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Frontiers in Neuroendocrinology Apr 2018As adolescents transition from childhood to adulthood, many physiological and neurobehavioral changes occur. Shifts in neuroendocrine function are one such change,... (Review)
Review
As adolescents transition from childhood to adulthood, many physiological and neurobehavioral changes occur. Shifts in neuroendocrine function are one such change, including the hormonal systems that respond to stressors. This review will focus on these hormonal changes, with a particular emphasis on the pubertal and adolescent maturation of the hypothalamic-pituitary-adrenal (HPA) axis. Furthermore, this review will concentrate on studies using animal models, as these model systems have contributed a great deal to our mechanistic understanding of how factors such as sex and experience with stressors shape hormonal reactivity during development. Continued study of the maturation of stress reactivity will undoubtedly shed much needed light on the stress-related vulnerabilities often associated with adolescence as well as providing us with possible strategies to mitigate these vulnerabilities. This area of research may lead to discoveries that enhance the well-being of adolescents, ultimately providing them with greater opportunities to mature into healthy adults.
Topics: Animals; Disease Models, Animal; Humans; Hypothalamo-Hypophyseal System; Pituitary-Adrenal System; Sexual Maturation; Stress, Psychological
PubMed: 29275000
DOI: 10.1016/j.yfrne.2017.12.003 -
British Medical Journal Apr 1953
Topics: Humans; Puberty; Puberty, Precocious; Sexual Maturation
PubMed: 13032541
DOI: No ID Found -
Frontiers in Neuroendocrinology Jan 2014Puberty and adolescence are major life transitions during which an individual's physiology and behavior changes from that of a juvenile to that of an adult. Here we... (Review)
Review
Puberty and adolescence are major life transitions during which an individual's physiology and behavior changes from that of a juvenile to that of an adult. Here we review studies documenting the effects of stressors during pubertal and adolescent development on the adult brain and behavior. The experience of complex or compound stressors during puberty/adolescence generally increases stress reactivity, increases anxiety and depression, and decreases cognitive performance in adulthood. These behavioral changes correlate with decreased hippocampal volumes and alterations in neural plasticity. Moreover, stressful experiences during puberty disrupt behavioral responses to gonadal hormones both in sexual performance and on cognition and emotionality. These behavioral changes correlate with altered estrogen receptor densities in some estrogen-concentrating brain areas, suggesting a remodeling of the brain's response to hormones. A hypothesis is presented that activation of the immune system results in chronic neuroinflammation that may mediate the alterations of hormone-modulated behaviors in adulthood.
Topics: Adolescent; Adolescent Behavior; Animals; Cognition; Gonadal Hormones; Humans; Puberty; Sexual Maturation; Stress, Psychological
PubMed: 24184692
DOI: 10.1016/j.yfrne.2013.10.004 -
Hormones and Behavior Jul 2013This article is part of a Special Issue "Puberty and Adolescence". Studies of birds and reptiles have provided many basic insights into the neuroendocrine control of... (Review)
Review
This article is part of a Special Issue "Puberty and Adolescence". Studies of birds and reptiles have provided many basic insights into the neuroendocrine control of reproductive processes. This research has elucidated mechanisms regulating both early development, including sexual differentiation, and adult neuroendocrine function and behavior. However, phenomena associated with the transition into sexual maturation (puberty) have not been a focus of investigators working on species in these taxonomic classes. Research is complicated in birds and reptiles by a variety of factors, including what can be extended times to maturation, the need to reach particular body size regardless of age, and environmental conditions that can support or inhibit endocrine responses. However, careful selection of model systems, particularly those with available genetic tools, will lead to important comparative studies that can elucidate both generalizability and diversity of mechanisms regulating the onset of reproductive maturity.
Topics: Animals; Birds; Neurosecretory Systems; Reproduction; Reptiles; Sex Differentiation; Sexual Maturation; Time Factors
PubMed: 23998665
DOI: 10.1016/j.yhbeh.2013.05.002 -
Proceedings of the Royal Society of... Jun 1951
Topics: Humans; Puberty; Puberty, Precocious; Sexual Maturation
PubMed: 14864526
DOI: No ID Found -
Proceedings of the Royal Society of... Sep 1952
Topics: Humans; Puberty; Puberty, Precocious; Sexual Maturation
PubMed: 13003950
DOI: No ID Found -
Experimental Physiology Nov 2013Determining the neural mechanisms controlling gonadotrophin-releasing hormone (GnRH) release is of pivotal importance in understanding central control of reproductive... (Review)
Review
Determining the neural mechanisms controlling gonadotrophin-releasing hormone (GnRH) release is of pivotal importance in understanding central control of reproductive physiology in vertebrates. Targeted genetic manipulation of kisspeptin and GPR54 neurons has provided new insights into the mechanisms modulating GnRH release and thereby regulating hypothalamic-pituitary-gonadal axis activity during reproductive maturation. While conditional ablation of the oestrogen receptor α gene in kisspeptin neurons results in a dramatic advancement of the onset of puberty in female mice, subsequent pubertal maturation is arrested in these animals, as they fail to acquire normal ovulatory cyclicity. These data suggest that two oestrogen receptor α-dependent mechanisms, one a 'brake' and the other an 'accelerator', are sequentially operated in kisspeptin neurons during pubertal development of female mice to gate and then to activate GnRH release. In a different experimental approach, we removed entire kisspeptin neurons from the mouse brain and thus from the neural circuits controlling reproduction. Surprisingly, the onset of puberty in females was unaffected by kisspeptin neuron ablation. Furthermore, the animals attained regular ovulatory cyclicity and were fertile. Consistent with this, female mice lacking neurons that express the kisspeptin receptor GPR54 were also fertile, suggesting female reproductive maturation in the absence of kisspeptin/GPR54 signalling. However, acute kisspeptin neuron ablation in adult mice inhibited fertility, indicating that there is developmental compensation for the loss of kisspeptin neurons during reproductive neural circuit formation. Finally, we showed that kisspeptin neurons become an indispensable part of reproductive neural circuitry in the mouse brain before postnatal day 20.
