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Nobel Del Mar

Researcher at University of Tennessee Health Science Center

Publications -  34
Citations -  1645

Nobel Del Mar is an academic researcher from University of Tennessee Health Science Center. The author has contributed to research in topics: Traumatic brain injury & Retinal. The author has an hindex of 16, co-authored 30 publications receiving 1449 citations.

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Pathway tracing using biotinylated dextran amines.

TL;DR: Biotinylated dextran amines (BDA) are highly sensitive tools for anterograde and retrograde pathway tracing studies of the nervous system and can, therefore, be readily used in ultrastructural studies.
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Evidence for Differential Cortical Input to Direct Pathway versus Indirect Pathway Striatal Projection Neurons in Rats

TL;DR: Results suggest that striatonigral neurons preferentially receive input from IT-type cortical neurons, whereas striatopallidal neurons receive greater input from PT- type cortical neurons.
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Differential morphology of pyramidal tract-type and intratelencephalically projecting-type corticostriatal neurons and their intrastriatal terminals in rats

TL;DR: The clear differences between these two corticostriatal neuron types in perikaryal size and laminar location in the cortex, and in the size and shape of their intrastriatal terminals, suggest that they may differ in the nature of their influence on the striatum.
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Cellular localization and development of neuronal intranuclear inclusions in striatal and cortical neurons in R6/2 transgenic mice.

TL;DR: The early accumulation ofNIIs in cortex and striatum in R6/2 mice is consistent with the early appearance of motor and learning abnormalities in these mice, and the eventual pervasiveness of NIIs at ages at which severe abnormalities are evident is inconsistent with their contribution to a neuronal dysfunction underlying the abnormalities.
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Abnormalities in the functioning of adipocytes from R6/2 mice that are transgenic for the Huntington’s disease mutation

TL;DR: The data suggest that the obesity observed at 8-9 weeks in R6/2 mice may stem from a defect in fat breakdown by adipocytes, which is not accompanied by symptoms associated with diabetes, as there were no abnormalities in serum glucose, serum insulin or the ability of insulin to stimulate glucose metabolism in epididymal adipose tissue.