Date: Wed, 6 Dec 1995 03:44:44 +0900
E-mail from feeney@unm.edu
Subject: recovery
Dr. Dennis Feeney says;
Dr. Jones et. al.,
After the rat recovers use of the impaired limb do the changes in the contralteral homtypical cortex reverse back to baseline? As you know, we have been studying recovery from hemiplegia and are able to promote recovery by combining the drug induced release of NA with "physical therapy" and have some evidence our effect is mediated by cerebellum (see Krobert, Sutton & Feeney J. Neurochem., 62, 2233-2240, 1994). Given that your animals have a transient hemiperesis, have you examined the cerebellum for simlar changes as described in cortex?
Thank you for preparing such an informative, and attractive poster.
Date: Thu, 7 Dec 1995 13:37:06 +0900
E-mail from tjones@ux1.cso.uiuc.edu
Subject: reply
Dr. Theresa Jones says;
Reply to Dr. Feeney
The issue of the persistence of the structural changes is an important one for
which we don't yet have a complete answer. At least some of the changes that
we have found are reduced at late time points after the lesion. For example,
increases in the dendritic bifurcations of Golgi-Cox stained pyramidal neurons
in layer V are reduced between 2 to 4 months after the lesion in comparison
to 18 days after the lesion, although higher order dendrites (those that are
topologically further from the soma) remain elevated in comparison to sham
animals (Jones & Schallert, 1992). These findings are based on relatively
insensitive means of detecting neuronal growth, however. They don't include,
for example, direct measurements of dendritic length, which is almost
certainly a more sensitive measure of dendritic growth. We also simply do
not yet know how enduring the synaptic increases may be.
It is interesting to speculate that the increased number of synapses per
neuron may require maintained expression of the behavioral changes. I think
a thorough assessment of this possibility will require a more sensitive means
of detecting qualitative changes in forelimb behavior in addition to the
magnitude of forelimb asymmetries. Data emerging from Tim Schallert's lab as
well as various unpublished observations indicate that the animals not only
use the non-impaired forelimb more relative to the impaired limb, but they
also develop different ways of using this limb in comparison to sham animals.
At least some of these changes are likely to be very enduring. Work in
our laboratory using intact animals strongly supports the possiblity that
learned changes in motor behavior can result in synaptogenesis in both the
motor cortex and the cerebellum (e.g., Black et al., Proc. Natl. Acad Sci,
87 (1990) 5568-5572).
It seems likely that the behavioral mediation of post-injury CNS plasticity
is not a phenomenon exclusive to the intact cortex or recovery processes in the
non-impaired forelimb. Your work on experience-dependent
recovery and cerebellar changes strongly suggests that the cerebellum is
importantly
involved in the recovery of the impaired body side following unilateral motor
cortex damage. In part because of your findings, we have started to assess
structural changes in the cerebellum following unilateral sensorimotor
cortex lesions. Our data are extremely preliminary, but they are
consistent with possible neural structural changes in the cerebellum and,
in particular, the hemisphere corresponding to the impaired forelimb.