http://cercor.oxfordjournals.org/content/early/2012/04/10/cercor.bhs092.abstract
Abstract
Most stroke survivors exhibit a partial
recovery from their deficits. This presumably occurs because of
remapping of lost
capabilities to functionally related brain areas.
Functional brain imaging studies suggest that remapping in the
contralateral
uninjured cortex might represent a transient stage
of compensatory plasticity. Some postmortem studies have also shown that
cortical lesions, including stroke, can trigger
dendritic plasticity in the contralateral hemisphere, but the data are
controversial.
We used longitudinal in vivo two-photon microscopy
in the contralateral homotopic cortex to record changes in dendritic
spines
of layer 5 pyramidal neurons in green fluorescent
protein mice. We could not detect de novo growth of dendrites or changes
in the density or turnover of spines for up to 4
weeks after stroke. We also used intrinsic optical signal imaging to
investigate
whether the forepaw (FP) sensory representation is
remapped to the spared homotopic cortex after stroke. Stimulation of the
contralateral FP reliably produced strong intrinsic
signals in the spared hemisphere, but we could never detect a signal
with
ipsilateral FP stimulation after stroke. This lack
of contralateral plasticity at the level of apical dendrites of layer 5
pyramidal neurons and FP sensory maps suggests that
the contralesional cortex may not contribute to functional recovery
after
stroke and that, at least in mice, the peri-infarct
cortex plays the dominant role in postischemic plasticity.
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