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Testosterone is a steroid sex hormone with an important role in the physiology in both sexes. It is involved in the development of morphological and functional parameters of the body via multiple molecular mechanisms. Intensive research focused on testosterone reveals associations with cognitive abilities and behavior and its causative role in sex differences in cognition. Testosterone modulates brain structure and the differentiation of neurons during intrauterine development with profound effects on brain functions during postnatal life. In this review we summarize the effects of testosterone on brain physiology and cognition with respect to the underlying molecular mechanisms.
The extraordinary giftedness is apparently a unique manifestation of a mutual interconnection between genes and environment. One of the possible etiological factors of intellectual giftedness is testosterone which is believed to affect the brain organization and function. The aim of our study was to analyze associations between 2D:4D digit ratio (a proxy of prenatal testosterone) and/or salivary testosterone levels with non-verbal IQ in intellectually gifted girls. Fifty-one girls with an age range of 10 to18 years and IQ scores higher than 130 were tested. Saliva samples were collected to obtain levels of salivary testosterone. 2D:4D digit ratio was measured on both hands as an indicator of prenatal testosterone. IQ parameters were assessed employing standardized set of tests. The CAG repeat polymorphism in exon 1 of the androgen receptor gene was analyzed to assess the sensitivity of androgen receptor. Testing of between-subjects effects proved significant interactions between right and left 2D:4D ratio, genetic variability in androgen receptor, and also salivary testosterone level with non-verbal IQ in gifted girls. Our results point out that the variability in parameters of androgenicity contributes to the variability of nonverbal IQ in gifted girls. However, the exact molecular mechanism of how testosterone acts on the brain and affects this cognitive domain remains still unclear.
Steroid hormones may act through a rapid mechanism that does not require an intracellular steroid receptor and its effects on gene expression. In this study we have analysed this so-called non-genomic effect of testosterone on social anxiety in rats of both sexes using androgen and oestrogen receptor blockers. Male rats were divided into four groups: SHAM-CTRL (a sham operated group treated with oil as vehicle, n=10), SHAM-TST (a sham operated group treated with testosterone at a dose of 1 mg/kg, n=10), GDX-CTRL (a castrated group treated with oil, n=10) and GDX-TST (a castrated group treated with testosterone at a dose of 1 mg/kg, n=10). Female rats were divided into two groups: OVX-CTRL (an ovariectomized group treated with oil, n=10) and OVX-TST (an ovariectomized group treated with testosterone, n=10). The intracellular androgen receptor was blocked with flutamide and both intracellular oestrogen receptors were blocked with tamoxifen (a selective oestrogen receptor modulator). Rats were tested one hour after oil or testosterone administration in the social interaction test. Although the concentration of testosterone was higher in testosterone groups, no significant difference in social interaction was observed between the groups. In summary, in this first study focusing on the non-genomic effects of testosterone on social interaction no rapid effects of testosterone in adult rats were found. Further studies should analyse potential nongenomic effects of testosterone on other forms of social behaviour.
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