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The Journal of Neuroscience, February 8, 2006, 26(6):1823-1832; doi:10.1523/JNEUROSCI.4127-05.2006

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Cellular/Molecular
Loss of Leukemia Inhibitory Factor Receptor or Cardiotrophin-1 Causes Similar Deficits in Preganglionic Sympathetic Neurons and Adrenal Medulla

Stephan Oberle,¹ Andreas Schober,¹ Verena Meyer,¹ Bettina Holtmann,² Christopher Henderson,³ Michael Sendtner,² and Klaus Unsicker¹

¹Neuroanatomy and Interdisciplinary Center for Neurosciences, University of Heidelberg, D-69120 Heidelberg, Germany, ²Department of Clinical Neurobiology, University of Würzburg, D-97080 Würzburg, Germany, and ³Hammer Health Sciences, Columbia University, New York, New York 10032

Correspondence should be addressed to Dr. Klaus Unsicker, Department of Neuroanatomy and IZN, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. Email: klaus.unsicker{at}urz.uni-heidelberg.de

Leukemia inhibitory factor (LIF) receptor (LIFR) is a receptor for a variety of neurotrophic cytokines, including LIF, ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1). These cytokines play an essential role for the survival and maintenance of developing and postnatal somatic motoneurons. CNTF may also serve the maintenance of autonomic, preganglionic sympathetic neurons (PSNs) in the spinal cord, as suggested by its capacity to prevent their death after destruction of one of their major targets, the adrenal medulla. Although somatic motoneurons and PSNs share a common embryonic origin, they are distinct in several respects, including responses to lesions. We have studied PSNs in mice with targeted deletions of the LIFR or CT-1 genes, respectively. We show that LIF, CNTF, and CT-1 are synthesized in embryonic adrenal gland and spinal cord and that PSNs express LIFR. In embryonic day 18.5 LIFR (–/–) and CT-1 (–/–) mice, PSNs were reduced by 20%. PSNs projecting to the adrenal medulla were more severely affected (–55%). Although LIFR (–/–) mice revealed normal numbers of adrenal chromaffin cells and axons terminating on chromaffin cells, levels of adrenaline and numbers of adrenaline-synthesizing cells were significantly reduced. We conclude that activation of LIFR is required for normal development of PSNs and one of their prominent targets, the adrenal medulla. Thus, both somatic motoneurons and PSNs in the spinal cord depend on LIFR signaling for their development and maintenance, although PSNs seem to be overall less affected than somatic motoneurons by LIFR deprivation.

Key words: preganglionic sympathetic neurons; intermediolateral column; adrenal medulla; LIFR; ciliary neurotrophic factor; cardiotrophin-1

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Received Sept. 28, 2005; revised Dec. 9, 2005; accepted Dec. 12, 2005.

Correspondence should be addressed to Dr. Klaus Unsicker, Department of Neuroanatomy and IZN, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. Email: klaus.unsicker{at}urz.uni-heidelberg.de

This article has been cited by other articles:

				J. Strelau, A. Strzelczyk, P. Rusu, G. Bendner, S. Wiese, F. Diella, A. L. Altick, C. S. von Bartheld, R. Klein, M. Sendtner, et al. Progressive Postnatal Motoneuron Loss in Mice Lacking GDF-15 J. Neurosci., October 28, 2009; 29(43): 13640 - 13648. [Abstract] [Full Text] [PDF]

				F. Sicard, M. Ehrhart-Bornstein, D. Corbeil, S. Sperber, A. W. Krug, C. G. Ziegler, V. Rettori, S. M. McCann, and S. R. Bornstein Age-dependent regulation of chromaffin cell proliferation by growth factors, dehydroepiandrosterone (DHEA), and DHEA sulfate PNAS, February 6, 2007; 104(6): 2007 - 2012. [Abstract] [Full Text] [PDF]

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