Topics: Animals; Estrogen Receptor alpha; Female; Gonadotropin-Releasing Hormone; Kisspeptins; Mice; Mice, Knockout; Models, Biological; Neurons; Periodicity; Receptors, G-Protein-Coupled; Receptors, Kisspeptin-1; Sexual Maturation
PubMed: 23955307
DOI: 10.1113/expphysiol.2013.071928 -
Hormones and Behavior Jul 2013This article is part of a Special Issue "Puberty and Adolescence". Puberty is the developmental period when the hypothalamic-pituitary-gonadal (HPG) axis is activated,... (Review)
Review
This article is part of a Special Issue "Puberty and Adolescence". Puberty is the developmental period when the hypothalamic-pituitary-gonadal (HPG) axis is activated, following a juvenile quiescent period, and reproductive capacity matures. Although pubertal events occur in a consistent sequence, there is considerable variation between individuals in the onset and timing of pubertal events, with puberty onset occurring earlier in girls than in boys. Evidence in humans demonstrates that social and environmental context influences the timing of puberty onset and may account for some of the observed variation. This review analyzes the nonhuman primate literature, focusing primarily on rhesus macaques (Macaca mulatta), to examine the social and environmental influences on puberty onset, how these factors influence puberty in males and females, and to review the relationship between puberty onset of adult neuroendocrine function and sexual behavior. Social and environmental factors influence the timing of puberty onset and pubertal events in nonhuman primates, as in humans, and the influences of these factors differ for males and females. In nonhuman primates, gonadal hormones are not required for sexual behavior, but modulate the frequency of occurrence of behavior, with social context influencing the relationship between gonadal hormones and sexual behavior. Thus, the onset of sexual behavior is independent of neuroendocrine changes at puberty; however, there are distinct behavioral changes that occur at puberty, which are modulated by social context. Puberty is possibly the developmental period when hormonal modulation of sexual behavior is organized, and thus, when social context interacts with hormonal state to strongly influence the expression of sexual behavior.
Topics: Animals; Behavior, Animal; Environment; Female; Macaca mulatta; Male; Neurosecretory Systems; Primates; Sexual Behavior; Sexual Maturation; Social Environment
PubMed: 23998667
DOI: 10.1016/j.yhbeh.2013.05.003 -
Frontiers in Neuroendocrinology Jan 2015Substantial progress has been made in recent years toward deciphering the molecular and genetic underpinnings of the pubertal process. The availability of powerful new... (Review)
Review
Substantial progress has been made in recent years toward deciphering the molecular and genetic underpinnings of the pubertal process. The availability of powerful new methods to interrogate the human genome has led to the identification of genes that are essential for puberty to occur. Evidence has also emerged suggesting that the initiation of puberty requires the coordinated activity of gene sets organized into functional networks. At a cellular level, it is currently thought that loss of transsynaptic inhibition, accompanied by an increase in excitatory inputs, results in the pubertal activation of GnRH release. This concept notwithstanding, a mechanism of epigenetic repression targeting genes required for the pubertal activation of GnRH neurons was recently identified as a core component of the molecular machinery underlying the central restraint of puberty. In this chapter we will discuss the potential contribution of various mechanisms of epigenetic regulation to the hypothalamic control of female puberty.
Topics: Animals; Epigenesis, Genetic; Female; Gonadotropin-Releasing Hormone; Humans; Hypothalamus; Neurons; Puberty; Sexual Maturation
PubMed: 25171849
DOI: 10.1016/j.yfrne.2014.08.003 -
Brain Research Dec 2010The initiation of mammalian puberty requires a sustained increase in pulsatile release of gonadotrophin releasing hormone (GnRH) from the hypothalamus. This increase is... (Review)
Review
The initiation of mammalian puberty requires a sustained increase in pulsatile release of gonadotrophin releasing hormone (GnRH) from the hypothalamus. This increase is brought about by coordinated changes in transsynaptic and glial-neuronal communication, consisting of an increase in neuronal and glial stimulatory inputs to the GnRH neuronal network and the loss of transsynaptic inhibitory influences. GnRH secretion is stimulated by transsynaptic inputs provided by excitatory amino acids (glutamate) and at least one peptide (kisspeptin), and by glial inputs provided by growth factors and small bioactive molecules. The inhibitory input to GnRH neurons is mostly transsynaptic and provided by GABAergic and opiatergic neurons; however, GABA has also been shown to directly excite GnRH neurons. There are many genes involved in the control of these cellular networks, and hence in the control of the pubertal process as a whole. Our laboratory has proposed the concept that these genes are arranged in overlapping networks internally organized in a hierarchical fashion. According to this concept, the highest level of intra-network control is provided by transcriptional regulators that, by directing expression of key subordinate genes, impose genetic coordination to the neuronal and glial subsets involved in initiating the pubertal process. More recently, we have begun to explore the concept that a more dynamic and encompassing level of integrative coordination is provided by epigenetic mechanisms.
Topics: Animals; Epigenomics; Female; Humans; Neurosecretory Systems; Puberty; Sexual Maturation; Transcription, Genetic
PubMed: 20851111
DOI: 10.1016/j.brainres.2010.09.039