Activity-dependent enhancement in the reliability of correlated spike timings in cultured cortical neurons

1999 ◽  
Vol 80 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Takashi Tateno ◽  
Yasuhiko Jimbo
Keyword(s):  
Cortical Neurons ◽  
Cultured Cortical Neurons ◽  
Activity Dependent

Identification of synaptic activity-dependent genes by exposure of cultured cortical neurons to tetrodotoxin followed by its withdrawal

2007 ◽  
Vol 85 (11) ◽  
pp. 2385-2399 ◽  
Author(s):  
Chikara Kitamura ◽  
Masaki Takahashi ◽  
Yasumitsu Kondoh ◽  
Hideo Tashiro ◽  
Tomoko Tashiro
Keyword(s):  
Cortical Neurons ◽  
Synaptic Activity ◽  
Cultured Cortical Neurons ◽  
Activity Dependent

scholarly journals The Bacterial Enzyme Cas13 Interferes with Neurite Outgrowth from Cultured Cortical Neurons

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 262
Author(s):  
Qin-Wei Wu ◽  
Josef P. Kapfhammer
Keyword(s):  
Rna Editing ◽  
Cortical Neurons ◽  
High Efficiency ◽  
Primary Cultures ◽  
Cultured Neurons ◽  
Therapeutic Tool ◽  
Bacterial Enzyme ◽  
Rna Targeting ◽  
Cultured Cortical Neurons ◽  
New Generation

The CRISPR-Cas13 system based on a bacterial enzyme has been explored as a powerful new method for RNA manipulation. Due to the high efficiency and specificity of RNA editing/interference achieved by this system, it is currently being developed as a new therapeutic tool for the treatment of neurological and other diseases. However, the safety of this new generation of RNA therapies is still unclear. In this study, we constructed a vector expressing CRISPR-Cas13 under a constitutive neuron-specific promoter. CRISPR-Cas13 from Leptotrichia wadei was expressed in primary cultures of mouse cortical neurons. We found that the presence of CRISPR-Cas13 impedes the development of cultured neurons. These results show a neurotoxic action of Cas13 and call for more studies to test for and possibly mitigate the toxic effects of Cas13 enzymes in order to improve CRISPR-Cas13-based tools for RNA targeting.

Abstract 91: Remodeling After Stroke: The Recovering Brain Is Vulnerable To Lipoxygenase-dependent Semaphorin Signaling

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Anton Pekcec ◽  
Kazim Yigitkanli ◽  
Joo Eun Jung ◽  
Hulya Karatas ◽  
Eng H Lo ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Cortical Neurons ◽  
Second Messengers ◽  
Artery Occlusion ◽  
Tube Formation ◽  
Stroke Recovery ◽  
Experimental Stroke ◽  
Axon Extension ◽  
Cultured Cortical Neurons ◽  
Cerebral Artery Occlusion

Background and Purpose— Recovery from stroke is limited in part by an inhibitory environment in the post-ischemic brain, but factors preventing successful remodeling are not well known. We sought to investigate if signaling from the axon guidance molecule semaphorin 3A (Sema3A) via eicosanoid second messengers can contribute to this inhibitory environment, and if blocking the Sema3A pathway can provide a benefit following experimental stroke. Methods— Cultured cortical neurons from mice were treated with recombinant Sema3A, or with the eicosanoids 12-HETE and 12-HPETE. Neurons from ALOX15 knockout mice, and a human brain endothelial cell line, were treated similarly. The filament model of MCAO was used to induce experimental stroke in mice, in some of which Sema3A was injected stereotactically into the striatum. The 12/15-LOX inhibitor LOXBlock-1 was injected intraperitoneally one week after MCAO. Results— Expression levels of 12/15-lipoxygenase (12/15-LOX) were increased within two hours after exposure of primary neurons to 90nM recombinant Sema3A. Either Sema3A, or the 12/15-lipoxygenase (12/15-LOX) metabolites 12-HETE and 12-HPETE at 300nM, blocked axon extension in neurons compared to solvent controls, and decreased tube formation in endothelial cells. The Sema3A effect was reversed by inhibiting 12/15-LOX, and neurons derived from 12/15-LOX knockout mice were insensitive to Sema3A. Following middle cerebral artery occlusion to induce stroke in mice, immunohistochemistry showed both Sema3A and 12/15-LOX are increased in the cortex up to two weeks. To determine if a Sema3A-dependent damage pathway is activated following ischemia, we injected recombinant Sema3A into the striatum. Sema3A alone did not cause injury in normal brains. But when injected into post-ischemic brains, Sema3A increased cortical damage by 79%, and again this effect was reversed by 12/15-LOX inhibition. Administration of the 12/15-LOX inhibitor LOXBlock-1 7 days after transient MCAO increased vascularization in the infarcted and peri-infarct area one week later. Conclusions— Our findings suggest that blocking the semaphorin pathway may provide a novel therapeutic strategy to improve stroke recovery.

scholarly journals Bifemelane Protects Cultured Cortical Neurons Against N-Methyl-D-aspartate Receptor-Mediated Glutamate Cytotoxicity

1998 ◽  
Vol 76 (3) ◽  
pp. 313-316 ◽  
Author(s):  
Akinori Akaike ◽  
Takehiko Maeda ◽  
Toshiaki Kume ◽  
Satoshi Kaneko
Keyword(s):  
Cortical Neurons ◽  
Aspartate Receptor ◽  
Cultured Cortical Neurons

scholarly journals Self-amplified BDNF transcription is a regulatory system for synaptic maturation in cultured cortical neurons

2015 ◽  
Vol 91 ◽  
pp. 55-61 ◽  
Author(s):  
Shingo Nakajima ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Yoshiko Ooshima ◽  
Haruki Odaka ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Regulatory System ◽  
Cultured Cortical Neurons ◽  
Synaptic Maturation ◽  
Bdnf Transcription
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