Induction of MAP1B phosphorylation in target-deprived afferent fibers after kainic acid lesion in the adult rat.

We have previously shown that the phosphorylated form of microtubule-associated protein 1B (MAP1B-P), which is located in growing axons during development and regeneration, remains detectable in the adult central nervous system only in areas that undergo morphologic plasticity (Nothias et al. [1996] J. Comp. Neurol. 368:317-334). Our objective in the present study was to determine whether lesion-induced axonal remodeling, in the adult rat, is associated with reinduction of MAP1B phosphorylation. MAP1B-P was not detectable in intact adult thalamic ventrobasal complex (VB), although low levels of MAP1B and its mRNA were present. A neuron-depletion of VB by in situ injection of kainic acid was followed by an induction of MAP1B phosphorylation by 24 hours postlesion. MAP1B-P was detected in fibers originating from undamaged neurons that were not located in the lesion, as demonstrated by the absence of hybridized MAP1B-mRNA. Ultrastructural analysis confirmed the exclusive location of MAP1B-P in axons in a proximodistal gradient. MAP1B phosphorylation appeared to be regulated by posttranslational modification of existing protein because the levels of MAP1B-mRNA did not change. The number of MAP1B-P-labeled fibers increased during the first month postlesion and remained high for a long period. Double staining by using axonal tracing with dextran-biotin and tyrosine hydroxylase immunohistochemistry, showed the presence of MAP1B-P in VB afferents from somatosensory relays and the locus coeruleus. This study supports the hypothesis that MAP1B, at a particular state of phosphorylation, is correlated with axonal remodeling in the adult central nervous system (CNS). We suggest that the interaction of MAP1B-P with microtubules allows the modulation of their dynamic properties during periods of increased axonal plasticity.