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1.
J Neurotrauma ; 31(16): 1396-404, 2014 Aug 15.
Article in English | MEDLINE | ID: mdl-24749541

ABSTRACT

Traumatic brain injury (TBI) afflicts up to 2 million people annually in the United States and is the primary cause of death and disability in young adults and children. Previous TBI studies have focused predominantly on the morphological, biochemical, and functional alterations of gray matter structures, such as the hippocampus. However, little attention has been given to the brain ventricular system, despite the fact that altered ventricular function is known to occur in brain pathologies. In the present study, we investigated anatomical and functional alterations to mouse ventricular cilia that result from mild TBI. We demonstrate that TBI causes a dramatic decrease in cilia. Further, using a particle tracking technique, we demonstrate that cerebrospinal fluid flow is diminished, thus potentially negatively affecting waste and nutrient exchange. Interestingly, injury-induced ventricular system pathology resolves completely by 30 days after injury as ependymal cell ciliogenesis restores cilia density to uninjured levels in the affected lateral ventricle.


Subject(s)
Brain Injuries/pathology , Brain Injuries/physiopathology , Cerebrospinal Fluid/physiology , Cilia/pathology , Ependyma/pathology , Animals , Cerebral Ventricles/pathology , Disease Models, Animal , Fluorescent Antibody Technique , Hydrocephalus/etiology , Immunohistochemistry , Magnetic Resonance Imaging , Male , Mice , Mice, Inbred C57BL , Microscopy, Confocal , Microscopy, Electron, Scanning , Microscopy, Electron, Transmission
2.
Proc Natl Acad Sci U S A ; 107(1): 366-71, 2010 Jan 05.
Article in English | MEDLINE | ID: mdl-19995960

ABSTRACT

Neurological dysfunction caused by traumatic brain injury results in profound changes in net synaptic efficacy, leading to impaired cognition. Because excitability is directly controlled by the balance of excitatory and inhibitory activity, underlying mechanisms causing these changes were investigated using lateral fluid percussion brain injury in mice. Although injury-induced shifts in net synaptic efficacy were not accompanied by changes in hippocampal glutamate and GABA levels, significant reductions were seen in the concentration of branched chain amino acids (BCAAs), which are key precursors to de novo glutamate synthesis. Dietary consumption of BCAAs restored hippocampal BCAA concentrations to normal, reversed injury-induced shifts in net synaptic efficacy, and led to reinstatement of cognitive performance after concussive brain injury. All brain-injured mice that consumed BCAAs demonstrated cognitive improvement with a simultaneous restoration in net synaptic efficacy. Posttraumatic changes in the expression of cytosolic branched chain aminotransferase, branched chain ketoacid dehydrogenase, glutamate dehydrogenase, and glutamic acid decarboxylase support a perturbation of BCAA and neurotransmitter metabolism. Ex vivo application of BCAAs to hippocampal slices from injured animals restored posttraumatic regional shifts in net synaptic efficacy as measured by field excitatory postsynaptic potentials. These results suggest that dietary BCAA intervention could promote cognitive improvement by restoring hippocampal function after a traumatic brain injury.


Subject(s)
Amino Acids, Branched-Chain/metabolism , Amino Acids, Branched-Chain/therapeutic use , Brain Injuries , Cognition Disorders , Diet , Amino Acids, Branched-Chain/administration & dosage , Animals , Brain Injuries/complications , Brain Injuries/physiopathology , Cognition Disorders/diet therapy , Cognition Disorders/etiology , Cognition Disorders/physiopathology , Glutamic Acid/metabolism , Hippocampus/metabolism , Hippocampus/physiopathology , Humans , Male , Mice , Mice, Inbred C57BL , Synaptic Transmission/physiology
3.
J Neurosci Methods ; 174(2): 177-85, 2008 Sep 30.
Article in English | MEDLINE | ID: mdl-18674561

ABSTRACT

Measuring extracellular dopamine in the brain of living animals by means of microdialysis and/or voltammetry is a route towards understanding both normal brain function and pathology. Previous reports, however, suggest that the tissue response to implantation of devices may affect the outcome of the measurements. To address the source of the tissue response and its impact on striatal dopamine systems microdialysis probes were placed in the striatum of anesthetized rats. Images obtained by dual-label fluorescence microscopy show signs of ischemia and opening of the blood-brain barrier near the probe tracks. Opening of the blood-brain barrier was further examined by determining dialysate concentrations of carbi-DOPA, a drug that normally does not penetrate the brain. Although carbi-DOPA was recovered in brain dialysate, it did not alter dialysate dopamine levels or evoked dopamine release as measured by voltammetry near the probes. Microdialysis probes also significantly diminished the effect of intrastriatal infusion of kynurenate on extracellular dopamine levels as measured by voltammetry near the probes.


Subject(s)
Corpus Striatum/blood supply , Corpus Striatum/pathology , Dopamine/analysis , Electrodes, Implanted/adverse effects , Microdialysis/instrumentation , Microelectrodes/adverse effects , Animals , Carbidopa/administration & dosage , Carbidopa/analysis , Cerebrovascular Circulation , Chromatography, High Pressure Liquid , Corpus Striatum/drug effects , Dopamine Agents/administration & dosage , Dopamine Agents/analysis , Excitatory Amino Acid Antagonists/administration & dosage , Excitatory Amino Acid Antagonists/analysis , Extracellular Space/drug effects , Extracellular Space/metabolism , Fluorescent Antibody Technique , Injections, Intraventricular , Kynurenic Acid/administration & dosage , Kynurenic Acid/analysis , Male , Microscopy, Confocal , Nanocapsules/administration & dosage , Nanocapsules/analysis , Rats , Rats, Sprague-Dawley
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