Correlation Between Circulating Adult Gonadal Steroids Essay

Correlation Between Circulating Adult Gonadal Steroids Essay

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Our studies will focus on interactions between circulating adult gonadal steroids (i.e., testosterone, estrogen) and neurotrophin-Trk (tyrosine receptor kinase), particularly Brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B T1 (TrkB T1) influences on adult sex behavior. Neurotrophin-Trk signaling is essential for mammal health. Numerous amounts of evidence suggest that the expression of neurotrophin-Trk and splice variant signaling regulates synaptic plasticity, neuronal and nonneuronal cells survival and differentiation (1-6). In humans and rodents, it has profound impact on reproduction (5). In addition, sex steroids are crucial for human and rodent’s health maintenance and survival. For instance, the level of gonadal steroid reduces with age particularly in women during menopause or post- oophorectomy (removal of ovaries). Studies in rodents correlating with humans demonstrates the removal of gonads reduces circulating gonadal steroids and affects sexual motivation and daily life activities. While reintroducing hormones via injection, patch or oral ingestion systematically raises the level of hormones to a normal baseline. Despite these findings, there are limited data on how adult sex hormones influences neurotrophin-Trk signaling and sex behavior. My lab is interested in the mechanism by which differential expression of testosterone, BDNF, and its receptor TrkB T1 causes differing mating behaviors in males and females. Thus, this is a novel study that will examine if Trkb T1 acts as a molecular break that inhibits male sex behaviors within females. And if removing this break will in turn reveal male sex behaviors in females.

This proposal underline three specific aims.
First,to determine the effect ...


... middle of paper ...


...d male-typical mating behavior.

Another factor that might be involved in the sex difference in testosterone’s effects on neural plasticity and behavior is TrkB(T1), a highly expressed isoform of TrkB, that lacks the kinase binding intracellular domain and absorbs BDNF inhibiting its function (1,2). It is possible that high levels of TrkB (T1) in the female inhibit the actions of testosterone on synaptic plasticity and thereby establishes the sex differences in the brain and behavior. There is precedence for this mechanism in the mammary gland. Dimorphisms in the development of the mammary gland are mediated by androgen actions on TrkB (T1) (5). T1 is present in the male mammary gland due to circulating androgens and absent in the female (5). TrkB (T1) in the male prevents BNDF from attracting axons to the gland, creating a degenerate mammary gland in the males (5).

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