Galectin-1 in regenerating motoneurons

• Published in: The European journal of neuroscience Vol. 20; no. 11; pp. 2872 - 2880
• Main Authors: McGraw, J., McPhail, L. T., Oschipok, L. W., Horie, H., Poirier, F., Steeves, J. D., Ramer, M. S., Tetzlaff, W.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.12.2004
• Subjects: Animals; Axotomy - methods; Cell Count - methods; Colchicine - pharmacology; Facial Nerve Injuries - metabolism; Facial Nerve Injuries - physiopathology; Functional Laterality - physiology; Galectin 1 - genetics; Galectin 1 - metabolism; GDNF; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Glial Cell Line-Derived Neurotrophic Factor; In Situ Hybridization - methods; L-14; Mice; Mice, Knockout; motoneurons; Motor Neurons - drug effects; Motor Neurons - metabolism; Nerve Crush - methods; Nerve Growth Factors - pharmacology; Nerve Regeneration - physiology; Recovery of Function; regeneration-associated genes; RL14; RNA, Messenger - metabolism; Time Factors; Vibrissae - physiology
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/j.1460-9568.2004.03802.x

The exogenous application of recombinant galectin‐1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal galectin‐1 expression has recently been demonstrated to increase after axotomy. Here we demonstrate a significant increase in the endogenous neuronal expression of galectin‐1 mRNA in facial motoneurons after either a nerve resection or crush injury in mice. This increase in galectin‐1 expression was due in part to the loss of target‐derived factor(s) as indicated by both the return of galectin‐1 expression to control levels following target re‐innervation and the increase in galectin‐1 expression after blockade of axonal transport by an interneuronal colchicine injection. Furthermore, interneuronal injections of glial‐derived neurotrophic factor into the uninjured nerve also increased galectin‐1 mRNA expression within facial motoneurons suggesting that positive signals may also be involved in the regulation of galectin‐1 expression. Galectin‐1 null mutant mice showed an attenuated rate of functional recovery of whisking movement after a facial nerve crush.