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Reduced axon sprouting after treatment that diminishes microglia accumulation at lesions in the leech CNS
Author(s) -
Ngu Emmanuel Mbaku,
Sahley Christie L.,
Muller Kenneth J.
Publication year - 2007
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21386
Subject(s) - microglia , sprouting , axon , biology , hirudo medicinalis , leech , central nervous system , neuroscience , nitric oxide , inflammation , immunology , endocrinology , botany , world wide web , computer science
The role of mammalian microglia in central nervous system (CNS) repair is controversial. Microglia accumulate at lesions where they act as immune cells and phagocytize debris, and they may secrete neurotrophins, but they also produce molecules that can be cytotoxic, like nitric oxide (NO). To determine the importance of microglial accumulation at lesions on growth of severed CNS axons in the leech ( Hirudo medicinalis ), in which axon and synapse regeneration are notably successful even when isolated in tissue culture medium, microglial migration to lesions was reduced. Pressure (P) sensory neurons were injected with biocytin to reveal the extent of their sprouting 24 hours after lesioning. To reduce microglia accumulation at lesions, cords were treated for 3.5 hours with 3 mM ATP or 2 mM N ω ‐nitro‐ L ‐arginine methyl ester (L‐NAME) or 50 μM Reactive blue‐2 (RB2) beginning 30 minutes before injury. Lesioned controls were either not treated with drug or treated 3 hours later with one of the drugs, after the migration and subsequent accumulation of most microglia had occurred, but before the onset of axon sprouting, for a total of seven separate conditions. There was a significant reduction in total sprout lengths compared with controls when microglial accumulation was reduced. The results suggest that microglial cells are necessary for the usual sprouting of injured axons. J. Comp. Neurol. 503:101–109, 2007. © 2007 Wiley‐Liss, Inc.