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Here, we have investigated, using patch-clamp recordings and optogenetic tools, the functional properties and synaptic integration of DA neurons, generated from neural stem/progenitor cells in mouse ventral mesencephalic neurospheres (VMNs), when grafted into striatum of organotypic mouse hemisphere slice cultures.
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Whole brains were dissected from P0 mice and the ventral mesencephalic region containing the substantia nigra (A9) and VTA (A10) was stereoscopically isolated and dissociated in media containing papain (20 U/ml).
This cell line originates from mice and was generated from a fusion of embryonic ventral mesencephalic and neuroblastoma cells.
In order to further evaluate the therapeutic potential of cell-specific Pten deletion, in this communication we transplanted ventral mesencephalic tissue from DA-PTEN-KO or control mice into the dopamine depleted striatum of MitoPark mice.
We prepared N/G cultures from the ventral mesencephalic tissues of embryonic day 13 14 rats or day 12 13 mice as described previously (Liu et al. 2000).
To examine whether Akt activation can protect vulnerable dopamine neurons after transplantation, we grafted ventral mesencephalic embryonic tissue from conditional DA-PTEN-KO and control mice bilaterally into the dopamine depleted striata of MitoPark mice (Ekstrand et al., 2007; Harvey et al., 2008; Ekstrand and Galter, 2009; Beal, 2010; Dawson et al., 2010; Galter et al., 2010; Good et al., 2011).
They served as a model system for the development of glial cell line-derived neurotrophic factor (GDNF -releasing PAM conveyinGDNF -releasingl mesencePAMliconveyingells.
Interestingly, this report described stereotaxic injection of the complexes into the mouse ventral midbrain and lateral ventricle.
Brain-derived neurotropic factor (BDNF) activity was confirmed by demonstrating enhanced generation of GABAergic neurons in embryonic (E15) striatal cultures and AAV-mediated glial-derived neurotrophic factor (GDNF) function using an assay for dopaminergic differentiation of embryonic (E14) ventral mesencephalic cultures.
We next examined whether PDE7 inhibition could also have neuroprotective effects on primary ventral mesencephalic cultures.
Here, we provide evidence that m-aconitase plays a significant role in death of neurons from primary ventral mesencephalic cultures.
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