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Christopher M. Sinton

Researcher at University of Texas Southwestern Medical Center

Publications -  6
Citations -  571

Christopher M. Sinton is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Striatum & Substantia nigra. The author has an hindex of 6, co-authored 6 publications receiving 550 citations.

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The neurotoxin MPTP causes degeneration of specific nucleus A8, A9 and A10 dopaminergic neurons in the mouse.

TL;DR: It is indicated that MPTP produces midbrain dopaminergic neuronal degeneration in the same nuclei in the C57BL16 mouse that degenerate in humans with Parkinson's disease.
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Evidence for a deficit in cholinergic interneurons in the striatum in schizophrenia

TL;DR: A decrease in the number or function of the cholinergic interneurons of the striatum may disrupt activity in the ventral striatal-pallidal-thalamic-prefrontal cortex pathway and thereby contribute to abnormalities infunction of the prefrontal cortex in schizophrenia.
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Midbrain dopaminergic neurons in the mouse: computer-assisted mapping.

TL;DR: The dopaminergic neurons in the midbrain play a role in cognition, affect and movement and their distribution within the nuclei that constitute cell groups A8, A9 and A10, in the mouse is mapped and quantify.
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Midbrain Dopaminergic Neurons in the Mouse that Contain Calbindin-D28kExhibit Reduced Vulnerability to MPTP-induced Neurodegeneration

TL;DR: It is demonstrated that the presence of CB in midbrain DA neurons identifies a population of cells in the mouse that are less vulnerable to MPTP-induced degeneration, and the mouse can serve as a useful model in which to investigate the putative neuroprotective effects ofCB in an animal model of Parkinson's disease.
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Upregulation of estrogen receptors in the forebrain of aromatase knockout (ArKO) mice.

TL;DR: Data indicate that in the absence of estrogens there is as much as a 2-fold increase in the number of cells with ERalpha-immunoreactivity in certain hypothalamic and limbic regions, indicating that estrogens can down-regulate ERalpha in brain.