Opposite impacts of tenascin-C and tenascin-R deficiency in mice on the functional outcome of facial nerve repair
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Opposite impacts of tenascin-C and tenascin-R deficiency in mice on the functional outcome of facial nerve repair. / Guntinas-Lichius, Orlando; Angelov, Doychin N; Morellini, Fabio; Lenzen, Mithra; Skouras, Emmanouil; Schachner, Melitta; Irintchev, Andrey.
in: EUR J NEUROSCI, Jahrgang 22, Nr. 9, 11.2005, S. 2171-9.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Opposite impacts of tenascin-C and tenascin-R deficiency in mice on the functional outcome of facial nerve repair
AU - Guntinas-Lichius, Orlando
AU - Angelov, Doychin N
AU - Morellini, Fabio
AU - Lenzen, Mithra
AU - Skouras, Emmanouil
AU - Schachner, Melitta
AU - Irintchev, Andrey
PY - 2005/11
Y1 - 2005/11
N2 - The glycoproteins tenascin-C (TNC) and tenascin-R (TNR) are extracellular matrix proteins involved in the development, plasticity and repair of the nervous system. Altered expression patterns after nerve lesions in adult animals have suggested that these molecules influence axonal regeneration. To test this hypothesis, we investigated adult mice constitutively deficient in the expression of TNC, TNR or both, using the facial nerve injury paradigm. Quantitative analysis of vibrissal movements prior to nerve transection and repair (facial-facial anastomosis) did not reveal genotype-specific differences, and thus impacts of the mutations on motor function in intact animals. Two months after nerve repair, recovery of vibrissal whisking was poor in wild-type mice, a typical finding after facial-facial anastomosis in rodents. Differential effects of the mutations on whisking were found: recovery of function was worse in TNC-deficient and better in TNR null mice compared with wild-type littermates. In double-knockout animals, vibrissal performance was insufficient, but to a lesser extent compared with TNC null mutant mice. Retrograde labelling of motoneurons in the same animals showed that similar numbers of motoneurons had reinnervated the whisker pads in all experimental groups precluding varying extents of motoneuron death and/or axon regeneration failures as causes for the different outcomes of nerve repair. Our results provide strong evidence that TNC promotes and TNR impedes recovery after nerve lesion. These findings are of particular interest with regard to the scanty knowledge about factors determining success of regeneration in the peripheral nervous system of mammals.
AB - The glycoproteins tenascin-C (TNC) and tenascin-R (TNR) are extracellular matrix proteins involved in the development, plasticity and repair of the nervous system. Altered expression patterns after nerve lesions in adult animals have suggested that these molecules influence axonal regeneration. To test this hypothesis, we investigated adult mice constitutively deficient in the expression of TNC, TNR or both, using the facial nerve injury paradigm. Quantitative analysis of vibrissal movements prior to nerve transection and repair (facial-facial anastomosis) did not reveal genotype-specific differences, and thus impacts of the mutations on motor function in intact animals. Two months after nerve repair, recovery of vibrissal whisking was poor in wild-type mice, a typical finding after facial-facial anastomosis in rodents. Differential effects of the mutations on whisking were found: recovery of function was worse in TNC-deficient and better in TNR null mice compared with wild-type littermates. In double-knockout animals, vibrissal performance was insufficient, but to a lesser extent compared with TNC null mutant mice. Retrograde labelling of motoneurons in the same animals showed that similar numbers of motoneurons had reinnervated the whisker pads in all experimental groups precluding varying extents of motoneuron death and/or axon regeneration failures as causes for the different outcomes of nerve repair. Our results provide strong evidence that TNC promotes and TNR impedes recovery after nerve lesion. These findings are of particular interest with regard to the scanty knowledge about factors determining success of regeneration in the peripheral nervous system of mammals.
KW - Anastomosis, Surgical
KW - Animals
KW - Cell Count
KW - Cell Death
KW - Disease Models, Animal
KW - Facial Nerve Injuries
KW - Mice
KW - Mice, Knockout
KW - Motor Neurons
KW - Muscle, Skeletal
KW - Nerve Regeneration
KW - Recovery of Function
KW - Stilbamidines
KW - Tenascin
KW - Tibial Nerve
KW - Vibrissae
U2 - 10.1111/j.1460-9568.2005.04424.x
DO - 10.1111/j.1460-9568.2005.04424.x
M3 - SCORING: Journal article
C2 - 16262655
VL - 22
SP - 2171
EP - 2179
JO - EUR J NEUROSCI
JF - EUR J NEUROSCI
SN - 0953-816X
IS - 9
ER -
