Neuroendocrine mechanisms in women's mating psychology

2008 ◽  
Author(s):  
James Roney
2020 ◽  
Vol 20 (4) ◽  
pp. 546-557
Author(s):  
Anna Rizzi ◽  
Matteo Saccia ◽  
Vincenzo Benagiano

Background: According to the views of psychoneuroendocrinoimmunology, many interactions exist between nervous, endocrine and immune system the purpose of which is to achieve adaptive measures restoring an internal equilibrium (homeostasis) following stress conditions. The center where these interactions converge is the hypothalamus. This is a center of the autonomic nervous system that controls the visceral systems, including the immune system, through both the nervous and neuroendocrine mechanisms. The nervous mechanisms are based on nervous circuits that bidirectionally connect hypothalamic neurons and neurons of the sympathetic and parasympathetic system; the neuroendocrine mechanisms are based on the release by neurosecretory hypothalamic neurons of hormones that target the endocrine cells and on the feedback effects of the hormones secreted by these endocrine cells on the same hypothalamic neurons. Moreover, the hypothalamus is an important subcortical center of the limbic system that controls through nervous and neuroendocrine mechanisms the areas of the cerebral cortex where the psychic functions controlling mood, emotions, anxiety and instinctive behaviors take place. Accordingly, various studies conducted in the last decades have indicated that hypothalamic diseases may be associated with immune and/or psychic disorders. Objective: Various researches have reported that the hypothalamus is controlled by the cerebellum through a feedback nervous circuit, namely the hypothalamocerebellar circuit, which bi-directionally connects regions of the hypothalamus, including the immunoregulatory ones, and related regions of the cerebellum. An objective of the present review was to analyze the anatomical bases of the nervous and neuroendocrine mechanisms for the control of the immune system and, in particular, of the interaction between hypothalamus and cerebellum to achieve the immunoregulatory function. Conclusion: Since the hypothalamus represents the link through which the immune functions may influence the psychic functions and vice versa, the cerebellum, controlling several regions of the hypothalamus, could be considered as a primary player in the regulation of the multiple functional interactions postulated by psychoneuroendocrinoimmunology.


2021 ◽  
Vol 22 (14) ◽  
pp. 7287
Author(s):  
Masaki Tanaka ◽  
Shunji Yamada ◽  
Yoshihisa Watanabe

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.


2021 ◽  
Vol 129 ◽  
pp. 104933
Author(s):  
Natanja F. Peen ◽  
Natalia Duque-Wilckens ◽  
Brian C. Trainor

1999 ◽  
Vol 77 (12) ◽  
pp. 1874-1890 ◽  
Author(s):  
C D Rollo ◽  
C V Ko ◽  
JG A Tyerman ◽  
L J Kajiura

Sleep is required for the consolidation of memory for complex tasks, and elements of the growth-hormone (GH) axis may regulate sleep. The GH axis also up-regulates protein synthesis, which is required for memory consolidation. Transgenic rat GH mice (TRGHM) express plasma GH at levels 100-300 times normal and sleep 3.4 h longer (30%) than their normal siblings. Consequently, we hypothesized that they might show superior ability to learn a complex task (8-choice radial maze); 47% of the TRGHM learned the task before any normal mice. All 17 TRGHM learned the task, but 33% of the 18 normal mice learned little. TRGHM learned the task significantly faster than normal mice (p < 0.05) and made half as many errors in doing so, even when the normal nonlearners were excluded from the analysis. Whereas normal mice expressed a linear learning curve, TRGHM showed exponentially declining error rates. The contribution of the GH axis to cognition is conspicuously sparse in literature syntheses of knowledge concerning neuroendocrine mechanisms of learning and memory. This paper synthesizes the crucial role of major components of the GH axis in brain functioning into a holistic framework, integrating learning, sleep, free radicals, aging, and neurodegenerative diseases. TRGHM show both enhanced learning in youth and accelerated aging. Thus, they may provide a powerful new probe for use in gaining an understanding of aspects of central nervous system functioning, which is highly relevant to human health.


1977 ◽  
Vol 179 (2) ◽  
Author(s):  
DavidE. Scott ◽  
Gerda Krobisch-Dudley ◽  
WillisK. Paull ◽  
GeraldP. Kozlowski

1992 ◽  
Vol 160 (S15) ◽  
pp. 7-17 ◽  
Author(s):  
Stuart Checkley

It is now generally accepted that stressful life events and chronic difficulties can trigger the onset of depression in predisposed individuals. However, although much is known of the neurobiology of stress, few attempts have been made to provide a biological explanation for the mechanisms whereby life events might trigger depression. Enough is now known of the central control of hypothalamic pituitary adrenal (HPA) function and its response to stress to permit an examination of its role in the neurobiology of the triggering of depression by stress. This evidence is reviewed, and the proposal explored that stress triggers depression by a genomic action of corticosteroids.


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