QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Schober, A. Articles by Unsicker, K. Search for Related Content PubMed PubMed Citation Articles by Schober, A. Articles by Unsicker, K. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH

 Previous Article  |  Next Article 

Volume 17, Number 3, Issue of February 1, 1997 pp. 891-903
Copyright ©1997 Society for Neuroscience

Reduced Acetylcholinesterase (AChE) Activity in Adrenal Medulla and Loss of Sympathetic Preganglionic Neurons in TrkA-Deficient, But Not TrkB-Deficient, Mice

Received Sept. 9, 1996; revised Nov. 1, 1996; accepted Nov. 11, 1996.

Andreas Schober¹, Liliana Minichiello², Markus Keller³, Katrin Huber¹, Paul G. Layer³, José L. Roig-López⁴, José E. García-Arrarás⁴, Rüdiger Klein², and Klaus Unsicker¹

¹ Department of Anatomy and Cell Biology III, University of Heidelberg, D-69120 Heidelberg, Germany, ² European Molecular Biology Laboratory, Differentiation Programme, D-69117 Heidelberg, Germany, ³ Department of Zoology, Technical University of Darmstadt, D-64287 Darmstadt, Germany, and ⁴ Department of Biology, University of Puerto Rico, Rio Piedras, Puerto Rico 000931-3360

TrkA high-affinity receptors are essential for the normal development of sympathetic paravertebral neurons and subpopulations of sensory neurons. Paravertebral sympathetic neurons and chromaffin cells of the adrenal medulla share an ontogenetic origin, responsiveness to NGF, and expression of TrkA. Which aspects of development of the adrenal medulla might be regulated via TrkA are unknown. In the present study we demonstrate that mice deficient for TrkA, but not the neurotrophin receptor TrkB, show an early postnatal progressive reduction of acetylcholinesterase (AChE) enzymatic activity in the adrenal medulla and in preganglionic sympathetic neurons within the thoracic spinal cord, which are also significantly reduced in number. Quantitative determinations of specific AChE activity revealed a massive decrease (62%) in the adrenal gland and a lesser, but still pronounced, reduction in the thoracic spinal cord (40%). Other markers of the adrenal medulla and its innervation, including various neuropeptides, chromogranin B, secretogranin II, amine transporters, the catecholamine-synthesizing enzymes tyrosine hydroxylase and PNMT, synaptophysin, and L1, essentially were unchanged. Interestingly, AChE immunoreactivity appeared unaltered, too. Preganglionic sympathetic neurons, in contrast to adrenal medullary cells, do not express TrkA. They must, therefore, be affected indirectly by the TrkA knock-out, possibly via a retrograde signal from chromaffin cells. Our results suggest that signaling via TrkA, but not TrkB, may be involved in the postnatal regulation of AChE activity in the adrenal medulla and its preganglionic nerves.

Key words: adrenal gland; spinal cord neurons; acetylcholinesterase; chromaffin cells; neurotrophin receptors; knock-out mice

This article has been cited by other articles:

				Y. Takei and R. Laskey Tumor Necrosis Factor {alpha} Regulates Responses to Nerve Growth Factor, Promoting Neural Cell Survival but Suppressing Differentiation of Neuroblastoma Cells Mol. Biol. Cell, March 1, 2008; 19(3): 855 - 864. [Abstract] [Full Text] [PDF]

				J. Deschenes-Furry, K. Mousavi, F. Bolognani, R. L. Neve, R. J. Parks, N. I. Perrone-Bizzozero, and B. J. Jasmin The RNA-Binding Protein HuD Binds Acetylcholinesterase mRNA in Neurons and Regulates its Expression after Axotomy J. Neurosci., January 17, 2007; 27(3): 665 - 675. [Abstract] [Full Text] [PDF]

				S. Oberle, A. Schober, V. Meyer, B. Holtmann, C. Henderson, M. Sendtner, and K. Unsicker Loss of Leukemia Inhibitory Factor Receptor beta or Cardiotrophin-1 Causes Similar Deficits in Preganglionic Sympathetic Neurons and Adrenal Medulla J. Neurosci., February 8, 2006; 26(6): 1823 - 1832. [Abstract] [Full Text] [PDF]

				A. Roosen, A. Schober, J. Strelau, M. Bottner, J. Faulhaber, G. Bendner, S. L. McIlwrath, H. Seller, H. Ehmke, G. R. Lewin, et al. Lack of Neurotrophin-4 Causes Selective Structural and Chemical Deficits in Sympathetic Ganglia and Their Preganglionic Innervation J. Neurosci., May 1, 2001; 21(9): 3073 - 3084. [Abstract] [Full Text] [PDF]

				S Finotto, K Krieglstein, A Schober, F Deimling, K Lindner, B Bruhl, K Beier, J Metz, J. Garcia-Arraras, J. Roig-Lopez, et al. Analysis of mice carrying targeted mutations of the glucocorticoid receptor gene argues against an essential role of glucocorticoid signalling for generating adrenal chromaffin cells Development, January 7, 1999; 126(13): 2935 - 2944. [Abstract] [PDF]

				A. Schober, N. Wolf, K. Huber, R. Hertel, K. Krieglstein, L. Minichiello, N. Kahane, J. Widenfalk, C. Kalcheim, L. Olson, et al. TrkB and Neurotrophin-4 Are Important for Development and Maintenance of Sympathetic Preganglionic Neurons Innervating the Adrenal Medulla J. Neurosci., September 15, 1998; 18(18): 7272 - 7284. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help