Ovariectomy attenuates dendritic growth in hormone‐sensitive spinal motoneurons

Abstract

The lumbar spinal cord of rats contains the sexually dimorphic, steroid-sensitive spinal nucleus of the bulbocavernosus (SNB). Dendritic development of SNB motoneurons in male rats is biphasic, initially showing exuberant growth through 4 weeks of age followed by a retraction to mature lengths by 7 weeks of age. The initial growth is steroid dependent, attenuated by castration or aromatase inhibition, and supported by hormone replacement. Dendritic retraction is also steroid sensitive and can be prevented by testosterone treatment, but is unaffected by aromatase inhibition. Together, these results suggest a role for estrogens during the initial growth phase of SNB development. In this study, we tested whether ovarian hormones could support SNB somal and dendritic development. Motoneuron morphology was assessed in normal males and in females perinatally masculinized with dihydrotestosterone and then either ovariectomized or left intact. SNB motoneurons were retrogradely labeled with cholera toxin-HRP at 4 or 7 weeks of age and reconstructed in three dimensions. Initial growth of SNB dendrites was reduced after ovariectomy in masculinized females. However, no differences in dendritic length were seen at 7 weeks of age between intact and ovariectomized masculinized females, and lengths in both groups were significantly lower than those of normal males. Together with previous findings, these results suggest that estrogens are involved in the early growth of SNB dendrites, but not in their subsequent retraction.

The spinal nucleus of the bulbocavernosus: Firsts in androgen-dependent neural sex differences

“…As described above, females masculinized by perinatal DHT treatment retain their SNB motoneurons and target musculature. Ovarian hormones support SNB dendritic growth in these females, because at P28, SNB dendritic length in intact females is significantly greater than that of ovariectomized females (Hebbeler et al, 2001).…”

“…Local blockade of estrogen receptors at the BC muscle of gonadally intact males results in severely reduced dendritic lengths similar to those seen in castrates, whereas local administration of estradiol to the BC muscle of castrated males supports dendritic growth. This estrogenic influence is limited to the early postnatal period: the morphology of SNB motoneurons is insensitive to estrogens after 4 weeks of age (Goldstein and Sengelaub, 1994;Hebbeler et al, 2001;Warren and Sengelaub, 2002) or in adulthood (Forger et al, 1992;Fargo and Sengelaub, 2007). The transient influence of estrogens on SNB dendritic growth is coincident with a period in which high levels of NMDA receptors are expressed in the spinal cord, and locally in the SNB nucleus (Verhovshek et al, 2005).…”

Testosterone manipulation protects motoneurons from dendritic atrophy after contralateral motoneuron depletion

“…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 and 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, , 2002, changes in dendritic interactions , and changes in afferent input (Kalb, 1994;Hebbeler et al, 2002).…”

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

“…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).…”