Induction of MAP1B phosphorylation in target‐deprived afferent fibers after kainic acid lesion in the adult rat-猫眼课题宝

成年大鼠红藻氨酸损伤后靶标剥夺传入纤维中 MAP1B 磷酸化的诱导

DOI：

10.1002/(sici)1096-9861(19980629)396:2

发表时间：

1998

期刊：

Journal of Comparative Neurology

影响因子：

2.5

通讯作者：

中科院分区：

医学3区

文献类型：

作者：

S. Soares;I. Fischer;M. Ravaille;J. Vincent;F. Nothias

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. J. Comp. Neurol. 396:193–210, 1998. © 1998 Wiley‐Liss, Inc.