k.p.collins at worldnet.att.net
Sun Nov 3 01:38:04 EST 2002
Unilateral sensorimotor cortex lesions in adult rats facilitate motor
skill learning with the "unaffected" forelimb and training-induced
dendritic structural plasticity in the motor cortex.
Bury SD, Jones TA.
Department of Psychology, University of Washington, Seattle,
Washington 98195, USA. sbury at uci.edu
In humans and other animals, sufficient unilateral damage to the
sensorimotor cortex can cause impairments in the opposite forelimb
and the development of a hyper-reliance on the nonimpaired limb. This
hyper-reliance is adaptive to the extent that it contributes to
functional compensation for lesion-induced impairments. We have found
that unilateral lesions of the forelimb region of the sensorimotor
cortex (FLsmc) in rats, or callosal transections, cause neurons of
the opposite motor cortex to become exceptionally responsive to
changes in forelimb behavior. This enhanced responsiveness might
facilitate learning of compensatory strategies with the nonimpaired
forelimb after unilateral FLsmc lesions. The possibility that these
lesions facilitate learning with the nonimpaired forelimb was
addressed in this study. Rats were required to learn a skilled
forelimb reaching task after either unilateral FLsmc lesions or sham
operations. The trained limb in animals with lesions was the
nonimpaired limb. Compared with shams, rats with unilateral lesions
had a greater rate of acquisition and asymptotic performance level on
the task, which was especially evident on more difficult trials.
Quantitative measures of microtubule associated protein-2 (MAP2)
immunostained dendrites indicated an enhancement of training-induced
dendritic cytoskeletal changes in the motor cortex opposite lesions.
Thus, unilateral FLsmc lesions facilitate learning of at least some
types of motor skills using the nonimpaired forelimb as well as some
of the neuronal changes associated with this learning. This
facilitation could be a substrate underlying behavioral compensation
for unilateral FLsmc damage and may contribute to the phenomenon of
learned nonuse of the impaired limb.
PMID: 12351733 [PubMed - indexed for MEDLINE]
© by someone other than me.
The 'concluding' suppositions are incorrect. It's just an instance of
decreased quantity of activation that has to be dealt with by the TD
E/I-minimization mechanisms that is responsible for the augmented
rate of learning, and the correlated structural changes all
directly-reflect the new rate of TD E/I-minimization on the
That's activation-dependence coupled to TD E/I-minimization, good
There's more than one form of backward propagation.
K. P. Collins
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