This should be continued as a test for the next week so the neuronal cascade of death could be observed and maybe figure out how long it lasts.
Shining a Light on Stroke
Stroke remains a common and serious consequence of numerous underlying illnesses and risk factors, such as hypertension and diabetes.
Understanding how the brain changes after stroke may help to advance treatments for this illness. To this end, Barth and Mody have developed an improved in vivo model of the anatomy and physiology of ischemic stroke
that uses photothrombosis—occlusion of a blood vessel through injection
of a dye followed by irradiation—combined with stereotaxic
localization (the use of a three-dimensional
coordinate system to place the optic fiber) to monitor neurological
changes before
and after ischemic stroke.
The researchers inserted the optic fiber into the hippocampal artery of mice to isolate blood flow to the hippocampus, a brain
region that is important in learning and memory and is particularly vulnerable to ischemic stroke.
Blood flow was then selectively blocked in the artery through light
activation of a photosensitive dye, rose bengal, which
induced blood clot formation. Measuring neuron
population activity in the hippocampus before and after this procedure,
the
authors observed a massive, brief high-frequency
epileptiform discharge (HFD) in affected neurons, followed by a negative
shift in the baseline electrical potential, which
is consistent with neuronal depolarization due to hypoxia (inadequate
oxygen).
This was followed by a long-lasting decrease in
neuron oscillatory activity in the gamma range (30 to 119 Hz), which is
generally
important to complex cognitive processes such as
memory. Interestingly, only the initial HFD was also observed in the
contralateral
hippocampus, which is often affected by the spread
of seizure activity from the other side of the brain.
This work elegantly characterizes the neurophysiological changes that unfold in the wake of stroke,
thus setting the stage for elaboration of the biochemical basis and
time course of these changes. These findings also suggest
that events, such as the HFD and subsequent
negative electrical potential, might provide specific targets for
therapeutic
intervention aimed at attenuating epileptiform
activity or other disturbances in electrical activity, ultimately to
mitigate
the deleterious effects of these processes on the
brain. Such knowledge should aid in the development of new therapies
designed
to restore brain function in stroke survivors.
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