Prolactin-releasing peptide (PrRP) has been proposed to mediate the central satiating effects of cholecystokinin (CCK) through the vagal CCK1 receptor. PrRP acts as an endogenous ligand of G protein-coupled receptor 10 (GPR10), which is expressed at the highest levels in brain areas related to food intake regulation, e.g., the paraventricular hypothalamic nucleus (PVN) and nucleus of the solitary tract (NTS). The NTS and PVN are also significantly activated after peripheral CCK administration. The aim of this study was to determine whether the endogenous PrRP neuronal system in the brain is involved in the central anorexigenic effect of the peripherally administered CCK agonist JMV236 or the CCK1 antagonist devazepide and whether the CCK system is involved in the central anorexigenic effect of the peripherally applied lipidized PrRP analog palm-PrRP31 in fasted lean mice. The effect of devazepide and JMV236 on the anorexigenic effects of palm-PrRP31 as well as devazepide combined with JMV236 and palm-PrRP31 on food intake and Fos cell activation in the PVN and caudal NTS was examined. Our results suggest that the anorexigenic effect of JMV236 is accompanied by activation of PrRP neurons of the NTS in a CCK1 receptor-dependent manner. Moreover, while the anorexigenic effect of palm-PrRP31 was not affected by JMV236, it was partially attenuated by devazepide in fasted mice. The present findings indicate that the exogenously influenced CCK system may be involved in the central anorexigenic effect of peripherally applied palm-PrRP31, which possibly indicates some interaction between the CCK and PrRP neuronal systems.

• MeSH
• Appetite Depressants administration & dosage   MeSH
• Hormone Antagonists administration & dosage   MeSH
• Chemokines, CC drug effects   metabolism   MeSH
• Cholecystokinin metabolism   MeSH
• Devazepide administration & dosage   MeSH
• Prolactin-Releasing Hormone administration & dosage   analogs & derivatives   MeSH
• Injections, Intraperitoneal MeSH
• Injections, Subcutaneous MeSH
• Mice, Inbred C57BL MeSH
• Mice MeSH
• Paraventricular Hypothalamic Nucleus drug effects   metabolism   MeSH
• Solitary Nucleus drug effects   metabolism   MeSH
• Fasting MeSH
• Peptide Fragments administration & dosage   MeSH
• Eating drug effects   MeSH
• Proto-Oncogene Proteins c-fos metabolism   MeSH
• Signal Transduction MeSH
• Sincalide administration & dosage   analogs & derivatives   MeSH
• Feeding Behavior drug effects   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Appetite Depressants MeSH
• Hormone Antagonists MeSH
• Ccl28 protein, mouse MeSH Browser
• Chemokines, CC MeSH
• Cholecystokinin MeSH
• Devazepide MeSH
• Fos protein, mouse MeSH Browser
• Prolactin-Releasing Hormone MeSH
• JMV 236 MeSH Browser
• palm11-PrRP31 MeSH Browser
• Peptide Fragments MeSH
• Proto-Oncogene Proteins c-fos MeSH
• Sincalide MeSH

The aim of the present work was to study the influence of variable stress on the expression of 11β-hydroxysteroid dehydrogenase type 1 (11HSD1) and the neuropeptides corticotropin-releasing hormone (CRH), urocortins 2 and 3(UCN2, UCN3), arginine vasopressin (AVP), oxytocin (OXT) and adenylate cyclase-activating polypeptide (PACAP) in two inbred rat strains: stress hypo-responsive Lewis (LEW) and hyper-responsive Fisher 344 (F344) rats. We found site-specific and strain-dependent differences in the basal and stress-stimulated expression of 11HSD1, CRH, UCN2, UCN3 and PACAP. In LEW rats, stress upregulated 11HSD1 in the prefrontal cortex and lateral amygdala, whereas in F344 rats 11HSD1 was upregulated in the central amygdala and hippocampal CA2 and ventral but not dorsal CA1 region; no effect was observed in the paraventricular nucleus, pituitary gland and adrenal cortex of both strains. The expression of glucocorticoid receptors did not parallel the upregulation of 11HSD1. Stress also stimulated the expression of paraventricular OXT, CRH, UCN3 and PACAP in both strains but amygdalar CRH only in LEW and UCN2/UCN3 in F344 rats, respectively. The upregulation of PACAP and CRH was paralleled only by increased expression of PACAP receptor PAC1 but not CRH receptor type 1. These observations provide evidence that inbred F344 and LEW rats exhibit not only the well-known phenotypic differences in the activity of the HPA axis but also strain- and stress-dependent differences in the expression of genes encoding 11HSD1 and neuropeptides associated with the HPA axis activity. Moreover, the differences in 11HSD1 expression suggest different local concentration of corticosterone and access to GR in canonical and noncanonical structures of the HPA axis.

