Immature rat brain slices exposed to oxygen–glucose deprivation as an in vitro model of neonatal hypoxic–ischemic encephalopathy

2005 ◽  
Vol 145 (1-2) ◽  
pp. 205-212 ◽  
Author(s):  
David Fernández-López ◽  
José Martínez-Orgado ◽  
Ignacio Casanova ◽  
Bartolomé Bonet ◽  
Juan Carlos Leza ◽  
...  
Keyword(s):  
Rat Brain ◽  
In Vitro Model ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Hypoxic Ischemic Encephalopathy ◽  
Oxygen Glucose Deprivation ◽  
Immature Rat ◽  
Vitro Model ◽  
Ischemic Encephalopathy

Hyperhomocysteinemia increases damage on brain slices exposed to in vitro model of oxygen and glucose deprivation: prevention by folic acid

2006 ◽  
Vol 24 (4) ◽  
pp. 285-291 ◽  
Author(s):  
Bárbara Tagliari ◽  
Lauren L. Zamin ◽  
Christianne G. Salbego ◽  
Carlos Alexandre Netto ◽  
Angela T.S. Wyse
Keyword(s):  
Folic Acid ◽  
In Vitro Model ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Vitro Model

scholarly journals An improved in-vitro model for the study of gonadotrophin secretion from immature rat pituitaries

Reproduction ◽  
1977 ◽  
Vol 50 (2) ◽  
pp. 347-348 ◽  
Author(s):  
Y. Koch ◽  
R. Meidan ◽  
P. Chobsieng ◽  
Z. Naor
Keyword(s):  
In Vitro Model ◽  
Immature Rat ◽  
Gonadotrophin Secretion ◽  
Vitro Model

scholarly journals Reappraisal of anoxic spreading depolarization as a terminal event during oxygen–glucose deprivation in brain slices in vitro

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Elvira Juzekaeva ◽  
Azat Gainutdinov ◽  
Marat Mukhtarov ◽  
Roustem Khazipov
Keyword(s):  
Membrane Potential ◽  
Brain Slices ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Terminal Event ◽  
Irreversible Damage ◽  
Neuronal Viability ◽  
Spreading Depolarization ◽  
Cortical Slices

Abstract Anoxic spreading depolarization (aSD) has been hypothesized as a terminal event during oxygen–glucose deprivation (OGD) in submerged cortical slices in vitro. However, mechanical artifacts caused by aSD-triggered edema may introduce error in the assessment of neuronal viability. Here, using continuous patch-clamp recordings from submerged rat cortical slices, we first confirmed that vast majority of L4 neurons permanently lost their membrane potential during OGD-induced aSD. In some recordings, spontaneous transition from whole-cell to out-side out configuration occurred during or after aSD, and only a small fraction of neurons survived aSD with reperfusion started shortly after aSD. Secondly, to minimize artifacts caused by OGD-induced edema, cells were short-term patched following OGD episodes of various duration. Nearly half of L4 cells maintained membrane potential and showed the ability to spike-fire if reperfusion started less than 10 min after aSD. The probability of finding live neurons progressively decreased at longer reperfusion delays at a rate of about 2% per minute. We also found that neurons in L2/3 show nearly threefold higher resistance to OGD than neurons in L4. Our results suggest that in the OGD ischemia model, aSD is not a terminal event, and that the “commitment point” of irreversible damage occurs at variable delays, in the range of tens of minutes, after OGD-induced aSD in submerged cortical slices.

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