-
Current Opinion in Neurobiology Jun 2016The adolescent transition from childhood to adulthood requires both reproductive and behavioral maturation as individuals acquire the ability to procreate. Gonadal... (Review)
Review
The adolescent transition from childhood to adulthood requires both reproductive and behavioral maturation as individuals acquire the ability to procreate. Gonadal steroid hormones are key players in the maturation of behaviors required for reproductive success. Beyond activating behavior in adulthood, testicular and ovarian hormones organize the adolescent brain and program adult-typical and sex-typical expression of sociosexual behaviors. Testicular hormones organize sexual and agonistic behaviors, including social proficiency-the ability to adapt behavior as a function of social experience. Ovarian hormones organize behaviors related to energy balance and maternal care. These sex differences in the behaviors that are programmed by gonadal hormones during adolescence suggest that evolution has selected for hormone-dependent sex-specific organization of behaviors that optimize reproductive fitness.
Topics: Animals; Gonadal Steroid Hormones; Humans; Mammals; Sex Characteristics; Sexual Behavior; Sexual Maturation
PubMed: 26963894
DOI: 10.1016/j.conb.2016.02.004 -
Basic & Clinical Pharmacology &... Feb 2008Onset and development of puberty is regulated by the neuroendocrine system. Population-based studies worldwide have observed secular trends towards earlier puberty... (Review)
Review
Onset and development of puberty is regulated by the neuroendocrine system. Population-based studies worldwide have observed secular trends towards earlier puberty development. These changes are apparently caused by environmental factors such as improved socio-economic status, improved health care and nutrition. However, they may also partly result from endocrine-disrupting chemicals in the environment. Epidemiological studies have investigated the relationship between pubertal development and exposure to endocrine-disrupting chemicals (polychlorinated biphenyls, polybrominated biphenyls, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, phthalate esters, furans and the pesticide endosulfan). Associations with both perinatal and postnatal exposure have been reported. Studies in experimental animals support some of these findings and point to differential endocrine regulatory mechanisms linked to pubertal development acting in the perinatal and the pre-pubertal period. Pubertal development is naturally associated with growth and body composition. There is increasing evidence for a link between prenatal development and pubertal onset. In girls born small for gestational age (SGA), pubertal onset and age at menarche often are advanced, especially if there has been an extensive catch-up growth during the first months of life. In utero growth retardation may have multiple causes including exposure to xenobiotic substances as was suggested for some endocrine-disrupting chemicals. An abnormal perinatal environment of children born SGA may alter the endocrine status and the sensitivity of the receptors for endocrine and metabolic signalling that may have effects on maturation of brain and gonads. However, the causal pathways and the molecular mechanisms that may link the pubertal growth pattern of children born SGA, pubertal development and endocrine-disrupting chemicals need further study.
Topics: Animals; Endocrine Disruptors; Female; Humans; Pregnancy; Prenatal Exposure Delayed Effects; Puberty; Sexual Maturation
PubMed: 18226071
DOI: 10.1111/j.1742-7843.2007.00180.x -
Human Reproduction Update Nov 2017Puberty is a complex developmental event, controlled by sophisticated regulatory networks that integrate peripheral and internal cues and impinge at the brain centers... (Review)
Review
BACKGROUND
Puberty is a complex developmental event, controlled by sophisticated regulatory networks that integrate peripheral and internal cues and impinge at the brain centers driving the reproductive axis. The tempo of puberty is genetically determined but is also sensitive to numerous modifiers, from metabolic and sex steroid signals to environmental factors. Recent epidemiological evidence suggests that the onset of puberty is advancing in humans, through as yet unknown mechanisms. In fact, while much knowledge has been gleaned recently on the mechanisms responsible for the control of mammalian puberty, fundamental questions regarding the intimate molecular and neuroendocrine pathways responsible for the precise timing of puberty and its deviations remain unsolved.
OBJECTIVE AND RATIONALE
By combining data from suitable model species and humans, we aim to provide a comprehensive summary of our current understanding of the neuroendocrine mechanisms governing puberty, with particular focus on its central regulatory pathways, underlying molecular basis and mechanisms for metabolic control.