• Keywords
• 11β-Hydroxysteroid dehydrogenase type 1, Brain, Fisher rat, Lewis rat, Neuropeptides, Stress,
• MeSH
• 11-beta-Hydroxysteroid Dehydrogenase Type 1 genetics   metabolism   MeSH
• Amygdala metabolism   MeSH
• Arginine Vasopressin genetics   metabolism   MeSH
• Hippocampus metabolism   MeSH
• Corticotropin-Releasing Hormone genetics   metabolism   MeSH
• Pituitary Gland metabolism   MeSH
• Pituitary Adenylate Cyclase-Activating Polypeptide genetics   metabolism   MeSH
• Rats MeSH
• Adrenal Cortex metabolism   MeSH
• RNA, Messenger metabolism   MeSH
• Brain metabolism   MeSH
• Paraventricular Hypothalamic Nucleus metabolism   MeSH
• Oxytocin genetics   metabolism   MeSH
• Rats, Inbred F344 MeSH
• Rats, Inbred Lew MeSH
• Prefrontal Cortex metabolism   MeSH
• Stress, Psychological genetics   metabolism   MeSH
• Receptors, Glucocorticoid genetics   metabolism   MeSH
• Gene Expression Profiling MeSH
• Pituitary-Adrenal System metabolism   MeSH
• Hypothalamo-Hypophyseal System metabolism   MeSH
• Urocortins genetics   metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Comparative Study MeSH
• Names of Substances
• 11-beta-Hydroxysteroid Dehydrogenase Type 1 MeSH
• Arginine Vasopressin MeSH
• Corticotropin-Releasing Hormone MeSH
• Pituitary Adenylate Cyclase-Activating Polypeptide MeSH
• RNA, Messenger MeSH
• Oxytocin MeSH
• Receptors, Glucocorticoid MeSH
• Urocortins MeSH

Generation of reactive oxygen species significantly contributes to the pathogenesis of acute renal failure (ARF) induced by myoglobin release. Ginsenosides (GS), the principal active ingredients of ginseng, is considered as an extremely good antioxidative composition of Chinese traditional and herbal drugs. The purpose of the present study was to investigate the protective effect of ginsenoside in rats with ARF on the changes of cholinergic nervous system in the kidney as well as on the involvement of mitogen-activated protein kinases (MAPK) in the hypothalamic paraventricular nuclei (PVN). In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced lipid peroxidation, restored the superoxide dismutase (SOD) level. Meanwhile, the obvious increase of choline acetyltransferase-immunoreactivity (ChAT-IR) in the proximal convoluted tubular cells (PCT) was observed by immunohistochemistry in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the hypothalamic paraventricular nuclei. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, reduce the renal oxidative stress, and ginsenoside can also activate the cholinergic system in PCT, simultaneously MAPK signal pathway in the PVN was also activated.

