INDUCTION OF MAP1B PHOSPHORYLATION IN TARGET-DEPRIVED AFFERENT-FIBERSAFTER KAINIC ACID LESION IN THE ADULT-RAT

We have previously shown that the phosphorylated form of microtubule-a ssociated protein 1B (MAP1B-P), which is located in growing axons duri ng development and regeneration, remains detectable in the adult centr al nervous system only in areas that undergo morphologic plasticity (N othias et al. [1996] J. Comp. Neurol. 368:317-334). Our objective in t he present study was to determine whether lesion-induced axonal remode ling, in the adult rat, is associated with reinduction of MAP1B phosph orylation. MAP1B-P was not detectable in intact adult thalamic ventrob asal complex (VB), although low levels of MAP1B and its mRNA were pres ent. A neuron-depletion of VB by in situ injection of kainic acid was followed by an induction of MAP1B phosphorylation by 24 hours postlesi on. 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 exclusi ve location of MAP1B-P in axons in a proximodistal gradient. MAP1B pho sphorylation appeared to be regulated by posttranslational modificatio n 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 us ing axonal tracing with dextran-biotin and tyrosine hydroxylase immuno histochemistry, showed the presence of MAP1B-P in VB afferents from so matosensory relays and the locus coeruleus. This study supports the hy pothesis that MAP1B, at a particular state of phosphorylation, is corr elated 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 increase d axonal plasticity. (C) 1998 Wiley-Liss, Inc.