SEARCH METHODS
A comprehensive MEDLINE search of articles published mostly from 2003 to 2017 has been carried out. Data from cellular and animal models (including our own results) as well as clinical studies focusing on the pathophysiology of puberty in mammals were considered and cross-referenced with terms related with central neuroendocrine mechanisms, metabolic control and epigenetic/miRNA regulation.
OUTCOMES
Studies conducted during the last decade have revealed the essential role of novel central neuroendocrine pathways in the control of puberty, with a prominent role of kisspeptins in the precise regulation of the pubertal activation of GnRH neurosecretory activity. In addition, different transmitters, including neurokinin-B (NKB) and, possibly, melanocortins, have been shown to interplay with kisspeptins in tuning puberty onset. Alike, recent studies have documented the role of epigenetic mechanisms, involving mainly modulation of repressors that target kisspeptins and NKB pathways, as well as microRNAs and the related binding protein, Lin28B, in the central control of puberty. These novel pathways provide the molecular and neuroendocrine basis for the modulation of puberty by different endogenous and environmental cues, including nutritional and metabolic factors, such as leptin, ghrelin and insulin, which are known to play an important role in pubertal timing.
WIDER IMPLICATIONS
Despite recent advancements, our understanding of the basis of mammalian puberty remains incomplete. Complete elucidation of the novel neuropeptidergic and molecular mechanisms summarized in this review will not only expand our knowledge of the intimate mechanisms responsible for puberty onset in humans, but might also provide new tools and targets for better prevention and management of pubertal deviations in the clinical setting.
Topics: Animals; Epigenesis, Genetic; Humans; Mammals; Neurosecretory Systems; Reproduction; Sexual Maturation; Signal Transduction
PubMed: 28961976
DOI: 10.1093/humupd/dmx025 -
International Journal of Andrology Feb 2006Sexual development and mature reproductive function are controlled by a handful of neurones that, located in the basal forebrain, produce the decapeptide luteinizing... (Review)
Review
Sexual development and mature reproductive function are controlled by a handful of neurones that, located in the basal forebrain, produce the decapeptide luteinizing hormone releasing hormone (LHRH). LHRH is released into the portal system that connects the hypothalamus to the pituitary gland and act on the latter to stimulate the synthesis and release of gonadotrophin hormones. The pubertal activation of LHRH release requires coordinated changes in excitatory and inhibitory inputs to LHRH-secreting neurones. These inputs are provided by both transsynaptic and glia-to-neurone communication pathways. Using cellular and molecular approaches, in combination with transgenic animal models and high-throughput procedures for gene discovery, we are gaining new insight into the basic mechanisms underlying this dual control of LHRH secretion and, hence, the initiation of mammalian puberty. Our results suggest that the initiation of puberty requires reciprocal neurone-glia communication involving excitatory amino acids and growth factors, and the coordinated actions of a group of transcriptional regulators that appear to represent a higher level of control governing the pubertal process.
Topics: Animals; Animals, Genetically Modified; Astrocytes; Female; Gonadotropin-Releasing Hormone; Humans; Hypothalamus; Neuroglia; Neurons; Neurosecretory Systems; Puberty; Sexual Maturation
PubMed: 16466547
DOI: 10.1111/j.1365-2605.2005.00619.x -
The Journal of Clinical Investigation Jan 2011Leptin exerts a permissive action on puberty by stimulating release of gonadotropin-releasing hormone (GnRH) in the hypothalamus. However, GnRH neurons lack leptin...
Leptin exerts a permissive action on puberty by stimulating release of gonadotropin-releasing hormone (GnRH) in the hypothalamus. However, GnRH neurons lack leptin receptor (LepR), indicating that leptin must indirectly regulate these neurons. The Kiss1 gene produces kisspeptins that stimulate GnRH secretion. Because Kiss1 neurons express LepR and inactivation of Kiss1 causes hypogonadotropic hypogonadism, Donato et al., in this issue of the JCI, assessed whether deletion of LepR from Kiss1 neurons would prevent sexual maturation. Unexpectedly, mice lacking LepR in Kiss1 neurons had normal pubertal development and fertility. In contrast, deletion of LepR from the ventral premammillary nucleus, a region of the brain involved in sexual behavior, prevented puberty and fertility. These findings highlight the complex biology of leptin in reproduction.
