Sex kontakte

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Try out PMC Labs and tell us what you think. Learn More. Language: English Spanish French. Contrary to popular belief, sex hormones act throughout the entire brain of both males and females via both genomic and nongenomic receptors. Many neural and behavioral functions are affected by estrogens, including mood, cognitive function, blood pressure regulation, motor coordination, pain, and opioid sensitivity.

Subtle sex differences exist for many of these functions that are developmentally programmed by hormones and by not yet precisely defined genetic factors, including the mitochondrial genome. These sex differences, and responses to sex hormones in brain regions and upon functions not ly regarded as subject to such differences, indicate that we are entering a new era in our ability to understand and appreciate the diversity of gender-related behaviors and brain functions.

Realization that the brain is a target of sex hormones began with studies of reproductive hormone actions on the hypothalamus, regulating not only gonadotropin secretion and ovulation in females but also sex behavior. Then, the identification of cell nuclear hormone receptors in peripheral tissues 67 by use of tritiated 3 H steroid and iodinated thyroid hormones led to the demonstration by Don Pfaff, as well as Walter Stumpf, of similar receptor mechanisms in the hypothalamus and pituitary gland. Although the focus at the time was on sexual behavior, 110 there were other behaviors and neurological states that were known to be influenced by estrogens involving brain regions besides the hypothalamus, including fine motor control, pain mechanisms, seizure activity, mood, cognitive function, and neuroprotection.

A further serendipitous finding of nuclear estrogen receptors ERs in the hippocampus 13 also represented a turning point in the realization that not all steroid hormone actions occur via cell nuclear receptors, but rather operate via receptors in other parts of the cell through a variety of aling pathways Figure 1.

Long regarded as a rather static and unchanging organ, except for electrophysiological responsivity, such as long-term potentiation, 16 the brain has gradually been recognized as capable of undergoing rewiring after brain damage 17 and also able to grow and change, as seen by dendritic branching, angiogenesis, and glial cell proliferation during cumulated experience. In the original steroid autoradiography studies, a few scattered cells in hippocampus demonstrated strong cell nuclear labeling by 3 H estradiol in inhibitory intemeurons.

Thus, estradiol does not work alone in causing this synapse formation, and the study of underlying mechanisms is revealing some remarkable new aspects not only of hormone action, but also of neuronal plasticity. Paradoxically, male rats treated with aromatase inhibitors at birth, which inhibit defeminization of the brain by endogenous androgen sex kontakte conversion to estradiol, do respond to estradiol in adulthood with spine synapse induction. Furthermore, androgens are also able to induce spine synapses in the female rat hippocampus see ref 32 et al.

In the CA1 pyramidal neurons, nongenomic actions of estrogens via phosphatidylinositol 3 PI3 kinase promote actin polymerization and fllopodia outgrowth to form putative synaptic contacts by dendrites with presynaptic elements. Subsequent PI3 kinase sex kontakte via ERs stimulated translation of postsynaptic density protein 95 PSD in dendrites to provide a postsynaptic scaffold for spine synapse maturation.

It is important to note that the cofilin pathway is implicated in spinogenesis in the ventromedial hypothalamus that contributes to activating lordosis behavior. Curiously, the classical progestin receptor is not detectable in cell nuclei within the rat hippocampus, but it is expressed in non-nuclear sites in hippocampal neurons, and virtually all sex kontakte the detectable progestin receptor is estrogen inducible. The mechanism of progesterone action on synapse downregulation is presently unknown.

Besides hippocampus, other brain regions demonstrate estrogen-regulated spine synapse formation and turnover, 3237 including the prefrontal cortex PFC 38 and primary sensory-motor cortex. Developmentally programmed sex differences arise not only from secretion of sex hormones during sensitive periods in development but also through contributions of genes on Y and X chromosomes. In females, there is inactivation of one or the other X chromosome, 40 ; moreover, mitochondria derive from the mother, and mitochondrial genes make important contributions to brain and body functions.

