Abstract
The thymidine analogue, 5-bromodeoxyuridine (BrdU), has been used in an attempt to manipulate experimentally the proliferative response of the Schwann cell population that follows induction of segmental demyelination in the peripheral nervous system. It was found that in the presence of BrdU, a significant number of Schwann cells displayed a susceptibility to the agent, in that they could be 'held' in the pro-myelinated state. It is suggested that there is some regulatory transition requiring the priming of the Schwann cell genome for myelination that occurs before the remyelinating phase of repair can be started, but after the establishment of the Schwann cell/axon relationship.
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