Topics: Animals; Brain; Female; Kisspeptins; Leptin; Male; Mice; Mice, Knockout; Models, Neurological; Proteins; Receptors, Leptin; Sexual Behavior, Animal; Sexual Maturation
PubMed: 21183781
DOI: 10.1172/JCI45813 -
Journal of Dairy Science Apr 2018The aim of this study was (1) to examine the effect of plane of nutrition during the first and second 6 mo of life on systemic concentrations of reproductive hormones...
Plane of nutrition before and after 6 months of age in Holstein-Friesian bulls: II. Effects on metabolic and reproductive endocrinology and identification of physiological markers of puberty and sexual maturation.
The aim of this study was (1) to examine the effect of plane of nutrition during the first and second 6 mo of life on systemic concentrations of reproductive hormones and metabolites in Holstein-Friesian dairy bulls, and (2) to establish relationships with age at puberty and postpubertal semen production potential. Holstein-Friesian bull calves (n = 83) with a mean (standard deviation) age and body weight of 17 (4.4) d and 52 (6.2) kg, respectively, were assigned to a high or low plane of nutrition for the first 6 mo of life. At 24 wk of age, bulls were reassigned, within treatment, either to remain on the same diet or to switch to the opposite diet until puberty, resulting in 4 treatment groups: high-high, high-low, low-low, and low-high. Monthly blood samples were analyzed for metabolites (albumin, urea, total protein, β-hydroxybutyrate, glucose, nonesterified fatty acid, triglycerides and creatinine), insulin, insulin-like growth factor-1, leptin, adiponectin, FSH, and testosterone. A GnRH challenge was carried out at 16 and 32 wk of age (n = 9 bulls per treatment). Blood was collected at 15-min intervals for 165 min, with GnRH administered (0.05 mg/kg of body weight, i.v.) immediately after the third blood sample. Blood samples were subsequently analyzed for LH, FSH, and testosterone. Stepwise regression was used to detect growth and blood measurements to identify putative predictors of age at puberty and subsequent semen quality traits. Metabolic hormones and metabolites, in general, reflected metabolic status of bulls. Although FSH was unaffected by diet, it decreased with age both in monthly samples and following GnRH administration. Testosterone was greater in bulls on the high diet before and after 6 mo of age. Testosterone concentrations increased dramatically after 6 mo of age. Luteinizing hormone was unaffected by diet following GnRH administration but basal serum LH was greater in bulls on a high diet before 6 mo of age. In conclusion, the plane of nutrition offered before 6 mo of age influenced metabolic profiles, which are important for promoting GnRH pulsatility, in young bulls.
Topics: Animal Nutritional Physiological Phenomena; Animals; Cattle; Gonadotropins; Male; Nutritional Status; Semen; Semen Analysis; Sexual Maturation
PubMed: 29397166
DOI: 10.3168/jds.2017-13720 -
Neuroscience and Biobehavioral Reviews Apr 2023Syrian hamsters show complex social play behavior and provide a valuable animal model for delineating the neurobiological mechanisms and functions of social play. In... (Review)
Review
Syrian hamsters show complex social play behavior and provide a valuable animal model for delineating the neurobiological mechanisms and functions of social play. In this review, we compare social play behavior of hamsters and rats and underlying neurobiological mechanisms. Juvenile rats play by competing for opportunities to pin one another and attack their partner's neck. A broad set of cortical, limbic, and striatal regions regulate the display of social play in rats. In hamsters, social play is characterized by attacks to the head in early puberty, which gradually transitions to the flanks in late puberty. The transition from juvenile social play to adult hamster aggression corresponds with engagement of neural ensembles controlling aggression. Play deprivation in rats and hamsters alters dendritic morphology in mPFC neurons and impairs flexible, context-dependent behavior in adulthood, which suggests these animals may have converged on a similar function for social play. Overall, dissecting the neurobiology of social play in hamsters and rats can provide a valuable comparative approach for evaluating the function of social play.
