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There is growing appreciation for the numerous and often dramatic differences in the nervous system of males and females and the importance of these sex differences for behavioral traits. Sex differences in the nervous system and behavior result from a process of sexual differentiation that is carried out by the interplay of genetic, hormonal, and environmental factors throughout the life span. Although the preponderance of mechanistic study of mammalian sexual differentiation has occurred in traditional laboratory rodents, this field of study has benefitted from comparative studies, which highlight the diversity in sexual polymorphism in vertebrates and also point to strongly conserved mechanisms whereby these sexually differentiated traits develop.

Article

Kalynn Schulz, Marcia Chavez, and Arthur Castaneda

Nicotinic acetylcholine receptors (nAChRs) are present throughout the central nervous system and involved in a variety of physiological and behavioral functions. Nicotinic acetylcholine receptors are receptive to the presence of nicotine and acetylcholine and can be modulated through a variety of agonist and antagonist actions. These receptors are complex in their structure and function, and they are composed of multiple α and β subunits. Many affective disorders have etiological links with developmental exposure to the nAChR agonist nicotine. Given that abnormalities in nAChRs are associated with affective disorders such as depression and anxiety, pharmacological interventions targeting nAChRs may have significant therapeutic benefits.

Article

James Burkett and Farzaneh Naghavi

“Empathy” is an umbrella term for any type of process in which one is affected by the emotional state of others, and it is of great importance for daily social interaction. Empathic processes are thought to have evolved in the context of parental care to motivate caregivers to respond to helpless neonates’ needs, but over time may have been generalized outside the rearing context to make a wider social network and help shape social behaviors. It is becoming more apparent that in several psychiatric disorders, such as major depressive disorder, autism spectrum disorder, and antisocial personality disorder, impaired empathic behaviors are correlated with the severity of the disease and a reduced quality of life. Therefore, developing scientific avenues for the study of empathy, its mechanisms, and origins is important for human health and understanding the human condition.

Article

Craig Heller

The words “regulation” and “control” have different meanings. A rich literature exists on the control mechanisms of sleep—the genomic, molecular, cellular, and circuit processes responsible for arousal state changes and characteristics. The regulation of sleep refers to functions and homeostatic maintenance of those functions. Much less is known about sleep regulation than sleep control, largely because functions of sleep are still unknown. Regulation requires information about the regulated variable that can be used as feedback information to achieve optimal levels. The circadian timing of sleep is regulated, and the feedback information is entraining stimuli such as the light–dark cycle. Sleep itself is homeostatically regulated, as evidenced by sleep deprivation experiments. Eletroenceophalography (EEG) slow-wave activity (SWA) is regulated, and it appears that adenosine is the major source of feedback information, and that fact indicates an energetic function for sleep. The last aspect of sleep regulation discussed in this short article is the non-rapid eye movement (NREM) and rapid eye movement (REM) sleep cycling. Evidence is discussed that supports the argument that NREM sleep is in a homeostatic relationship with wake, and REM sleep is in a homeostatic relationship with NREM sleep.

Article

Mohammed H. Abdulla and Edward J. Johns

A potential role for the renal innervation was first described in 1859 by Claude Bernard, who observed an increase in urine flow following section of the greater splanchnic nerve, which included the renal nerves. Subsequent studies provided little further clarity, leading Homer Smith in 1951 to declare that the renal innervation had little or no significance in controlling kidney hemodynamic or excretory function. However, since the 1960s, there has been increased attention to how the renal nerves may contribute to the deranged control of blood pressure and heart function cardiovascular diseases. The efferent (sympathetic) nerves have neuroeffector junctions which provide close contact with all vascular and tubular elements of the kidney. Activation of the sympathetic nerves at the resistance vessels, that is, the interlobular arteries afferent and even arterioles, modulates both renal blood flow and glomerular filtration rate; at the juxtaglomerular granular cells, they cause renin release and subsequent angiotensin II generation, and at the tubules there is a neurally stimulated increase in epithelial cell sodium transport. Less is known of the role of the afferent nerves, which primarily innervate the renal pelvis, and to a lesser degree the cortex and medulla. Their role is uncertain but sensory information passing to the brain can influence renal efferent nerve activity, forming the basis of both inhibitory and excitatory reno-renal reflexes. Increasingly, it is perceived that in a range of cardiovascular diseases such as cardiac failure, chronic renal disease, and hypertension, there is an inappropriate sympatho-excitation related to alterations in afferent renal nerve activity, which exacerbates the disease progression. The importance of the renal innervation in these disease processes has been emphasized in clinical studies where renal denervation in humans has been found to reduce blood pressure in resistant hypertensive patients and to ameliorate the progression of cardiac and kidney diseases, diabetes, and obesity and hypertension. The importance of both systemic and renal inflammatory responses in activating the neurohumoral control of the kidney is a continuing source of investigation.

