Critical period for estrogen-dependent motoneuron dendrite growth is coincident with ERα expression in target musculature.
The spinal cord of rats contains the sexually dimorphic, steroid-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB). In males, SNB dendrite growth is dependent on gonadal steroids: dendrite growth is inhibited after castration, but supported in androgen- or estrogen-treated castrated males. Furthermore, estrogenic support of SNB dendrite growth is mediated by estrogen action at the target musculature, inhibited by estrogen receptor (ER) blockade at the muscle and supported by local estradiol treatment. However, this estrogenic support is restricted to the early postnatal period, after which the morphology of SNB dendrites is insensitive to estrogens. To test if the developmentally restricted effects of estrogens on SNB dendrite growth coincide with the transient expression of ER in the target musculature, ERα expression was assessed during development and in adulthood. ERα expression in extra-Muscle fiber cells was greatest from postnatal day 7 (P7) to P14 and declined after P21. Because this pattern of ERα expression coincided with the period of estrogen-dependent dendrite growth, we tested if limiting hormone exposure to the period of maximal ERα expression in extra-muscle fiber cells could fully support estrogen-dependent SNB dendrite growth. We restricted estradiol treatment in castrated males from P7 to P21 and assessed SNB dendritic morphology at P28. Treating castrates with estradiol implants at the muscle from P7 to P21 supported dendrite growth to normal levels through P28. These data suggest that the transient ERα expression in target muscle could potentially define the critical period for estrogen-dependent dendrite growth in SNB motoneurons.
Department of Psychological and Brain Sciences and Program in Neuroscience, Indiana University, Bloomington, IN 47405, USA.
Lauren M
LM
Rudolph
Dale R
DR
Sengelaub
D000367:Age Factors; D000818:Animals; D002369:Castration; D002772:Cholera Toxin / Q000378:metabolism; D003423:Critical Period, Psychological; D003712:Dendrites / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D004958:Estradiol / Q000378:metabolism* / Q000494:pharmacology; D047628:Estrogen Receptor alpha / Q000378:metabolism*; D004967:Estrogens / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects*; D006735:Horseradish Peroxidase / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009046:Motor Neurons / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012727:Sex Characteristics; D013116:Spinal Cord / Q000166:cytology / Q000254:growth & development
D047628:Estrogen Receptor alpha; D004967:Estrogens; C052635:cholera toxin, B subunit-horseradish peroxidase; D004958:Estradiol; D002772:Cholera Toxin; D006735:Horseradish Peroxidase