The dynamics of a neuronal culture of dissociated cortical neurons of neonatal rats

2000 ◽  
Vol 83 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Yasuhiko Jimbo ◽  
Akio Kawana ◽  
Pietro Parodi ◽  
Vincent Torre
Keyword(s):  
Cortical Neurons ◽  
Neuronal Culture ◽  
Neonatal Rats ◽  
Dissociated Cortical Neurons

Interaction of electrically evoked responses in networks of dissociated cortical neurons

2009 ◽  
Vol 80 (3) ◽  
Author(s):  
Pieter Laurens Baljon ◽  
Michela Chiappalone ◽  
Sergio Martinoia
Keyword(s):  
Cortical Neurons ◽  
Evoked Responses ◽  
Dissociated Cortical Neurons

Effects of simulated microgravity on the development and maturation of dissociated cortical neurons.

2004 ◽  
Author(s):  
Alessio Crestini ◽  
Cristina Zona ◽  
Pierluigi Sebastiani ◽  
Massimo Pieri ◽  
Valentina Caracciolo ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Simulated Microgravity ◽  
Dissociated Cortical Neurons

EFFECTS OF SIMULATED MICROGRAVITY ON THE DEVELOPMENT AND MATURATION OF DISSOCIATED CORTICAL NEURONS

2004 ◽  
Vol 40 (5) ◽  
pp. 159 ◽  
Author(s):  
ALESSIO CRESTINI ◽  
CRISTINA ZONA ◽  
PIERLUIGI SEBASTIANI ◽  
MASSIMO PIERI ◽  
VALENTINA CARACCIOLO ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Simulated Microgravity ◽  
Dissociated Cortical Neurons

scholarly journals Spatiotemporal Memory Is an Intrinsic Property of Networks of Dissociated Cortical Neurons

2015 ◽  
Vol 35 (9) ◽  
pp. 4040-4051 ◽  
Author(s):  
H. Ju ◽  
M. R. Dranias ◽  
G. Banumurthy ◽  
A. M. J. VanDongen
Keyword(s):  
Cortical Neurons ◽  
Intrinsic Property ◽  
Dissociated Cortical Neurons

scholarly journals COX5A over-expression protects cortical neurons from hypoxic ischemic injury in neonatal rats associated with TPI up-regulation

2020 ◽  
Author(s):  
Ya Jiang ◽  
Xue Bai ◽  
Ting-Ting Li ◽  
Mohammed AL Hawwas ◽  
Yuan Jin ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Molecular Mechanisms ◽  
Cerebral Injury ◽  
Neurological Dysfunction ◽  
Neurological Injury ◽  
Immunofluorescent Staining ◽  
Neonatal Rats ◽  
Over Expression ◽  
Qrt Pcr

Abstract Background: Neonatal hypoxic-ischemic encephalopathy (HIE) represents as a major cause of neonatal morbidity and mortality. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. This study was conducted to determine the specific potential molecular mechanism in the hypoxic-ischemic induced cerebral injury. Methods: Here, hypoxic-ischemic (HI) animal models were established and primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in - vitro . The HI-induced neurological injury was evaluated by Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl Transferased Utp Nick End Labeling (TUNEL) and immunofluorescent staining. Then the expression of Cytochrome c oxidase subunit 5a (COX5A) was determined by immunohistochemistry, western blotting (WB) and quantitative real time Polymerase Chain Reaction (qRT-PCR) techniques. Moreover, HSV-mediated COX5A over-expression virus was transducted into OGD neurons to explore the role of COX5A in - vitro , and the underlying mechanism was predicted by GeneMANIA, then verified by WB and qRT-PCR. Results: HI induced a severe neurological dysfunction, brain infarction, and cell apoptosis as well as obvious neuron loss in neonatal rats, in corresponding to the decrease on the expression of COX5A in both sides of the brain . What’s more, COX5A over-expression significantly promoted the neuronal survival, reduced the apoptosis rate, and markedly increased the neurites length after OGD. Moreover, Triosephosephate isomerase (TPI) was predicted as physical interactions with COX5A, and COX5A over-expression largely increased the expressional level of TPI. Conclusions: The present findings suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-regulation.

scholarly journals Blue light-induced gene expression alterations in cultured neurons are the result of phototoxic interactions with neuronal culture media

2019 ◽  
Author(s):  
Corey G. Duke ◽  
Katherine E. Savell ◽  
Robert A. Phillips ◽  
Jeremy J. Day
Keyword(s):  
Gene Expression ◽  
Blue Light ◽  
Cortical Neurons ◽  
Clock Genes ◽  
Culture Media ◽  
Light Exposure ◽  
Neuronal Culture ◽  
Gene Expression Alterations

Blue waveform light is used as an optical actuator in numerous optogenetic technologies employed in neuronal systems. However, the potential side effects of blue waveform light in neurons has not been thoroughly explored, and recent reports suggest that neuronal exposure to blue light can induce transcriptional alterations in vitro and in vivo. Here, we examined the effects of blue waveform light in cultured primary rat cortical neurons. Exposure to blue light (470nm) resulted in upregulation of several immediate early genes (IEGs) traditionally used as markers of neuronal activity, including Fos and Fosb, but did not alter the expression of circadian clock genes Bmal1, Cry1, Cry2, Clock, or Per2. IEG expression was increased following 4 hours of 5% duty cycle light exposure, and IEG induction was not dependent on light pulse width. Elevated levels of blue light exposure induced a loss of cell viability in vitro, suggestive of overt phototoxicity. Changes in gene expression induced by blue waveform light were prevented when neurons were cultured in a photoinert media supplemented with a photostable neuronal supplement instead of commonly utilized neuronal culture media and supplements. Together, these findings suggest that light-induced gene expression alterations observed in vitro stem from a phototoxic interaction between commonly used media and neurons, and offer a solution to prevent this toxicity when using photoactivatable technology in vitro.

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