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Harnessing activity-dependent plasticity to repair the damaged corticospinal tract in an animal model of cerebral palsy

MARTIN JH; CHAKRABARTY S; FRIEL KM
DEV MED CHILD NEUROL , 2011, vol. 534, n° Suppl. 4, p. 9-13
Doc n°: 153889
Localisation : Documentation IRR

D.O.I. : http://dx.doi.org/DOI:10.1111/j.1469-8749.2011.04055.x
Descripteurs : AJ23 - PARALYSIE CEREBRALE

The corticospinal tract (CST) is the principal motor control pathway for skilled
movements. It has a protracted postnatal development, creating a protracted
period of vulnerability to perinatal brain and spinal cord injury. Research has
shown that the motor signs in cerebral palsy (CP) reflect the loss of CST
connections as well as development of abnormal motor systems connections,
especially between the developing CST and spinal motor circuits.
In this paper,
we discuss a feline model of CP that we have developed. The animals develop a
pattern of abnormal CST connections that is remarkably similar to that seen in
hemiplegic CP and visuomotor impairments. Using this model we devised neural
activity-based therapeutic approaches to repair the abnormal CST connections and
restore normal skilled movement control. Our studies stress that more active CST
connections are better able to maintain strong synaptic connections with spinal
motor circuits. We propose that perinatal trauma initiates a vicious cycle in
which CST axons that are spared after an injury are at a disadvantage for
maintaining spinal connections, leading to further reductions in connections and
motor signs. If this is so, targeted activation of the spared CST might interrupt
this process and lead to functional improvement.
CI - (c) The Authors. Developmental Medicine & Child Neurology (c) 2011 Mac Keith
Press.

Langue : ANGLAIS

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