Sentence examples for mouse brain leads from inspiring English sources

The present data suggest that the lack of dopamine D3 receptor genes in the mouse brain leads to the aggravation of the development of physical dependence on ethanol.

Furthermore, conditional loss of PS in adult mouse brain leads to loss of synaptic plasticity, memory impairments, and age-dependant neurodegeneration through the loss of Notch activation of CRE-dependent gene expression [59].

Our observation that PINK1 deficiency in mouse brain leads to a combined impairment of activity of respiratory complex I+III+IV and II+III+IV, mitochondrial membrane potential Δψm and ATP generation at old age are consistent with a defect in mitochondrial bioenergetic function.

Similarly, iatrogenic inoculation of alpha-synuclein oligomers into mouse brain leads to widespread Lewy-like pathology, albeit requiring endogenous alpha-synuclein for transmission [ 16].

In vivo overexpression of BMP4 in developing mouse brain leads to an increase in astrocyte number (Gomes et al., 2003); mice deficient in both Bmpr1a and Bmpr1b show a 25-40% decrease in the number of astrocytes expressing either S100β or GFAP (See et al., 2007).

Since removal of amphiphysins from mouse brain led to some defects in the synaptic vesicles endocytosis (SVE) (31), we tested whether Ophn1 null mice displayed a similar deficit.

In accordance, simultaneous ablation of HDAC1 and HDAC2 in the developing mouse brain led to DNA damage and enhanced H3K56 acetylation (Hagelkruys et al. 2013).

Inhibition of miR-29b by in utero electroporation of anti-miR-29b into embryonic mouse brains led to premature outward cortical migration.

Robustly genetic loss of HDACs may block the process of neural differentiation in mouse brain and lead to developmental defects, whereas inhibition of HDACs to some extent could enhance the NPC commitment.

However, previous work with cultured cortical neurons from GFPu mice showed that GFP fluorescence accumulated in response to proteasome inhibition in a dose-dependent manner [32], and stereotaxic injection of the proteasome inhibitor MG-132 to GFPu mouse brains also lead to GFPu accumulation (manuscript in preparation).

This, together with the emergence of aggregated α-Synuclein in transplanted embryonic nigral cells in PD patients and cell to cell transfer of α-Synuclein in mouse brain and cell culture leads to the assumption of interneuronal spreading of disease pathology [ 13, 14, 27, 44].