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Tenascin-R knock-out mice

Reference Number 21-00013b


Genetically modified animals are essential research tools in modern neuroscience, since they allow researchers to study the role of specific genes in pathological processes leading to neurodegenerative diseases. Tenascin-R (TNR) is an extracellular matrix glycoprotein expressed predominantly in the central nervous system and localizes to the nodes of Ranvier and perineuronal nets. TNR has also been implicated to have a positive effect on nerve regeneration.

Open field behavior of TN-R-/- and wild-type mice: representative paths of wild-type (left) and TNR-/- (right) mouse during the first 5 min of test. TNR-/- mice spend considerably more time in the central area of the maze.

TNR -/- mice were generated by inactivating the Tnr gene via homologous recombination in embryonic stem cells and creating transgenic mice. Although TNR -/- mice appear to be normal with regard to general health condition and neurological state, deficits in the rota-rod, open field, water maze and two-way active avoidance paradigms have been observed, which indicate impairment in motor coordination and in spatial and associative learning. Furthermore, the knock-out animals displayed a significant decrease in conduction velocity of compound action potential recordings from optic nerves.

Commercial Opportunity
Breeding pairs are available under a Tangible Property License Agreement.

Further Reading

  • Weber et al.: Mice deficient for Tenascin-R display alterations of extracellular matrix and decreased axonal conduction velocities in the CNS. J of Neuroscience, 1999, 19(11): 4245-4262.
  • Montag-Sallaz and Montag: Severe cognitive and motor coordination deficits in Tenascin-R-deficient mice. Genes, Brain and Behaviour (2003) 2: 20-31.
  • Hargus et al.: Tenascin-R promotes neuronal differentiation of embryonic stem cells and recruitment of host-derived neural precursor cells after cytotoxic lesion of the mouse striatum. Stem Cells. 2008 Aug;26(8):1973-84. Epub 2008 May 22.