MOTONEURON DEVELOPMENT AFTER DEAFFERENTATION .2. DORSAL RHIZOTOMY DOES NOT BLOCK ESTROGEN-SUPPORTED GROWTH IN THE DORSOLATERAL NUCLEUS (DLN)

Citation
Tc. Hays et al., MOTONEURON DEVELOPMENT AFTER DEAFFERENTATION .2. DORSAL RHIZOTOMY DOES NOT BLOCK ESTROGEN-SUPPORTED GROWTH IN THE DORSOLATERAL NUCLEUS (DLN), Developmental brain research, 91(1), 1996, pp. 20-28
Citations number
69
Categorie Soggetti
Neurosciences
ISSN journal
01653806
Volume
91
Issue
1
Year of publication
1996
Pages
20 - 28
Database
ISI
SICI code
0165-3806(1996)91:1<20:MDAD.D>2.0.ZU;2-2
Abstract
The lumbar spinal cord of the rat contains two sexually dimorphic moto r nuclei, the spinal nucleus of the bulbocavernosus (SNB) and the dors olateral nucleus (DLN). Postnatally, SNB and DLN motoneurons grow subs tantially and reach their adult morphology by 7 weeks of age. The masc ulinization of SNB and DLN motoneuron dendrites depends upon steroid h ormones. After early castration, the growth of SNB and DLN dendrites i s markedly attenuated, but testosterone replacement restores this grow th. In the SNB, initial dendritic growth is also supported in castrate s treated with estrogen. By using castration and hormone replacement t echniques, we examined the development of DLN motoneuron morphology in estrogen-treated castrated rats to determine if estrogen also support s the growth of DLN motoneurons. In addition, given that dorsal root g anglia may be a site of estrogen action, we tested the hypothesis that estrogen acts at primary afferents to support DLN dendritic growth. T hus, we attempted to block the potential trophic effect of estrogen by performing unilateral dorsal rhizotomies in estrogen-treated castrate s. DLN motoneuron morphology was analyzed at 4 and 7 weeks of age by u sing cholera toxin horseradish peroxidase (BHRP) histochemistry. As fo und for SNB motoneurons, estrogen treatment transiently supported deve lopment. DLN motoneurons in estrogen-treated castrates developed norma lly through 4 weeks of age, but by 7 weeks, DLN motoneuron morphology in estrogen-treated castrates was no longer different from that in oil -treated castrates. Moreover, deafferentation via unilateral dorsal rh izotomy did not inhibit estrogen's ability to masculinize the early de velopment of DLN motoneurons. Thus, the trophic effect of estrogen did not appear to act via the dorsal root ganglia to support the early po stnatal development of DLN motoneurons.