Topics: Cricetinae; Animals; Rats; Sexual Maturation; Mesocricetus; Aggression; Neurons
PubMed: 36804399
DOI: 10.1016/j.neubiorev.2023.105102 -
Developmental Psychology Jun 2015Evolutionary-minded developmentalists studying predictive-adaptive-response processes linking childhood adversity with accelerated female reproductive development and... (Observational Study)
Observational Study
Evolutionary-minded developmentalists studying predictive-adaptive-response processes linking childhood adversity with accelerated female reproductive development and health scientists investigating the developmental origins of health and disease (DOoHaD) may be tapping the same process, whereby longer-term health costs are traded off for increased probability of reproducing before dying via a process of accelerated reproductive maturation. Using data from 73 females, we test the following propositions using path analysis: (a) greater exposure to prenatal stress predicts greater maternal depression and negative parenting in infancy, (b) which predicts elevated basal cortisol at 4.5 years, (c) which predicts accelerated adrenarcheal development, (d) which predicts more physical and mental health problems at age 18. Results prove generally consistent with these propositions, including a direct link from cortisol to mental health problems. DOoHaD investigators should consider including early sexual maturation as a core component linking early adversity and stress physiology with poor health later in life in females.
Topics: Adolescent; Adrenarche; Adult; Child; Depression; Female; Health Status; Humans; Hydrocortisone; Life Change Events; Longitudinal Studies; Mental Health; Parenting; Pregnancy; Prenatal Exposure Delayed Effects; Puberty, Precocious; Sexual Maturation; Stress, Psychological; Young Adult
PubMed: 25915592
DOI: 10.1037/dev0000017 -
Scientific Reports Feb 2023Photoperiod, the portion of 24-h cycle during which an organism is exposed to illumination, is an important phenological cue in many animals. However, despite its...
Photoperiod, the portion of 24-h cycle during which an organism is exposed to illumination, is an important phenological cue in many animals. However, despite its influence on critical biological processes, there remain many unknowns regarding how variations in light intensity translate into perceived photoperiod. This experiment examined how light intensity variations affect perceived photoperiod in Atlantic salmon (Salmo salar) to determine whether photoperiod interpretation is, a) fixed such that anything above a minimum detection threshold is regarded as 'illumination', or b) adaptive and varies with recent light exposure. To do this we compared the frequency of smoltification and sexual maturation between groups of male parr which were exposed to one of eight light regimes on a 12:12 cycling regime (12-hour day/12-hour night). The eight regimes were divided into two treatments, four with 'High' daytime light intensity and four with 'Low' daytime light intensity. The 'High' and 'Low' intensity treatments were each sub-divided into four groups for which the subjective 'night' light intensity was 100%, 10%, 1% and 0% of the daytime light intensity, with four replicate tanks of each treatment. The results show that above a minimum detection threshold, Atlantic salmon have adaptive photoperiod interpretation which varies with recent light exposure, and that adaptive photoperiod interpretation modulates the timing of the parr-smolt transformation and sexual maturation. Further, we show that photoperiod interpretation varies between closely related families. Given the influence of phenological timing on species survival, our results reveal a critical role for integration of photoperiod interpretation in attempts to understand how geographically shifting thermal niches due to climate change will affect future populations.
Topics: Animals; Male; Salmo salar; Photoperiod; Light; Sexual Maturation; Climate Change
PubMed: 36788276
DOI: 10.1038/s41598-023-27583-7 -
Hormones and Behavior Jul 2013Throughout the past several decades, studies have uncovered a wealth of information about the neural circuitry underlying fear learning and extinction that has helped to... (Review)
Review
Throughout the past several decades, studies have uncovered a wealth of information about the neural circuitry underlying fear learning and extinction that has helped to inform treatments for fear-related disorders such as post-traumatic stress and anxiety. Yet, up to 40% of people do not respond to such treatments. Adolescence, in particular, is a developmental stage during which anxiety disorders peak, yet little is known about the development of fear-related neural circuitry during this period. Moreover, pharmacological and behavioral therapies that have been developed are based on mature circuitry and function. Here, we review neural circuitry implicated in fear learning and data from adolescent mouse and human fear learning studies. In addition, we propose a developmental model of fear neural circuitry that may optimize current treatments and inform when, during development, specific treatments for anxiety may be most effective.
Topics: Adolescent; Adolescent Development; Animals; Conditioning, Psychological; Fear; Humans; Learning; Memory; Mice; Sexual Maturation; Stress, Psychological
PubMed: 23998679
DOI: 10.1016/j.yhbeh.2013.01.016