Sex kontakte brain, there are few sexual dimorphisms, ie, complete differences between males and females. The sexually dimorphic nucleus of the preoptic area SDN-POA in the rodent brain comes close, 41 and Witelson has described an apparent sex dimorphism in the human brain. Parsch and Ellegren 46 suggested that sex-specific effects on reproduction drive the rapid evolution of sex-biased genes. Males and females adopt different sex kontakte to cope with environmental challenges. Indeed, the response to stress induces sex-specific effects on brain plasticity 364748 and activation of neuronal circuitry, 4950 as well as distinct behavioral phenotypes in males and females.

Transcriptional regulation helps explain the sex-dependent sensitivity to stressful stimuli and the associated risk of neuropsychiatric disorders in males versus females. The incidence of mood disorders is 1. A whole-brain transcriptome analysis showed that the gene expression difference between males and females changes over the lifetime and that the greatest expression divergence occurs during the perinatal and peripubertal periods.

They found that the transcriptomal difference between females with high and low ovarian hormone levels was greater than the difference between both female conditions and males. Thus, endogenous fluctuation of gonadal hormones may induce alternative gene networks within the same sex. In nucleus accumbens, male and female mice exposed to the same stressors display different transcriptional regulation, and the transcriptional phenotype of the nucleus accumbens predicts the increased behavioral susceptibility to stress in females versus males.

The stress-vulnerable CA3 neurons respond differentially to chronic stress in males and females. Moreover, we found that one episode of acute stress dramatically decreased the gene expression changes observed in unstressed female mice during endogenous fluctuation of estradiol levels see Figure 3. Thus, targeting discrete brain regions paves the way for novel insights into the molecular underpinnings sex kontakte hormonal actions and sex differences.

Sex differences emerge in many brain regions throughout the life course via both genetic and epigenetic mechanisms because of the widespread distribution of nongenomic, as well as genomic, forms of sex hormone receptors. Below, we present some examples, by no means exhaustive, to illustrate both the widespread nature of sex hormone influences but also the unexpectedly widespread nature of subtle sex differences.

Twenty-one days of chronic restraint stress CRS causes apical dendrites of CA3 neurons to retract; these changes do not occur after CRS in female rats. Female and male rats show opposite effects of chronic stress on hippocampal-dependent memory, with males showing impairment and females showing enhancement or no effect.

Exposure of male and female rats to restraint plus intermittent tail shock yields opposite effects on classical eyeblink conditioning, inhibiting it in females and enhancing it in males; in females, this effect is abolished by ovariectomy and is therefore estrogen dependent.

Neonatal masculinization of females makes them respond positively, like genetic males, to shock stressor. Females have a heightened sensitivity to stress 7071 and can show enhanced cognitive performance after stress, 72 which may contribute to their accelerated course of addiction. Sex differences in chronic stress effects on dendrite length and branching appear after puberty.

Stress in the pubertal transition causes qualitatively similar responses in males and females in hippocampus, PFC, and amygdala; however, after puberty, distinct sex differences in response to chronic stress become evident. CRS for 21 days causes neurons in the medial PFC of the male rat to show dendritic debranching and shrinkage. However, neurons that project to the sex kontakte from the medial PFC undergo sex kontakte expansion in females but not in males; this expansion in the female is estrogen-dependent, evidenced by ovariectomized females not showing such changes.

Estradiol stimulates dopamine release independently of nuclear ERs. The cerebellum is responsive to estrogens, generates both estradiol and progesterone during its development, and in humans is implicated in disorders that show sex differences. Morphine is less potent in alleviating pain in women than in men. Assessments of empathy in male and female volunteers, in which both sexes perform equally well on three separate tests, reveal different brain regional patterns of activation as seen by functional magnetic resonance imaging fMRI.

Estradiol protects neurons from excitotoxic damage due to seizures and stroke, as sex kontakte as in Alzheimer disease. Investigation of the ability of estrogens to protect against stroke damage, as well as Alzheimer and Parkinson disease, has demonstrated that the brain is capable of locally generating estrogens either from androgens or possibly directly from cholesterol. Estrogen actions have also illuminated the aging process insofar as they have revealed the progressive loss of plasticity and hormone responsiveness, which is not necessarily irreversible.

