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Showing papers by "Jiang-Ning Zhou published in 2000"


Journal ArticleDOI
TL;DR: The present findings of somatostatin neuronal sex differences in the BSTc and its sex reversal in the transsexual brain clearly support the paradigm that in transsexuals sexual differentiation of the brain and genitals may go into opposite directions and point to a neurobiological basis of gender identity disorder.
Abstract: Transsexuals experience themselves as being of the opposite sex, despite having the biological characteristics of one sex. A crucial question resulting from a previous brain study in male-to-female transsexuals was whether the reported difference according to gender identity in the central part of the bed nucleus of the stria terminalis (BSTc) was based on a neuronal difference in the BSTc itself or just a reflection of a difference in vasoactive intestinal polypeptide innervation from the amygdala, which was used as a marker. Therefore, we determined in 42 subjects the number of somatostatin-expressing neurons in the BSTc in relation to sex, sexual orientation, gender identity, and past or present hormonal status. Regardless of sexual orientation, men had almost twice as many somatostatin neurons as women (P < 0.006). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of the females (P = 0.83). In contrast, the neuron number of a female-to-male transsexual was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood did not seem to have influenced BSTc neuron numbers. The present findings of somatostatin neuronal sex differences in the BSTc and its sex reversal in the transsexual brain clearly support the paradigm that in transsexuals sexual differentiation of the brain and genitals may go into opposite directions and point to a neurobiological basis of gender identity disorder.

400 citations


Journal ArticleDOI
TL;DR: In this paper, the expression of vasopressin (AVP) mRNA in the human suprachiasmatic nucleus (SCN) was investigated and it was shown that the amount of AVP mRNA expressed as masked silver grains in the SCN was 3 times lower in AD patients than in age-and time-of-death-matched controls.
Abstract: Circadian rhythm disturbances are frequently present in Alzheimer disease (AD). In the present study, we investigated the expression of vasopressin (AVP) mRNA in the human suprachiasmatic nucleus (SCN). The in situ hybridization procedure on formalin-fixed paraffin-embedded material was improved to such a degree that we could, for the first time, visualize AVP mRNA expressing neurons in the human SCN and carry out quantitative measurements. The total amount of AVP mRNA expressed as masked silver grains in the SCN was 3 times lower in AD patients (n = 14; 2,135 +/- 597 microm2) than in age- and time-of-death-matched controls (n = 11; 6,667 +/- 1466 microm2) (p = 0.003). No significant difference was found in the amount of AVP mRNA between AD patients with depression (n = 7) and without depression (n = 7) (2,985 +/-1103 microm2 and 1,285 +/- 298 microm2, respectively; p = 0.38). In addition, the human SCN AVP mRNA expressing neurons showed a marked day-night difference in controls under 80 years of age. The amount of AVP mRNA was more than 3 times higher during the daytime (9,028 +/- 1709 microm2, n = 7) than at night (2,536 +/- 740 microm2, n = 4; p = 0.02), whereas no clear diurnal rhythm of AVP mRNA in the SCN was observed in AD patients. There was no relationship between the amount of AVP mRNA in the SCN and age at onset of dementia, duration of AD and the neuropathological changes in the cerebral cortex. These findings suggest that the neurobiological basis of the circadian rhythm disturbances that are responsible for behavioral rhythm disorders is located in the SCN. It also explains the beneficial effects of light therapy on nightly restlessness in AD patients.

146 citations


Book ChapterDOI
TL;DR: Hypofrontality and hyperactivity of the HPA-axis reinforce each other's actions in the development of the signs and symptoms of depression.
Abstract: Publisher Summary Hypothalamo-pituitary adrenal (HPA)-axis hyperactivity leads to increased production of corticotrophin-releasing hormone (CRH) and cortisol; the central effects of these hormones form the final common pathway in the pathogenesis of symptoms of depression. HPAaxis activity may not only be caused by glucocorticoid receptor resistance, developmental sequelae or stress in adulthood, but also by stroke, especially if the left prefrontal cortex is affected. Transcranial cortical stimulation seems to be an effective new treatment for depression. HPA hyperactivity leads, in addition, to a decreased frontal metabolism, probably due to the inhibiting effect of glucocorticoids on the brain metabolism. The hyperactivity of the HPA axis may also explain at least part of the changes in the HPT-axis and contribute to decreased bioavailability of T3 in the brain. Hypofrontality and hyperactivity of the HPA-axis reinforce each other's actions in the development of the signs and symptoms of depression.

73 citations


01 Jan 2000
TL;DR: The finding of SOM neuronal sex Differences in the BSTc and the sex reversal of these differences in the brains of gender dysphoric individuals, clearly supports the paradigm that in these individuals, the sex differentiation of the brain and the genitals may go in opposite directions.
Abstract: This study followed one similar piece of research on much of the same brain material, and was thus only the second of its kind to be done on human brains. The research team focussed on a part of the brain understood to be sexually dimorphic, the central subdivision of the bed-nucleus of the stria terminalis [BSTc]. The main neuron population of the BSTc is somatostatin-expressing [SOM] neurons.* The team sought to determine the number of SOM neurons in the BSTc [only those with visible nucleolus were counted], in relation to sex, sexual orientation, gender identity and past or present hormonal status. 42 human brains were collected in total: eight [8] gender dysphoric individuals, six [6] of whom were male-to-female individuals ( MtF, transwomen) and had undergone transition, including hormone treatment and surgery, one [1] male-to-female individual who had undergone no treatment whatever, but who had always strongly identified as female, and one [1] female-to-male individual (FtM, transman). The control group of 34 individuals included: nine [9] homosexual men, nine [9] heterosexual men, ten [10] presumed heterosexual women, three [3] women with hormone disorders, three [3] men with hormone disorders. The findings indicated that, regardless of sexual orientation, men had almost twice as many SOM neurons as women (P< 0.006). The number of SOM neurons in the BSTc of the transwomen [MtF] was similar to the other women (P= 0.83). In contrast, the neuron number of a transman [FtM] was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood seemed to have no impact on BSTc neuron numbers. The relative volumes of the BSTc were also measured. All of the men, regardless of sexual orientation, had volumes which were similar; the women and the transwomen [MtF] had similar volumes; the transman [FtM] fell into the same range as the other men. The volumes of all men versus all women and transwomen [MtF] were statistically highly significant (P< 0.01) No statistical differences were found for age, post-mortem time, fixation time, storage time or cause of death, nor were any differences found between early, rather than late, recognition of gender dysphoria/transsexualism. The effects of variations in levels of estrogen, testosterone, antiandrogen treatments and orchidectomy were also tested and appeared to have no effect on the BSTc. The finding of SOM neuronal sex differences in the BSTc and the sex reversal of these differences in the brains of gender dysphoric individuals, clearly supports the paradigm that in these individuals, the sex differentiation of the brain and the genitals may go in opposite directions. This points to a neurobiological basis, established during early development, for the condition of gender dysphoria.

2 citations