Loading…

Effects of Leukemia Inhibitory Factor on Galanin Expression and on Axonal Growth in Adult Dorsal Root Ganglion Neurons in Vitro

Synthesis of leukemia inhibitory factor (LIF) is increased in lesioned peripheral nerves and it is thought that this may cause increased expression of galanin (GAL) in axotomized dorsal root ganglia (DRG) neurons and also to promote axonal regeneration. We therefore compared effects of LIF and nerve...

Full description

Saved in:
Bibliographic Details
Published in:Experimental neurology 2001-06, Vol.169 (2), p.376-385
Main Authors: Öztürk, G., Tonge, D.A.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Synthesis of leukemia inhibitory factor (LIF) is increased in lesioned peripheral nerves and it is thought that this may cause increased expression of galanin (GAL) in axotomized dorsal root ganglia (DRG) neurons and also to promote axonal regeneration. We therefore compared effects of LIF and nerve growth factor (NGF) on galanin expression and axonal growth using cultured intact DRGs of adult mice. In control lumbar DRGs cultured for 3 days, only 16% of neurons were immunoreactive for GAL, but this was increased to 38% in preparations cultured with LIF. NGF by itself had no effect on GAL expression, but the proportion of GAL-positive neurons in cultures incubated with LIF and NGF together (22%) was less than that observed in DRGs cultured with LIF alone. Similar results were obtained using thoracic DRGs. In collagen gels, NGF caused marked increases in the numbers and lengths of outgrowing axons as observed in previous studies. In contrast, LIF did not stimulate axonal outgrowth but increased the proportions of axons which were immunoreactive for GAL. The results indicate that expression of LIF in lesioned nerves may affect expression of neuropeptides such GAL rather than stimulating axonal regeneration.
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.2001.7667