Article

Steven Kinsey, Olivia Vanegas, Kristen Trexler, Floyd Steele, and Matthew Eckard

The stress response evolved as a series of neural and endocrine mechanisms that protect the host organism from threats to homeostasis. Repeated use of psychotropic drugs can lead to the development of tolerance (i.e., decreased drug activity at a given dose) and drug dependence, as indicated by withdrawal syndromes following drug abstinence. Drug withdrawal is often overtly stressful, although acute drug exposure may also represent a threat to homeostasis. This article explores the neuroendocrine effects of drugs of abuse and some of the ways in which stress and appetitive mechanisms interact.

Article

Nicolas Rohleder

Stress is a condition or an experience that is pervasive throughout human life. While there are many definitions of stress, a common notion is that stress is processed in the central nervous system and has effects on health that are mediated by stress-modulated pathways. Several brain areas, such as the amygdala and the broader limbic system, are involved in interpreting situations as potentially stressful. The signals of these areas converge in the hypothalamus, which orchestrates peripheral stress-modulated pathways, mainly the hypothalamus-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS). Health effects of stress are mediated by long-term alterations of basic stress system activity, which has downstream effects on pathophysiological pathways such as the inflammatory system.

Article

Talita de Melo e Silva, Catherine Miriam Czeisler, and José Javier Otero

Breathing is essential for survival and is precisely regulated by the nervous system. From a neuroanatomical perspective, the respiratory tract is innervated by afferent and efferent autonomic nerves, which regulate aspects of airway function and ensure appropriate tissue oxygenation. The general concepts of how the peripheral nervous system (PNS) develops as it relates to lung function are reviewed. The vagus (cranial nerve X), a mixed motor and sensory nerve, supplies parasympathetic and sensory fibers to the airways. During development, preganglionic visceromotor efferent neurons of the cranial nerves arise in the hindbrain basal plate and later migrate dorsally through the neuroepithelium. The neural crest is a migratory and multipotent embryonic cell population that develops at the dorsal portion of the neural tube, which delaminates from the neuroepithelium to enter distinct pathways, forming various derivatives, among which include the peripheral nervous system. Neural crest cells emerging from the vagal region migrate into the ventral foregut and give rise to intrinsic ganglia in the respiratory tract that are innervated from the vagus and send out postganglionic fibers. The lung is innervated by sympathetic nerves derived from the upper thoracic and cervical ganglia. The sympathetic preganglionic neurons are derived from trunk neural crest cells that migrate, forming two chains of sympathetic ganglia referred to as the lateral vertebral sympathetic chains. Neural crest cells that migrate along defined pathways to generate sympathetic ganglia also derivate the dorsal root ganglia that send somatosensory afferent innervations to the respiratory tract.

Article

Steven Holfinger, M. Melanie Lyons, Nitin Bhatt, and Ulysses Magalang

Obstructive sleep apnea is recognized as a heterogeneous disease presenting with varying underlying risk factors, phenotypes, and responses to therapy. This clinical variance is in part due to the complex pathophysiology of sleep apnea. While multiple anatomical issues can predispose to the development of sleep apnea, factors that control the airway musculature also contribute via different pathophysiologic mechanisms. As sleep apnea does not occur during wakefulness, the impact of sleep stages on respiration is of critical importance. Altogether, understanding sleep apnea pathophysiology helps to guide current treatment modalities and helps identify potential targets for future therapies.

Article

In mammals, reproductive function is closely regulated by energy availability. It is influenced by both extremes of nutrition, too few calories (undernutrition) and an excessive amount of calories (obesity). Atypical decreases or increases in weight can have adverse effects on the reproductive axis. This includes suppression of reproductive function, decreases in ovarian cyclicity, reduction in fertility, anovulation, and dysregulation of spermatogenesis. The balance between energy regulation and reproduction is supervised by a complex system comprised of the brain and peripheral tissues. The brain senses and integrates various systemic and central signals that are indicative of changes in body physiology and energy status. This occurs via numerous factors, including metabolic hormones and nutrients. Adipokines, endocrine factors primarily secreted by white adipose tissue, and adipose tissue related cytokines (adipocytokines) contribute to the regulation of maturity, fertility, and reproduction. Indeed, some adipokines play a fundamental role in reproductive disorders. The brain, predominantly the hypothalamus, is responsible for linking adipose-derived signals to pathways controlling reproductive processes. Gonadotropin-releasing hormone (GnRH) cells in the hypothalamus are fundamental in relaying adipose-derived signals to the pituitary–gonadal axis, which consequently controls reproductive processes. Leptin, adiponectin, apelin, chermin, resistin, and visfatin are adipokines that regulate reproductive events via the brain.