P75-DEFICIENT SENSORY AXONS ARE IMMUNOREACTIVE FOR THE GLYCOPROTEIN L1 IN MICE OVEREXPRESSING NERVE GROWTH-FACTOR

Nerve growth factor (NGF) regulates the expression of the glycoprotein L1 among neural cell populations. The purpose of this investigation w as to determine whether NGF equally affects the immunolocalization of L1 on both sympathetic and sensory axons, and whether the functional e xpression of the p75 neurotrophin receptor (p75(NTR)) is required for the immunodetection of this glycoprotein on peripheral axons. Two line s of transgenic mice overexpressing NGF among glial cells were used in this study: (1) one line of mice possessing two normal alleles for p7 5(NTR), and (2) another line of mice possessing two mutated alleles fo r p75(NTR). In both types of animals, sensory axons stained immunohist ochemically for calcitonin gene-related peptide and sympathetic axons stained immunohistochemically for tyrosine hydroxylase invaded the dee p white matter portions of the cerebellum (a central structure contain ing high levels of transgene expression and synthesis); the cerebella of wild type (C57B1/6) and p75(NTR)-deficient mice lacked these sensor y and sympathetic fibers. Both lines of transgenic animals also posses sed a dense plexus of L1-immunoreactive axons in their cerebella; the spatial distribution of these L1-immunostained axone paralleled that s een for the sensory and sympathetic axons. A unilateral removal of the superior cervical ganglion in both lines of transgenic animals caused a complete reduction of tyrosine hydroxylase-immunopositive axons in the cerebellum but did not affect the density of L1-immunopositive axo ns. From these in vivo data, we conclude that collateral branches of s ensory axons which invade a NGF-rich target area display L1 immunoreac tivity, and that such immunodetection does not require the functional expression of p75NTR. (C) 1998 Elsevier Science B.V. All rights reserv ed.