Hypothalamus

About: Hypothalamus is a research topic. Over the lifetime, 22301 publications have been published within this topic receiving 1085925 citations.

Localization of oxytocin receptor messenger ribonucleic acid in the rat brain

Abstract: The expression of oxytocin receptor (OT-R) mRNA in the rat central nervous system was examined by in situ hybridization histochemistry using cRNA probe. Wide distribution of cells expressing OT-R mRNA was observed not only in the hypothalamus, but also in other regions. There were high levels of OT-R mRNA in the anterior olfactory nuclei, tenia tecta, olfactory tubercle, rostral most region of the frontal cortex, piriform cortex, layers 2 and 3 of the neocortex, bed nucleus of the stria terminalis, anterior medial preoptic nucleus (AV3V region), magnocellular preoptic nucleus, supraoptic nucleus, paraventricular hypothalamic nucleus, retrochiasmatic nucleus, ventromedial hypothalamic nucleus, paraventricular thalamic nucleus, central amygdaloid nucleus, medial amygdaloid nucleus, posterior cortical amygdaloid nucleus, amygdalohippocampal area, subiculum, prepositus hypoglossal nucleus, and dorsal motor nucleus of vagus. In most regions of the brain, our findings concurred with those obtained by receptor b...

De Novo Neurogenesis in Adult Hypothalamus as a Compensatory Mechanism to Regulate Energy Balance

Abstract: The ability to develop counter-regulatory mechanisms to maintain energy balance in response to environmental and physiologic insults is essential for survival, but the mechanisms underlying these compensatory regulations are poorly understood. Agouti-related peptide (AGRP) and Neuropeptide Y are potent orexigens and are coexpressed in neurons in the arcuate nucleus of the hypothalamus. Acute ablation of these neurons leads to severe anorexia and weight loss, whereas progressive degeneration of these neurons has minimal impact on food intake and body weight, suggesting that compensatory mechanisms are developed to maintain orexigenic drive. In this study, we show that cell proliferation is increased in the hypothalamus of adult mutant animals in which AgRP neurons undergo progressive neurodegeneration due to deletion of mitochondrial transcription factor A, and that a subset of these newly generated cells differentiate into AgRP neurons along with other resident neuronal subtypes. Furthermore, some of the newly generated cells are capable of responding to leptin, and a central blockade of cell proliferation in adult animals results in decreases in food intake and body adiposity in mutant but not in control animals. Our study indicates that neurons important for energy homeostasis can be regenerated in adult feeding centers under neurodegenerative conditions. It further suggests that de novo neurogenesis might serve as a compensatory mechanism contributing to the plastic control of energy balance in response to environmental and physiologic insults.

Evidence for the existence of atrial natriuretic factor-containing neurons in the rat brain.

Abstract: Immunoreactive atrial natriuretic factor- (ANF-)positive nerve fibers and cell bodies were observed in the preoptic area, hypothalamus, mesencephalon, and pons of rats. In colchicine-treated animals a large number of immunoreactive ANF-positive cell bodies were seen in the organum vasculosum of the lamina terminalis, in several hypothalamic nuclei (e.g. periventricular, arcuate, and ventral premammillary nuclei), and in the dorsolateral tegmental nuclei of the pons. Varicose nerve fibers containing ANF were generally observed in the vicinity of the cells. These findings indicate that a widespread network of ANF-containing neurons is present in the brain.

The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box.

Abstract: The hypothalamus is the focus of many peripheral signals and neural pathways that control energy homeostasis and body weight. Emphasis has moved away from anatomical concepts of 'feeding' and 'satiety' centres to the specific neurotransmitters that modulate feeding behaviour and energy expenditure. We have chosen three examples to illustrate the physiological roles of hypothalamic neurotransmitters and their potential as targets for the development of new drugs to treat obesity and other nutritional disorders. Neuropeptide Y (NPY) is expressed by neurones of the hypothalamic arcuate nucleus (ARC) that project to important appetite-regulating nuclei, including the paraventricular nucleus (PVN). NPY injected into the PVN is the most potent central appetite stimulant known, and also inhibits thermogenesis; repeated administration rapidly induces obesity. The ARC NPY neurones are stimulated by starvation, probably mediated by falls in circulating leptin and insulin (which both inhibit these neurones), and contribute to the increased hunger in this and other conditions of energy deficit. They therefore act homeostatically to correct negative energy balance. ARC NPY neurones also mediate hyperphagia and obesity in the ob/ob and db/db mice and fa/fa rat, in which leptin inhibition is lost through mutations affecting leptin or its receptor. Antagonists of the Y5 receptor (currently thought to be the NPY 'feeding' receptor) have anti-obesity effects. Melanocortin-4 receptors (MC4-R) are expressed in various hypothalamic regions, including the ventromedial nucleus and ARC. Activation of MC4-R by agonists such as alpha-melanocyte-stimulating hormone (a cleavage product of pro-opiomelanocortin which is expressed in ARC neurones) inhibits feeding and causes weight loss. Conversely, MC4-R antagonists such as 'agouti' protein and agouti gene-related peptide (AGRP) stimulate feeding and cause obesity. Ectopic expression of agouti in the hypothalamus leads to obesity in the AVY mouse, while AGRP is co-expressed by NPY neurones in the ARC. Synthetic MC4-R agonists may ultimately find use as anti-obesity drugs in human subjects Orexins-A and -B, derived from prepro-orexin, are expressed in specific neurones of the lateral hypothalamic area (LHA). Orexin-A injected centrally stimulates eating and prepro-orexin mRNA is up regulated by fasting and hypoglycaemia. The LHA is important in receiving sensory signals from the gut and liver, and in sensing glucose, and orexin neurones may be involved in stimulating feeding in response to falls in plasma glucose.

Migratory arrest of gonadotropin-releasing hormone neurons in transgenic mice.

Abstract: Gonadotropin-releasing hormone (GnRH) is important in reproduction, although the mechanism of central hypogonadism in humans remains unclear. Because the GnRH neuron originates from the olfactory placode and migrates to the hypothalamus during development, central hypogonadism in humans could be caused by failure in normal migration of GnRH neurons to the hypothalamus. We report that in transgenic mice expression of the simian virus 40 T antigen, driven by the promoter of human GnRH gene, resulted in central hypogonadism due to an arrest in neuronal migration during development and tumor formation along the migratory pathway. This system appears to be an important animal model of hypogonadotropic hypogonadism in humans. Additionally, olfactory bulb tumors from these animals were dispersed, and a GnRH-secreting neuronal cell line (GN cell line) was established.