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SUMMARY:Intrinsic and extrinsic controls on axon regeneration and plastici
 ty. -  James W. Fawcett Cambridge University Centre for Brain Repair\, Uni
 versity of Cambridge\, Cambridge\, UK
DTSTART:20090402T084500Z
DTEND:20090402T093000Z
UID:TALK17655@talks.cam.ac.uk
CONTACT:Anna Di Pietro
DESCRIPTION:Recovery of function in the damaged adult CNS is limited due t
 o the absence of axon regeneration and relatively low levels of plasticity
 . Both axon regeneration and plasticity are inhibited by molecules and str
 uctures in the extracellular matrix. \nThe role of  chondroitin sulphate p
 roteoglycans (CSPGs) in the extracellular matrix in the control of plastic
 ity was revealed because chondroitinase\, which degrades the glycosaminogl
 ycans (GAGs)\, promotes recovery of function in the damaged CNS. This reco
 very of function has now been demonstrated in spinal injury and peripheral
  nerve repair models. The formation of new circuits is controlled both by 
 levels of plasticity and by behaviour. We have therefore examined the inte
 raction of rehabilitation and plasticity\, based on skilled forelimb funct
 ion. A rehabilitation task for skilled forelimb use combined with chondroi
 tinase produces a dramatic increase in recovery compared to rehabilitation
  or chondroitinase alone. Plasticity in the adult CNS may be restricted by
  perineuronal nets (PNNs) around may neuronal cell bodies and dendrites. T
 hese contain inhibitory CSPGs\, hyaluronan\, link protein and tenascin R. 
 The components of PNNs are produced either by the neurones themselves or b
 y surrounding glial cells. All neurones with PNNs express both a hyalurona
 n synthase enzyme and a link protein\, and these are probably the key comp
 onents that trigger the formation of the structures. A link protein knocko
 ut animal lacks normal PNNs on its dendrites. The GAGs within PNNs have a 
 different sulphation pattern to those in the general CNS matrix\, giving t
 hem high affinity for binding molecules which may affect plastic behaviour
  in neurons. This may be a mechanism that concentrates active molecules in
  the regions of synapses. \nIn addition to inhibition by inhibitory molecu
 les in myelin and CSPGs in glial scar tissue\, CNS axons have a low intrin
 sic ability to regenerate. Part of this low regenerative ability can be ex
 plained by the fact that CNS axons lack the integrins needed to interact w
 ith the matrix of the damaged CNS. The presence of protein translational m
 echanisms in PNS but not CNS axons is also a factor. Changes in gangliosid
 es are also an important event in regeneration\, and these may also differ
  in the CNS.\n\n
LOCATION:Cripps Court\, Magdalene College
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