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 (15) Citing Articles via Google Scholar Google Scholar Articles by Pérez, J. Articles by Kelley, D. B. Search for Related Content PubMed PubMed Citation Articles by Pérez, J. Articles by Kelley, D. B.

 Previous Article  |  Next Article 

Volume 17, Number 19, Issue of October 1, 1997 pp. 7396-7403
Copyright ©1997 Society for Neuroscience

Androgen Mitigates Axotomy-Induced Decreases in Calbindin Expression in Motor Neurons

Received May 29, 1997; revised July 2, 1997; accepted July 21, 1997.

Julio Pérez and Darcy B. Kelley

Department of Biological Sciences, Columbia University, New York, New York 10027

Androgens can rescue axotomized motor neurons from cell death. Here we examine a possible mechanism for this trophic action in juvenile Xenopus laevis: regulation of a calcium-binding protein, calbindin, after axotomy. Western analysis revealed that a monoclonal antibody to calbindin D specifically recognizes a single ~28 kDa band in X. laevis CNS and rat cerebellum. Retrograde transport of peroxidase combined with immunohistochemistry demonstrated that somata, axons, and synaptic terminals of laryngeal motor neurons in nucleus (N.) IX-X of X. laevis are calbindin-positive. The number of calbindin-positive cells was compared in the intact and axotomized sides of N.IX-X of gonadectomized males that were either hormonally untreated or DHT-treated for 1 month. Although axotomy decreased the number of calbindin-positive cells by 86% in hormonally untreated males, the decrease was only 56% in DHT-treated animals. Compared with hormonally untreated animals, the number of calbindin-labeled cells in N.IX-X of DHT-treated males was increased in both the intact (14%) and axotomized sides (75%). We conclude that axotomy decreases and that DHT enhances calbindin immunoreactivity in N.IX-X. Axotomy-induced decrease in calbindin immunoreactivity precedes cell loss in N.IX-X and may impair the capacity of motor neurons to regulate cytoplasmic calcium. Androgen-mediated maintenance of calbindin expression is thus a candidate cellular mechanism for trophic maintenance of hormone target neurons.

Key words: dihydrotestosterone; motor neuron death; immunohistochemistry; calcium buffer; androgens; calbindin

This article has been cited by other articles:

				C. B. Huppenbauer, L. Tanzer, L. L. DonCarlos, and K. J. Jones Gonadal Steroid Attenuation of Developing Hamster Facial Motoneuron Loss by Axotomy: Equal Efficacy of Testosterone, Dihydrotestosterone, and 17-{beta} Estradiol J. Neurosci., April 20, 2005; 25(16): 4004 - 4013. [Abstract] [Full Text] [PDF]

				E. A. Brenowitz and K. Lent Afferent Input Is Necessary for Seasonal Growth and Maintenance of Adult Avian Song Control Circuits J. Neurosci., April 1, 2001; 21(7): 2320 - 2329. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help