Sentences with phrase «neuronal marker tuji»

After 4 weeks of differentiation, the majority of the cells (> 60 %) expressed the postmitotic neuronal marker β - III tubulin with a subset (about 50 % of total neurons) additionally expressing TH, a marker for midbrain dopaminergic neurons (Fig. 3A — D).
For the detection of specific antigens, the following primary antibodies were used: mouse monoclonal anti-Tuj1 (Covance, Princeton, NJ, USA) as a neuronal marker, rabbit anti-L1 (kindly provided from Dr. Asou)[52] and rat monoclonal anti-L1 (Millipore, Billerica, MA, USA) as granule cell markers, rabbit anti-calbindin D28K (Millipore) as a Purkinje cell marker, and rabbit anti-glial fibrillary acidic protein (GFAP, DAKO, Denmark) as an astrocyte marker.
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Neurons were detected using the pan neuronal marker TuJI (red) and the synaptic contact by alpha - Bungarotoxin (green).
We observed a modest decrease in cell cycling and some induction of the neuronal marker beta - III tubulin, as quantified here.
The green staining indicates the cortical marker CTIP2, the red stain is the neuronal marker TUJ1, and the blue stains the nuclei of the cells.
The neurons express a pan neuronal marker Map2 in green and a percentage of the cells express a marker for inhibitory neurons, GABA, in red.

Not exact matches

The neurons where then stained with a marker of neuronal processes in red.
For neuroscientists finishing a Ph.D. program or a postdoctoral position, the mysteries of neuronal circuits and genetic markers for disease pale compared to one puzzling question: Where are the jobs?
Whilst the immune response to TBM sets up some of the damage, this new research suggests that markers of ongoing neuronal injury are more predictive of disease severity than markers of immune response.
Based on anatomy and molecular markers, we propose that it arose by duplication of a neighboring stem cell, which may have enabled finer neuronal control over leg - related behaviors, such as walking and grooming.»
«We now have the first marker for the capacity of brain immune cells to remove toxic materials,» says Haass, «and its increase long before full Alzheimer's dementia shows that there is early neuronal injury that does not yet affect memory, but already triggers a microglia response.»
«Even more importantly, we were interested in determining whether inflammatory markers in plasma were independently linked to CSF markers of AD - related pathology and neuronal damage in a group of healthy, community dwelling older adults.»
Bettcher also emphasized that although participants had detectable levels of AD - related markers and markers of neuronal damage in their CSF, the presence of these markers alone does not indicate a diagnosis of AD, nor does it mean that they will develop AD in the future.
«Results from our study suggest that although CSF markers of inflammation are strong predictors, both plasma and CSF markers of inflammation independently relay information about AD - related pathology and neuronal damage in head - to - head comparisons,» Bettcher said.
The scientists had expected inflammation markers in the CSF to be more robust predictors of AD - related pathology and neuronal damage than those in the blood due to the «blood brain barrier.»
Conducted among more than 170 subjects at various stages of Alzheimer's disease, the study by the team led by Salah El Mestikawy (Douglas Mental Health University Institute, Canada) and Stéphanie Daumas (Université Pierre et Marie Curie, France) has shown instead that the disease is accompanied by a minor decline in neuronal and synaptic markers.
We combined a behavioral test for magnetic compass orientation in mole rats and immunocytochemical visualization of the transcription factor c - Fos as a marker of neuronal activity.
«Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects» prefrontal cortices, we only observed very minor neuronal and synaptic losses.
Using these direct electrical recordings, the team was able to test the level of high frequency neuronal activity (a marker of neurons firing) in this region, a very precise measure which captures activity tied to cognition processes lasting mere hundreds of milliseconds.
Hippocampus glutamate and N - acetyl aspartate markers of excitotoxic neuronal compromise in posttraumatic stress disorder Rosso IM, Crowley DJ, Silveri MM, Rauch SL, Jensen JE.
By combining neuronal tracing with behavioral experiments leading to sensory - driven gene expression of the neuronal activity marker ZENK during magnetic compass orientation, we demonstrate a functional neuronal connection between the retinal neurons and Cluster N via the visual thalamus.
The vast majority of forebrain neurons in songbirds can express ZENK as a marker for neuronal activity [13], [14], [24]--[26] Feenders, Liedvogel, Zapka, Mouritsen, Jarvis, personal communication].
To do this, we combined neuronal tracing with analyses of ZENK expression as a marker for neuronal activity induced during behavioral experiments.
The proper placement of retrograde tracer into Cluster N was proven by co-localization of tracer and the neuronal activity marker ZENK, since Cluster N is the only part of the forebrain displaying movement - independent ZENK activity in night - migratory birds sitting still or performing magnetic compass orientation under dim light conditions at night [13].
The most promising markers reflect neuronal and glial degeneration, particularly neurofilament light chain.
However, recent evidence indicates that apoE4 expression compromises the blood - brain barrier (as does apoE deficiency).40 Studies of brain histology, neurodegenerative markers, cholinergic activity, and neuronal function in knockout mice have been equivocal.39 Failure of detailed neurocognitive and retinal studies to demonstrate defects in our patient suggests either that the functions of apoE in the brain and eye are not critical or that they can be fulfilled by a surrogate protein.
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