Androgen regulation of dendritic growth and retraction in the development of a sexually dimorphic spinal nucleus

Abstract

The spinal nucleus of the bulbocavernosus (SNB) is a sexually dimorphic group of motoneurons whose development and maintenance are under androgenic control. Exposure to androgens early in development permanently alters SNB motoneuron number and soma size; in adulthood, androgens regulate dendritic and synaptic architecture. The present set of experiments investigates the influence of androgens on the development of SNB dendritic morphology. In normal males, SNB dendritic growth is biphasic, reaching exuberant lengths by the fourth postnatal week and then retracting to adult lengths by 7 weeks of age. This dendritic growth is androgen dependent--males castrated on postnatal day (P) 7 and given daily injections of testosterone propionate (TP) had exuberant dendritic lengths similar to those of normal males; dendritic length in oil-treated males remained at P7 levels. The early exuberant dendritic length was retained in TP-treated males through P49. The retraction of SNB dendrites after P28 is also influenced by androgens. Males castrated at P28 and given testosterone implants retained exuberant dendritic length at P49; blank-implanted males had significantly shorter dendritic lengths by P70. These results suggest that androgens are necessary for the early exuberant growth of SNB dendrites. Furthermore, the subsequent retraction of SNB dendrites may be halted when testosterone titers reach a critical level during puberty, stabilizing their adult length.

Androgenic, but not estrogenic, protection of motoneurons from somal and dendritic atrophy induced by the death of neighboring motoneurons

“…BHRP labeling permits population-level quantitative analysis of motoneuron somal and dendritic morphologies (Kurz et al, 1986;Goldstein et al, 1990). Animals were anesthetized with ether, and the left BC muscle was exposed and injected with 0.5 μL of a 0.2% solution of BHRP.…”

“…Animals were anesthetized with ether, and the left BC muscle was exposed and injected with 0.5 μL of a 0.2% solution of BHRP. Two days after BHRP injection, a period that ensures optimal labeling of SNB motoneurons (Kurz et al, 1986;Goldstein et al, 1990), animals were weighed, overdosed with urethane (approximately 0.25 g/100 g body weight), and perfused intracardially with saline followed by cold fixative (1% paraformaldehyde/1.25% glutaraldehyde). The BC/LA muscle complex was removed from each animal, bisected along the midline, and each side was weighed.…”

“…Average dendritic length per labeled motoneuron was estimated by summing the measured dendritic lengths of the series of sections, multiplying by two to correct for sampling, then dividing by the total number of labeled motoneurons in that series. This method does not attempt to assess the actual total dendritic length of labeled motoneurons (Kurz et al, 1991), but has been shown to be a sensitive and reliable indicator of changes in dendritic morphology in normal development (Goldstein et al, 1990, in response to hormonal manipulation (Kurz et al, 1986(Kurz et al, , 1991Forger and Breedlove, 1987;Goldstein et al, 1990;Sengelaub, 1993, 1994;Burke et al, 1997Burke et al, , 1999Hebbeler et al, 2001Hebbeler et al, , 2002Hebbeler and Sengelaub, 2003), after changes in dendritic interactions and afferent input (Kalb, 1994;Hebbeler et al, 2002;Hebbeler and Sengelaub, 2003), and after the death of nearby motoneurons (Fargo and Sengelaub, 2004a,b).…”

Inhibition of Cytosolic Phospholipase A2Has Neuroprotective Effects on Motoneuron and Muscle Atrophy after Spinal Cord Injury

“…BHRP labeling permits populationlevel quantitative analysis of motoneuron somal and dendritic morphologies 24,25 . Forty-eight hours after BHRP injection, a period that ensures optimal labeling of motoneurons 24,25 , animals were weighed and received a lethal dose of Nembutal (60 mg/kg, i.p. ), and were then perfused intracardially with saline followed by cold fixative (1% paraformaldehyde/1.25% glutaraldehyde).…”

“…normal development 24,33,34 , after changes in dendritic interactions 33 and afferent input [35][36][37] , and after injury 6,[21][22][23]38 .…”