Newborns and hatchlings can perform incredibly sophisticated behaviors, but many animals abstain from sexual activity at the beginning of life. Hormonal changes have long been known to drive both physical and behavioral changes during adolescence, leading to the largely untested assumption that sexuality emerges from organizational changes to neuronal circuitry. We show that the transition to sexuality in male is controlled by hormonal changes, but this regulation is functional rather than structural. In very young males, a broadly acting hormone directly inhibits the activity of three courtship-motivating circuit elements, ensuring the complete suppression of sexual motivation and behavior. Blocking or overriding these inhibitory mechanisms evokes immediate and robust sexual behavior from very young and otherwise asexual males. Similarities to mammalian adolescence suggest a general principle in which hormonal changes gate the transition to sexuality not by constructing new circuitry but by permitting activity in otherwise latent motivational circuit elements.
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http://dx.doi.org/10.1126/sciadv.abg6926 | DOI Listing |
BMJ Glob Health
January 2025
Population Council, Nairobi, Kenya.
Introduction: Climate change is shaping adolescent and young people's (AYP) transitions to adulthood with significant and often compounding effects on their physical and mental health. The climate crisis is an intergenerational inequity, with the current generation of young people exposed to more climate events over their lifetime than any previous one. Despite this injustice, research and policy to date lacks AYP's perspectives and active engagement.
View Article and Find Full Text PDFJ Eat Disord
January 2025
, London, UK.
Improvements to eating disorder (ED) care are urgently needed in the United Kingdom (UK) and around the world. Informed by my lived experiences, independent research, and involvement in the underappreciated field of quality improvement (QI), I have written this article to offer ideas on how to improve individuals' access to and experiences of ED care. As I live in the UK, my lived and QI experiences are of the UK's National Health Service (NHS).
View Article and Find Full Text PDFJ Clin Endocrinol Metab
January 2025
Department of Women's and Children's Health, Karolinska Institutet, SE-171 76 Stockholm, Sweden.
Classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH) is a rare genetic condition that results in cortisol deficiency and excess production of adrenal androgens. While the introduction of newborn screening for CAH has reduced morbidity and mortality, management of CAH remains challenging. Lifelong treatment with glucocorticoids is required to replace the endogenous cortisol deficiency and reduce excess adrenal androgens.
View Article and Find Full Text PDFFront Psychol
January 2025
Department of Human Neuroscience, Sapienza University of Rome, Rome, Italy.
Depression is presented as a multi-factorial bio-psycho-social expression that has evolved primarily as an effect of stressors related to the motivational/emotional systems that regulate the in our relationship with conspecifics. These stressors may be caused by two sources of threat, firstly, the loss of bonding with the caregiver and later with a partner and/or group which relates to the SEPARATION (PANIC/GRIEF) system, secondly, social defeat as an expression of the social competition and social dominance. The sexual maturity drives the individual to social competition and social dominance, even if the latter often occurs before sexual maturity, e.
View Article and Find Full Text PDFDevelopment
January 2025
School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland 4072, Australia.
A successful mitosis-to-meiosis transition in germ cells is essential for fertility in sexually reproducing organisms. In mice and humans, it is established that expression of STRA8 is critical for meiotic onset in both sexes. Here we show that BMP signalling is also essential, not for STRA8 induction but for correct meiotic progression in female mouse fetal germ cells.
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