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According this view, the lateral hypothalamus is "a unique arbitrator of learning capable of shifting behavior toward or away from important events". Lesions in this nucleus abolish passive defensive behavior, like freezing and the "on-the-back" posture. Moreover, the premammillary nucleus also is mobilized, the dorsomedial part but not the ventrolateral part. Fos-labeled cell analysis showed that the PMDvl is the most activated structure in the hypothalamus, and inactivation with muscimol prior to exposure to the context abolishes the defensive behavior. The medial zone of hypothalamus is part of a circuitry that controls motivated behaviors, like defensive behaviors. Further lesion of the lateral part of the ventromedial nucleus in the same animal produces complete cessation of food intake. Bilateral lesion of the medial part of the ventromedial nucleus causes hyperphagia and obesity of the animal.
The most obvious is the sex-determining region Y (SRY) gene on the Y chromosome, which codes the testis-determining factor and is responsible for the development of the testis and the production of testosterone.9 In addition, the gene for the AR is located on the X chromosome.19,20 Males with Klinefelter syndrome, who have an extra X chromosome, show excess abdominal adiposity and have an increased risk of T2D, suggesting that the additional X chromosome promotes metabolic dysfunction.31,32 Extensive evidence relates sexually dimorphic aspects of physiology to brain masculinization by the testicular perinatal testosterone surges in males.7-10 Hypothalamic structure and function are modified by testosterone, leading to sex differences in reproductive behavior and physiology.10 Testosterone deficiency predisposes men to metabolic dysfunction, with excess adiposity, insulin resistance, and type 2 diabetes, whereas androgen excess predisposes women to insulin resistance, adiposity, and type 2 diabetes. One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose and energy homeostasis by testosterone in males and females. This male predominance, particularly among those with testosterone deficiency, has sparked research into the potential role of androgens in PD pathogenesis and as a therapeutic target. Although considerable attempts have been made to assess the effects of TRT in men and MCI, there is a notable lack of research on the role of androgens in the development of neurodegenerative disease in women or comparing these effects across genders. This is postulated to contribute to the higher incidence of certain neurodevelopmental disorders as well as increased aggressive behaviors and diminished executive functioning in males with ASD as compared to females.
Androgens bind to these receptors and operate via genomic (DNA binding) or nongenomic pathways (non-DNA binding) that influence multiple signaling cascades essential for CNS function and neuroprotection. Following androgen binding, they convert to a nuclear receptor which influences gene expression through binding at specific DNA sequences. Testosterone is converted into dihydrotestosterone (DHT) by the action of 5-alpha reductase in the prostate and skin. Testosterone is the most potent androgen, produced primarily by the Leydig cells in the testis. Androstenedione acts as the precursor for both testosterone and estrogen.
The studies reviewed here demonstrate that testosterone acts in the CNS to differentially impact glucose homeostasis and energy balance in males and females. Female global ARKO mice display normal metabolic phenotypes on a chow diet, yet they develop insulin resistance, glucose intolerance, and obesity when on a high-fat diet relative to normal mice on a high-fat diet.87 However, the authors did not explore if this obesity was due to increased food intake or decreased energy expenditure. In these mice, androgen excess decreased hypothalamic POMC messenger RNA expression. In female mice with chronic androgen excess during adulthood, leptin fails to reduce body weight, leading to obesity. Testosterone action is probably mediated at least in part via the AR, as men that have AR variants with low transcriptional activity exhibit hyperinsulinemia and obesity69 However, ERs are also involved in testosterone's metabolic effect in men, as treatment with an aromatase inhibitor blocked the ability of testosterone replacement to suppress adiposity in men.70 More direct evidence for the role of the AR in metabolic homeostasis can be gathered from androgen-receptor knockout (ARKO) mouse models.
They typically contain ingredients like D-Aspartic Acid, Vitamin D, and Zinc, which have been shown to support testosterone production. This interplay between testosterone and the SNS could have significant implications for how individuals respond to stress and engage in risk-taking behaviors. A study examining testosterone reactivity during skydiving, a quintessential sensation-seeking activity, found that testosterone reactivity was significantly greater than basal day measurements. It interacts with various other physiological systems, including the endocrine system, which is responsible for hormone production and regulation.
Hypothalamic dimorphism underlies some known behavioral differences in mice, and has known physiological effects in humans, e.g. affecting thermoregulation and metabolism. The hypothalamus is highly interconnected with other parts of the central nervous system, in particular the brainstem and its reticular formation. These responses are triggered by the sympathetic nervous system, but, in order to fit the model of fight or flight, the idea of flight must be broadened to include escaping capture either in a physical or sensory way. Individuals with higher levels of emotional reactivity (Such as an anxiety disorder) may be prone to anxiety and aggression, which illustrates the implications of appropriate emotional reaction in the fight or flight response. The physiological changes that occur during the fight or flight response are activated to give the body increased strength and speed in anticipation of fighting or running. Additionally, the circulation of cortisol functions to turn fatty acids into available energy, which prepares muscles throughout the body for response.
As discussed above, the DMH is a key nucleus that regulates BAT thermogenesis and energy expenditure and could be a target of androgen action.81,100 Indeed, in female mice exposed to chronic androgen excess, we see reduced intensity of POMC fibers in the DMII and a reduced decrease in body weight in response to the melanocortin receptor agonist, melanotan II.80 The studies described above suggest that the ARC is a probable site at which androgen is acting to impact metabolism.43,53,60,71 Indeed, in mice, impairment of GABAergic signaling within the ARC reduces energy expenditure by reducing thermogenesis without altering food intake, a phenotype similar to that of the model of adult androgen excess in female mice.80,89 Additionally, androgen could target the ARC in females to induce leptin resistance and hepatic insulin resistance in female mice. Women with PCOS exhibit increased gonadotropin-releasing hormone (GnRII) pulsatility, suggesting impairment of hypothalamic GnRH neurons.88 It is proposed that androgen activation of AR in ARC y-aminobutyric acid (GABA)ergic neurons upstream of GnRII neurons downregulates the progesterone receptor, whose activity leads to suppression of GnRH pulsatility.88 Perhaps AR action in these ARC neurons also contributes to metabolic dysfunction. Interestingly, androgen signaling could be important for proper metabolic function in females. The central effects of testosterone excess in adult females are summarized in Figure 1.
The study also found that testosterone reactivity to skydiving was predicted by increased cortisol, increased sympathetic activity (heart rate), and reduced parasympathetic activity1. Recent research has questioned whether the lateral hypothalamus's role is only restricted to initiating and stopping innate behaviors and argued it learns about food-related cues. The defeated animal has an increase in Fos levels in sexually dimorphic structures, such as the medial pre-optic nucleus, the ventrolateral part of ventromedial nucleus, and the ventral premammilary nucleus. Therefore, the hypothalamus, mainly the PMDvl, has an important role in expression of innate and conditioned defensive behaviors to a predator.
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