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Cellular proliferation and migration following a controlled cortical impact in the mouse
TLDR
It is delineated that an increase in proliferation occurs in the dorsal-most aspect of the ipsilateral SVZ following impact and that proliferating cells migrate from the SVZ to cortical and subcortical structures affected by the injury and that some of these cells are migrating neuroblasts. Expand
Use-dependent exacerbation of brain damage occurs during an early post-lesion vulnerable period
TLDR
It is found that surviving neural tissue in the damaged hemisphere and recovery of function appear to be vulnerable to prolonged forced overuse of the impaired forelimb throughout the first 15 days, but tissue loss was detectable only when the animal was forced to use the impaired Forelimb during the first 7 days after injury. Expand
Differential activation of microglia in neurogenic versus non‐neurogenic regions of the forebrain
TLDR
The data show that both constitutive and postlesion levels of microglial activation differ between neurogenic and non‐neurogenic regions. Expand
Use-Dependent Exaggeration of Neuronal Injury after Unilateral Sensorimotor Cortex Lesions
TLDR
The results suggest that although behavioral experience can enhance neural growth after brain injury, the region surrounding the injury may be vulnerable to behavioral pressure during the early postlesion period. Expand
Use-dependent structural events in recovery of function.
TLDR
It is hypothesized that behaviorally driven neurotransmitter release relating to forced use of the forelimb may be toxic to surviving tissue that has been partially traumatized by the lesion. Expand
Ethanol reduces metabolic uncoupling following experimental head injury.
TLDR
Results indicate that low-dose ethanol is associated with a marked attenuation of immediate postinjury hyperglycolysis and with more normal glucose metabolism in the injury penumbra over the ensuing 3 days, which may likely explain the neuroprotective effect of ethanol. Expand
Differential effects of glial cell line-derived neurotrophic factor (GDNF) in the striatum and substantia nigra of the aged Parkinsonian rat
TLDR
It is demonstrated that increased levels of striatal, but not nigral, GDNF biosynthesis prevents DA neuronal loss and protects DA terminals from 6-OHDA-induced damage, thereby maintaining DA function in the aged rat. Expand
Glial Cell Line-Derived Neurotrophic Factor (GDNF) Gene Delivery Protects Dopaminergic Terminals from Degeneration
TLDR
The results suggest that GDNF gene delivery prior to a partial lesion ameliorates damage caused by 6-OHDA in aged rats by inhibiting the degeneration of DA terminals rather than by inducing sprouting of nigrostriatal axons. Expand
Delivery of a GDNF Gene into the Substantia Nigra after a Progressive 6-OHDA Lesion Maintains Functional Nigrostriatal Connections
TLDR
It is demonstrated that experimentally increasing levels of GDNF biosynthesis near the dopaminergic neuronal soma is effective in protecting the survival of these neurons and their function even when therapy is begun after 6-OHDA-induced degeneration has commenced, and GDNF gene therapy may ameliorate the consequences of Parkinson's disease through rescuing compromised dopamine neurons. Expand
Targeted Gene Inactivation of Calpain-1 Suppresses Cortical Degeneration Due to Traumatic Brain Injury and Neuronal Apoptosis Induced by Oxidative Stress*
TLDR
The findings suggest that the calpain-1 knock-out mice may serve as a useful model system for neuronal protection and apoptosis in traumatic brain injury and other neurodegenerative disorders in which oxidative stress plays a role. Expand
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