @default.
• W2016475345 cites W2066790769 @default.
• W2016475345 cites W2073554076 @default.
• W2016475345 cites W2073923559 @default.
• W2016475345 cites W2075390326 @default.
• W2016475345 cites W2077766248 @default.
• W2016475345 cites W2079412878 @default.
• W2016475345 cites W2080399942 @default.
• W2016475345 cites W2085338938 @default.
• W2016475345 cites W2086157846 @default.
• W2016475345 cites W2086279424 @default.
• W2016475345 cites W2086831569 @default.
• W2016475345 cites W2090245393 @default.
• W2016475345 cites W2111965631 @default.
• W2016475345 cites W2112136117 @default.
• W2016475345 cites W2118432415 @default.
• W2016475345 cites W2120494251 @default.
• W2016475345 cites W2126027530 @default.
• W2016475345 cites W2128008306 @default.
• W2016475345 cites W2128960139 @default.
• W2016475345 cites W2130374291 @default.
• W2016475345 cites W2134405071 @default.
• W2016475345 cites W2135374937 @default.
• W2016475345 cites W2144918294 @default.
• W2016475345 cites W2156566914 @default.
• W2016475345 cites W2163520260 @default.
• W2016475345 cites W4327766731 @default.
• W2016475345 cites W43432051 @default.
• W2016475345 doi "https://doi.org/10.1002/jnr.10191" @default.
• W2016475345 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11948665" @default.
• W2016475345 hasPublicationYear "2002" @default.
• W2016475345 type Work @default.
• W2016475345 sameAs 2016475345 @default.
• W2016475345 citedByCount "3" @default.
• W2016475345 crossrefType "journal-article" @default.
• W2016475345 hasAuthorship W2016475345A5070801908 @default.
• W2016475345 hasAuthorship W2016475345A5085980399 @default.
• W2016475345 hasConcept C118303440 @default.
• W2016475345 hasConcept C126322002 @default.
• W2016475345 hasConcept C134018914 @default.
• W2016475345 hasConcept C170493617 @default.
• W2016475345 hasConcept C178790620 @default.
• W2016475345 hasConcept C185592680 @default.

• next