High-performance and reliable site-directed in vivo genetic manipulation of mouse and rat brain by in utero electroporation with a triple-electrode probe.

2013 ◽  
Author(s):  
Laura Cancedda ◽  
Joanna Szczurkowska ◽  
Andrzej W. Cwetsch ◽  
Marco dal Maschio ◽  
Diego Ghezzi ◽  
...  
Keyword(s):  
Rat Brain ◽  
High Performance ◽  
Genetic Manipulation ◽  
In Utero ◽  
In Utero Electroporation

Targeted in vivo genetic manipulation of the mouse or rat brain by in utero electroporation with a triple-electrode probe

2016 ◽  
Vol 11 (3) ◽  
pp. 399-412 ◽  
Author(s):  
Joanna Szczurkowska ◽  
Andrzej W Cwetsch ◽  
Marco dal Maschio ◽  
Diego Ghezzi ◽  
Gian Michele Ratto ◽  
...  
Keyword(s):  
Rat Brain ◽  
Genetic Manipulation ◽  
In Utero ◽  
In Utero Electroporation

scholarly journals In Utero Electroporation as a Tool For Genetic Manipulation In Vivo to Study Psychiatric Disorders

2011 ◽  
Vol 18 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Yu Taniguchi ◽  
Tracy Young-Pearse ◽  
Akira Sawa ◽  
Atsushi Kamiya
Keyword(s):  
Psychiatric Disorders ◽  
Genetic Manipulation ◽  
In Utero ◽  
In Utero Electroporation

scholarly journals Evolution of structural abnormalities in the rat brain following in utero exposure to maternal immune activation: A longitudinal in vivo MRI study

2017 ◽  
Vol 63 ◽  
pp. 50-59 ◽  
Author(s):  
William R. Crum ◽  
Stephen J. Sawiak ◽  
Winfred Chege ◽  
Jonathan D. Cooper ◽  
Steven C.R. Williams ◽  
...  
Keyword(s):  
Rat Brain ◽  
Immune Activation ◽  
In Utero ◽  
In Utero Exposure ◽  
Maternal Immune Activation ◽  
Structural Abnormalities ◽  
Mri Study

scholarly journals High-performance and site-directed in utero electroporation by a triple-electrode probe

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Marco dal Maschio ◽  
Diego Ghezzi ◽  
Guillaume Bony ◽  
Alessandro Alabastri ◽  
Gabriele Deidda ◽  
...  
Keyword(s):  
High Performance ◽  
In Utero ◽  
In Utero Electroporation

Novel method for in vivo hydroxyl radical measurement by microdialysis in fetal sheep brain in utero

2005 ◽  
Vol 98 (6) ◽  
pp. 2304-2310 ◽  
Author(s):  
Edwin B. Yan ◽  
Jessica K. Unthank ◽  
Margie Castillo-Melendez ◽  
Suzanne L. Miller ◽  
Steven J. Langford ◽  
...  
Keyword(s):  
Hydroxyl Radical ◽  
High Performance ◽  
Fetal Brain ◽  
In Utero ◽  
In Vivo Studies ◽  
Fetal Sheep ◽  
Low Concentrations ◽  
Sheep Brain

Hydroxyl radical (·OH) is a reactive oxygen species produced during severe hypoxia, asphyxia, or ischemia that can cause cell death resulting in brain damage. Generation of ·OH may occur in the fetal brain during asphyxia in utero. The very short half-life of ·OH requires use of trapping agents such as salicylic acid or phenylalanine for detection, but their hydroxylated derivatives are either unstable, produced endogenously, or difficult to measure in the small volume of microdialysis samples. In the present study, we used terephthalic acid (TA), hydroxylation of which yields a stable and highly fluorometric isomer (excitation, 326 nm; emission, 432 nm). In vitro studies using ·OH generated by the Fenton reaction showed that hydroxylated TA formed quickly (<10 s), was resistant to bleaching (<5% change in fluorescence), and permitted detection of <0.5 pmol ·OH. In vivo studies were performed in fetal sheep using microdialysis probes implanted into the parasagittal cortex. The probe was perfused at 2 μl/min with artificial cerebrospinal fluid containing 5 mM TA, and samples were collected every 30 min. Fluorescence measured in 10 μl of dialysate was significantly greater than in the efflux from probes perfused without TA. High-performance liquid chromotography analysis showed that the fluorescence in dialysis samples was entirely due to hydroxylation of TA. Thus this study shows that it is possible to use TA as a trapping agent for detecting low concentrations of ·OH both in vitro and in vivo and that low concentrations of ·OH are present in fetal brain tissue and fluctuate with time.

In Vivo Targeting of Neural Progenitor Cells in Ferret Neocortex by In Utero Electroporation

10.3791/61171 ◽  
2020 ◽  
Author(s):  
Nereo Kalebic ◽  
Barbara Langen ◽  
Jussi Helppi ◽  
Hiroshi Kawasaki ◽  
Wieland B. Huttner
Keyword(s):  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
In Utero ◽  
In Utero Electroporation

scholarly journals NAc-DBS corrects depression-like behaviors in CUMS mouse model via disinhibition of DA neurons in the VTA

2021 ◽  
Author(s):  
Song Nan ◽  
Gao Yan ◽  
Lu Shanshan ◽  
Yang Shenglian ◽  
Yuan Chao ◽  
...  
Keyword(s):  
Mouse Model ◽  
High Performance ◽  
Genetic Manipulation ◽  
In Vivo Microdialysis ◽  
Antidepressant Effect ◽  
Neuron Activity ◽  
Mild Stress ◽  
Electrochemical Detector ◽  
Mesolimbic Pathway

Major depressive disorder (MDD) is characterized by diverse debilitating symptoms that include loss of motivation and anhedonia. If multiple medications, psychotherapy, and electroconvulsive therapy fail in some patients with MDD, their condition is then termed treatment – resistant depression (TRD). MDD can be associated with abnormalities in the reward – system – dopaminergic mesolimbic pathway, in which the nucleus accumbens (NAc) and ventral tegmental area (VTA) play major roles. Deep brain stimulation (DBS) applied to the NAc alleviates the depressive symptoms of MDD. However, the mechanism underlying the effects of this DBS has remained elusive. In this study, using the chronic unpredictable mild stress (CUMS) mouse model, we investigated the behavioral and neurobiological effects of NAc – DBS on the multidimensional depression – like phenotypes induced by CUMS by integrating behavioral, in vivo microdialysis coupled with high – performance liquid chromatography – electrochemical detector (HPLC – ECD), calcium imaging, pharmacological, and genetic manipulation methods in freely moving mice. We found that long – term and repeated, but not single, NAc – DBS induced robust antidepressant responses in CUMS mice. Moreover, even a single trial NAc – DBS led to the elevation of the γ – aminobutyric acid (GABA) neurotransmitter, accompanied by the increase in dopamine (DA) neuron activity in the VTA. Both the inhibition of the GABAA receptor activity and knockdown of the GABAA – α1 gene in VTA – GABA neurons blocked the antidepressant effect of NAc – DBS in CUMS mice. Our results showed that NAc – DBS could disinhibit VTA – DA neurons by regulating the level of GABA and the activity of VTA – GABA in the VTA and could finally correct the depression – like behaviors in the CUMS mouse model.

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