![]() ![]() Neurosecretory parvocellular neurons send their axons to the external zone of the median eminence to regulate the secretion of releasing factors into the hypothalamohypophyseal portal vasculature to control the secretion of corresponding anterior pituitary hormones. Further investigation is necessary to identify specific mechanisms that lead to these unique properties. In contrast, magnocellular neurons do not display low-threshold potentials but are characterized by a distinct return to baseline after depolarizing stimuli ( Hernandez et al., 2015 Israel et al., 2016). Parvocellular neurons display small low threshold depolarizations, while long-projecting neurons generate large low-threshold depolarizations. These neurons are characterized by their unique electrophysiological properties ( Tasker and Dudek, 1991). The paraventricular nucleus (PVN) houses three functional neuronal types that act as central regulators of the stress response: parvocellular, neurosecretory magnocellular, and long-projecting neurons. Components of the HPA Axis Morphology and Development of the Paraventricular Nucleus (PVN) The effect of environmental perturbations, such as prenatal stress or prenatal exposure to synthetic GC hormones, and the associated susceptibility to stress-related neuropathologies in adulthood are also addressed. ![]() We also examine the activational and organizational effects of hormones during critical periods of development that result in the sexually dimorphic responses of the HPA axis in adults. In this review, we discuss the HPA axis as the central regulator of various physiological responses to stressors. This may become detrimental to the fetus later in life as it leads to abnormal physiological function in adulthood, thereby increasing the risk for adult disease. Early life exposure of the offspring to excess fetal glucocorticoid (GC) hormones or environmental perturbations, such as maternal stressors, can alter normal neuropeptide synthesis and lead to a disruption in the development of the HPA axis. The HPA axis begins to develop as early as fetal life and becomes sexually dimorphic during puberty due to differing levels of gonadal hormones. There are several critical developmental stages must be attained to ensure proper functionality of the HPA axis and appropriate behavioral and physiological stress-responses in adulthood. The HPA axis consists of a cascade of endocrine pathways that respond to specific negative feedback loops involving the hypothalamus, anterior pituitary gland, and adrenal gland. A major component of the homeostatic response is the hypothalamic-pituitary-adrenal (HPA) axis, an intricate, yet robust, neuroendocrine mechanism that mediates the effects of stressors by regulating numerous physiological processes, such as metabolism, immune responses, and the autonomic nervous system (ANS). Humans and animals respond to environmental perturbations with a stress response that allows physiological adaptation to the stressor to maintain homeostasis. We will also examine the maternal-fetal hypothalamic-pituitary-adrenal axis and disruption of the normal fetal environment which becomes a major risk factor for many neurodevelopmental pathologies in adulthood, such as major depressive disorder, anxiety, schizophrenia, and others. ![]() In this review, we will discuss the regulation of the HPA axis and its development. ![]() Together, these changes can potentially lead to a disruption in neuroendocrine, behavioral, autonomic, and metabolic functions in adulthood. Abnormal development of the hypothalamic-pituitary-adrenal (HPA) axis can further result in long-term alterations in neuropeptide and neurotransmitter synthesis in the central nervous system, as well as glucocorticoid hormone synthesis in the periphery. The hypothalamic-pituitary-adrenal axis is a complex system of neuroendocrine pathways and feedback loops that function to maintain physiological homeostasis. 2Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, AZ, United States.1Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, United States. ![]()
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