Neonatal hormone manipulations and the maintenance of perineal muscles and their motor neurones in Albino Swiss rats

Currie, J. C.; Houston, Pamela A.; Henderson, Aubrien; Payne, A. P.

doi:10.1530/jrf.0.0890597

Cited by 6 publications

(2 citation statements)

References 21 publications

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“…By contrast, in the SNB, treatment of females with EB completely fails to alter cell number from the normal feminine pattern (Figure 1) (Breedlove et al, 1982;Breedlove, 1997). Similarly, SNB motoneuron number is not affected in males treated postnatally with the aromatase inhibitor 4-OH-androstenedione (Currie et al, 1990). The findings in Tfm rats, and the failure of estrogens to prevent SNB motoneuron death, suggests that the sparing of both the SNB and its target musculature specifically requires activation of the androgen receptor.…”

Section: Motoneuron Death and The Establishment Of Snb Cell Numbermentioning

confidence: 89%

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

Sengelaub

Forger

2008

Hormones and Behavior

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Cell number in the spinal nucleus of the bulbocavernosus (SNB) of rats was the first neural sex difference shown to differentiate under the control of androgens, acting via classical intracellular androgen receptors. SNB motoneurons reside in the lumbar spinal cord and innervate striated muscles involved in copulation, including the bulbocavernosus (BC) and levator ani (LA). SNB cells are much larger and more numerous in males than in females, and the BC/LA target muscles are reduced or absent in females. The relative simplicity of this neuromuscular system has allowed for considerable progress in pinpointing sites of hormone action, and identifying the cellular bases for androgenic effects. It is now clear that androgens act at virtually every level of the SNB system, in development and throughout adult life. In this review we focus on effects of androgens on developmental cell death of SNB motoneurons and BC/LA muscles; the establishment and maintenance of SNB motoneuron soma size and dendritic length; BC/LA muscle morphology and physiology; and behaviors controlled by the SNB system. We also describe new data on neurotherapeutic effects of androgens on SNB motoneurons after injury in adulthood.

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Section: Motoneuron Death and The Establishment Of Snb Cell Numbermentioning

confidence: 89%

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

Sengelaub

Forger

2008

Hormones and Behavior

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“…1). Similarly, SNB motoneuron number is not affected in males treated postnatally with the aromatase inhibitor 4-OH-androstenedione [24], indicating that conversion of testosterone to an estrogen is not necessary for the development of a masculine number of motoneurons in this system. The findings in Tfm rats, and the failure of estrogens to prevent SNB motoneuron death, suggests that the sparing of both the SNB and its target musculature specifically requires activation of the androgen receptor.…”

Section: Protection From Cell Death: Sexual Differentiationmentioning

confidence: 99%

Neuroprotective actions of androgens on motoneurons

Fargo

Foecking

Jones

et al. 2009

Frontiers in Neuroendocrinology

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Androgens have a variety of protective and therapeutic effects in both the central and peripheral nervous systems. Here we review these effects as they related specifically to spinal and cranial motoneurons. Early in development, androgens are critical for the formation of important neuromuscular sex differences, decreasing the magnitude of normally occurring cell death in select motoneuron populations. Throughout the lifespan, androgens also protect against motoneuron death caused by axonal injury. Surviving motoneurons also display regressive changes to their neurites as a result of both direct axonal injury and loss of neighboring motoneurons. Androgen treatment enhances the ability of motoneurons to recover from these regressive changes and regenerate both axons and dendrites, restoring normal neuromuscular function. Androgens exert these protective effects by acting through a variety of molecular pathways. Recent work has begun to examine how androgen treatment can interact with other treatment strategies in promoting recovery from motoneuron injury. Keywords motoneurons; androgens; axotomy; neuroprotection; cell death; sex differences; nerve regeneration; dendrites; testosterone; steroids From cellular and molecular perspectives, the consequences of gonadal steroid action in the nervous system include profound trophic effects on target neurons. During development, gonadal steroids are involved in the establishment of sex differences in neural structure and organization that underlie sex differences in behavior [122], promoting the differentiation of a masculine pattern of neural organization [3,111]. For example, androgens have been shown to exert a potent influence on the determination of sex differences in neuron number [116,

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Timing and duration of dihydrotestosterone treatment affect the development of motoneuron number and morphology in a sexually dimorphic rat spinal nucleus

Goldstein

Sengelaub

1992

J of Comparative Neurology

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The spinal nucleus of the bulbocavernosus (SNB) is a sexually dimorphic motor nucleus in the rat lumbar spinal cord. SNB motoneurons and their perineal target muscles are present in adult males, but reduced or absent in adult females. This dimorphism is due to the presence of androgens during development. Perinatal treatment of females with testosterone (T), or a combination of dihydrotestosterone (DHT) and estrogen (E+D females) from embryonic (E) day 16 through postnatal (P) day 5, results in a masculine number of SNB motoneurons and the retention of the target muscles. Perinatal treatment with estrogen alone does not masculinize the SNB; prenatal treatment with DHT alone from E17-E22 results in a feminine number of SNB motoneurons and a significantly altered motoneuron morphology and connectivity. To determine if masculinization of the SNB involves the interaction of estrogen and DHT or results from a longer exposure to DHT alone, the number, morphology, and connectivity of SNB motoneurons in females treated with DHT both pre- and post-natally (from E16-P5) were examined. At E22, DHTP (E16-P5) females have SNB motoneuron numbers identical to E+D and normal females, but far fewer than normal males, thus indicating that T is essential for prenatal masculinization. After E22, SNB motoneuron number declines precipitously in normal females but remains stable in DHTP (E16-P5) females and E+D females, which do not differ from normal males at P10. These results demonstrate that DHT can completely masculinize SNB motoneuron number without any synergistic actions with estrogen, and suggest that the development of SNB motoneuron number is strictly an androgen-mediated event. In adulthood, horseradish peroxidase histochemistry reveals that the connectivity, dendritic length, and soma size of SNB motoneurons in DHTP (E16-P5) females are identical to those of normal males but differ significantly from those of DHTP (E17-E22) females. These data suggest that the altered connectivity in DHTP (E17-E22) females is not simply a hormone-specific effect, but the result of a truncated hormone exposure. Thus, DHT can fully masculinize SNB morphology and connectivity if given during the appropriate period of development. It is suggested that while T may be required to masculinize the SNB prenatally, DHT may be involved in masculinizing postnatal aspects of SNB development.

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Neonatal hormone manipulations and the maintenance of perineal muscles and their motor neurones in Albino Swiss rats

Cited by 6 publications

References 21 publications

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

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

Neuroprotective actions of androgens on motoneurons

Timing and duration of dihydrotestosterone treatment affect the development of motoneuron number and morphology in a sexually dimorphic rat spinal nucleus

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