Hormonal control of neuron number in sexually dimorphic spinal nuclei of the rat: II. Development of the spinal nucleus of the bulbocavernosus in androgen-insensitive (Tfm) rats.
Hormonal control of neuron number in sexually dimorphic spinal nuclei of the rat: II. Development of the spinal nucleus of the bulbocavernosus in androgen-insensitive (Tfm) rats.
复制标题
大鼠性二形性脊髓核中神经元数量的激素控制：II。
DOI：
10.1002/cne.902800412
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Arnold,AP
中科院分区：
文献类型：
--
作者：
Sengelaub,DR;Jordan,CL;Kurz,EM;Arnold,AP
The spinal nucleus of the bulbocavernosus (SNB) is a sexually dimorphic motor nucleus whose development is under the control of steroid hormones. The SNB contains many more motoneurons in adult male rats than in females, and this sex difference is produced by a sexually dimorphic motoneuron death which is regulated by androgens. To study further the role of androgens in the development of sex differences in SNB motoneuron number, we examined SNB development in males with the testicular feminization mutation (Tfm) which renders them insensitive to androgens.Counts of SNB motoneurons perinatally revealed that SNB development in normal male and female King‐Holtzman rats was similar to that reported previously for Sprague‐Dawley rats; SNB motoneuron number increased from initially low levels at embryonic day 18 through the day before birth, when motoneuron numbers in both sexes were substantially higher than adult levels. After this prenatal increase, motoneuron number declined in both sexes, until by postnatal day 10 motoneuron numbers were in their adult ranges and the sex difference was fully expressed. Females lost more motoneurons than did males during this period, and this loss was due to motoneuron death as revealed by counts of degenerating cells.SNB development in King‐HoltzmanTfmmales was similar to that of normal males through embryonic day 20, suggesting that androgens may not be necessary for the initial increase in motoneuron numbers in the SNB. Thereafter, SNB motoneuron numbers inTfmmales declined in a female‐typical fashion;Tfmmales and normal females did not differ at any postnatal age. The incidence of degenerating cells inTfmmales over this period was like that of normal females and significantly higher than that of normal males. These results indicate that just as treatment of females with androgens during development attenuates cell death in the SNB to male‐typical levels, resulting in masculine motoneuron numbers, theTfmmale's insensitivity to androgens results in a female‐typical cell death resulting in feminine SNB motoneuron numbers.