In contrast to estrogen modulation of synaptic plasticity in young female rats, estrogen treatment failed to increase synapse density in CA1 of aged ovariectomized rats. In young, but not aged, ovariectomized rats, estrogen rescues the learning deficits associated with experimentally induced cholinergic impairment. The nonhuman primate model has provided the best insights into the aging effects on the PFC, which is important for working memory and self-regulation. In contrast, there was an estrogen-induced spinogenesis in the aged cohort, which occurred against the background of an age-related reduction in spine density of the aged vehicle- treated group.

Thus, the vulnerability to cognitive decline in the aged vehicle-treated group is explained by both an age-induced loss of spines on top of an estrogen deficiency-induced loss of spines. Because spine size is highly correlated with both synapse size as well as glutamate receptor37 it was noteworthy that estrogen shifts the distribution of spine-head diameter toward smaller size in both the young and aged animals, but aging dramatically reduced the representation of spines with small he and long necks.

When estrogen replacement is provided to the aged animals, their cognitive performance matches the performance of young animals in spite of having an overall smaller spine density than the young estrogen-treated animals. This could indicate that a modest increase in small spines goes a long way in providing neurobiological resilience.

Another finding from the infrahuman primate model is that surgical menopause impairs cognitive function in a manner that is ameliorated by estrogen treatment. In contrast, accuracy correlated inversely with the frequency of boutons containing donut-shaped mitochondria, and those terminals exhibited smaller active zone areas and fewer docked synaptic sex kontakte than those with straight or curved mitochondria.

Estrogen administration ameliorated cognitive performance deficits and reduced the s of donut-shaped mitochondria, suggesting that hormone therapy may benefit cognitive aging, in part by promoting mitochondrial and synaptic health in the PFC and possibly in other parts of the brain. The origins of sex differences in the brain and behavior depend not only on developmentally programmed secretion of hormones during sensitive periods of early life but also on genes and sex chromosomes, as well as mitochondria from the mother.

Knowing that the entire brain is affected by sex hormones with subtle sex differences, we are entering a new era in our ability to understand and appreciate the diversity of genderrelated behaviors and brain functions.

National Center for Biotechnology InformationU. Journal List Dialogues Clin Neurosci v. Dialogues Clin Neurosci. Bruce S. Author information Copyright and information Disclaimer. This article has been cited by other articles in PMC. Abstract Contrary to popular belief, sex hormones act throughout the entire brain of both males and females via both genomic and nongenomic receptors.

Keywords: agingandrogendepressionepigeneticsestradiolhippocampusmemoryprefrontal cortexprogesteronestructural plasticitysynapse formation. Introduction Realization that the brain is a target of sex hormones began with studies of reproductive hormone actions on the hypothalamus, regulating not only gonadotropin secretion and ovulation in females but also sex behavior. Open in a separate window. Figure 1. Steroid hormones are now known to act via genomic and nongenomic receptors. In many cases, the same receptor molecule has different functions in the nucleus and non-nuclear sites in the cell.

Plasticity of the adult brain Long regarded as a rather static and unchanging organ, except for electrophysiological responsivity, such as long-term potentiation, 16 the brain has gradually been sex kontakte as capable of undergoing rewiring after brain damage 17 and also able to grow sex kontakte change, as seen by dendritic branching, angiogenesis, and glial cell proliferation during cumulated experience. Sex hormone actions beyond the hypothalamus Hippocampus In the original steroid autoradiography studies, a few scattered cells in hippocampus demonstrated strong cell nuclear labeling by 3 H estradiol in inhibitory intemeurons.

Figure 2. The discovery of estrogen actions on synapse formation in hippocampus via both genomic and nongenomic mechanisms has opened the way to understanding actions of estrogens and other steroid hormones throughout the brain, where nuclear steroid hormone receptors are not evident.

J Endocrinol. Estrogen actions throughout the brain Besides hippocampus, other brain regions demonstrate estrogen-regulated spine synapse formation and turnover, 3237 including the prefrontal cortex PFC 38 and primary sensory-motor cortex. Developmental programming of sex differences Mechanisms Developmentally programmed sex differences arise not only from secretion of sex hormones during sensitive periods in development but also through contributions of genes on Y and X chromosomes.

Epigenetic regulation of gene expression Parsch and Ellegren 46 suggested that sex-specific effects on reproduction drive the rapid evolution of sex-biased genes. Epigenetics, brain-derived neurotrophic factor, and mental illness The incidence of mood disorders is 1.

Patterns of gene regulation A whole-brain transcriptome analysis showed that the gene expression difference between males and females changes over the lifetime and that the greatest expression divergence occurs during the perinatal and peripubertal periods. Figure 3.

Acute stress induces more genes in females pink than in males blue. The overlap purple represents the of genes commonly changed in males and females. B Venn diagram illustrating the of genes altered during endogenous fluctuation of estradiol levels high estradiol [proestrus] vs low estradiol [diestrus] in CA3 pyramidal neurons of female BAG-TRAP mice. Acute stress green dramatically decreases the estradiol-biased genes observed in unstressed mice orange.

The overlap brown represents the of genes commonly changed in unstressed and acutely stressed females. BAC-TRAP, bacterial artificial chromosome transgenic mouse; down arrow, downregulated genes; up arrow, upregulated genes.

Sex differences throughout the brain Sex differences emerge in many brain regions throughout the life sex kontakte via both genetic and epigenetic mechanisms because of the widespread distribution of nongenomic, as well as genomic, forms of sex hormone receptors. Hippocampus response to stressors Dendrite remodeling Twenty-one days of chronic restraint stress CRS causes apical dendrites of CA3 neurons to retract; these changes do not occur after CRS in female rats.

Spatial memory Female and male rats show opposite effects of chronic stress on hippocampal-dependent memory, with males showing impairment and females showing enhancement or no effect. Classical conditioning Exposure of male and female rats to restraint plus intermittent tail shock yields opposite effects on classical eyeblink conditioning, inhibiting it in females and enhancing it in males; in females, this effect is abolished by ovariectomy and is therefore estrogen dependent. Neonatal masculinization Neonatal masculinization of females makes them respond positively, like genetic males, to shock stressor.

Opioids Females have a heightened sensitivity to stress 7071 and can show enhanced cognitive performance after stress, 72 which may contribute to their accelerated course of addiction. Sex differences in prefrontal cortex CRS for 21 days causes neurons in the medial PFC of the male rat to show dendritic debranching and shrinkage. Dopaminergic systems Estradiol stimulates dopamine release independently of nuclear ERs. Sex differences in cerebellum The cerebellum is responsive to estrogens, generates both estradiol and progesterone during its development, and in humans is implicated in disorders that show sex differences.

Sex differences in pain sensitivity and circuitry Morphine is less potent in alleviating pain in women than in men. Empathy Assessments of empathy in male and female volunteers, in which both sexes perform equally well on three separate tests, reveal different brain regional patterns of activation as seen by functional magnetic resonance imaging fMRI. Neuroprotection Estradiol protects neurons from excitotoxic damage due to seizures and stroke, as well as in Alzheimer disease.

Estrogen and the aging hippocampus and prefrontal cortex Estrogen actions have also illuminated the aging process insofar as they have revealed the progressive loss of plasticity and hormone responsiveness, which is not necessarily irreversible. Hippocampus In contrast to estrogen modulation of synaptic plasticity in young female rats, estrogen treatment failed to increase synapse density in CA1 of aged ovariectomized rats.

Prefrontal cortex The nonhuman primate model has provided the best insights into the sex kontakte effects on the PFC, which is important for working memory and self-regulation. Conclusion The origins of sex differences in the brain and behavior depend not only on developmentally programmed secretion of hormones during sensitive periods of early life but also on genes and sex chromosomes, as well as mitochondria from the mother. Notes Conflict of Interest: The authors declare no conflict of interest.

Young WC. Hormones and sexual behavior. Harris GW. Sex kontakte stimulation of the hypothalamus and the mechanism of neural control of the adenohypophysis. J Physiol. Meites J. Short history of neuroendocrinology and the International Society of Neuroendocrinology.

Schally AV.

Sex kontakte

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