• MeSH
• Acute Kidney Injury chemically induced   enzymology   pathology   prevention & control   MeSH
• Antioxidants administration & dosage   pharmacology   MeSH
• Administration, Oral MeSH
• Time Factors MeSH
• Choline O-Acetyltransferase metabolism   MeSH
• Cytoprotection MeSH
• Phosphorylation MeSH
• Ginsenosides administration & dosage   pharmacology   MeSH
• Glycerol MeSH
• Malondialdehyde metabolism   MeSH
• Mitogen-Activated Protein Kinase 1 metabolism   MeSH
• Mitogen-Activated Protein Kinase 3 metabolism   MeSH
• Disease Models, Animal MeSH
• Paraventricular Hypothalamic Nucleus drug effects   enzymology   MeSH
• Oxidative Stress drug effects   MeSH
• Lipid Peroxidation drug effects   MeSH
• Rats, Sprague-Dawley MeSH
• Kidney Tubules, Proximal drug effects   enzymology   pathology   MeSH
• Signal Transduction drug effects   MeSH
• Superoxide Dismutase metabolism   MeSH
• Up-Regulation MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Antioxidants MeSH
• Choline O-Acetyltransferase MeSH
• Ginsenosides MeSH
• Glycerol MeSH
• Malondialdehyde MeSH
• Mapk1 protein, rat MeSH Browser
• Mitogen-Activated Protein Kinase 1 MeSH
• Mitogen-Activated Protein Kinase 3 MeSH
• Superoxide Dismutase MeSH

The hypothalamic supraoptic and paraventricular nuclei consist of oxytocin and arginine vasopressin synthesizing neurons that send projections to the neurohypophysis. A growing body of evidence in adult animals and young animals at near term confirmed the structure and function in the vasopressinergic and oxytocinergic network. However, whether those distinctive neural networks are formed before near term is largely unknown. This study determined the special patterns in location and distribution of oxytocin- and vasopressin-neurons in the paraventricular and supraoptic nuclei from preterm to term in the ovine fetuses. The results showed that oxytocin- and vasopressin-neurons were present in both nuclei at the three gestational time periods (preterm, near term, and term). In the paraventricular nuclei, vasopressin-cells concentrated mainly in the core of the middle magnocellular paraventricular nuclei, and oxytocin-cells were scattered surrounding the core. In the supraoptic nuclei, vasopressin-cells mostly located in the ventral part, and oxytocin-cells in the dorsal part. The data demonstrated that the special distributed patterns of vasopressin- and oxytocin-neuron network have formed in those two nuclei at least from preterm. Intracerebroventricular injection of angiotensin II significantly increased fetal plasma oxytocin and vasopressin levels at preterm, which was associated with an increase of oxytocin- and vasopressin-neuron activity marked with c-fos expression. The data provided new evidence for the structural and functional development of the oxytocin- and vasopressin-network before birth.

• MeSH
• Angiotensin II administration & dosage   MeSH
• Arginine Vasopressin blood   metabolism   MeSH
• Time Factors MeSH
• Gestational Age MeSH
• Injections, Intraventricular MeSH
• Nerve Net embryology   metabolism   MeSH
• Neurons drug effects   metabolism   MeSH
• Paraventricular Hypothalamic Nucleus drug effects   embryology   metabolism   MeSH
• Supraoptic Nucleus drug effects   embryology   metabolism   MeSH
• Sheep MeSH
• Oxytocin blood   metabolism   MeSH
• Proto-Oncogene Proteins c-fos metabolism   MeSH
• Pregnancy MeSH
• Animals MeSH
• Check Tag
• Pregnancy MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Angiotensin II MeSH
• Arginine Vasopressin MeSH
• Oxytocin MeSH
• Proto-Oncogene Proteins c-fos MeSH

OBJECTIVE: Obesity represents a low-grade inflammatory disease and appears a risk factor for insulin resistance, but little is known on whether this may contribute to the development of autoimmune inflammatory diseases. The aim of this work was to study the early-life diet-induced obesity in Lewis rats which are known to be highly susceptible to autoimmunity. METHODS: Obesity was induced by reduced litter size (4 pups per litter) followed by high-fat diet (SHF rats). Control rats (8 pups per litter) were fed with standard diet (CN rats). Oral glucose tolerance test (3 g glucose per kg b.w.) was performed by intra-gastric tube in conscious rats after 12 h fast. Adipocyte size was assessed by light microscope after collagenase digestion. Hypothalamic arcuate (ARC) and paraventricular nuclei (PVN) were isolated by the punching technique. Target mRNAs were quantified by real-time PCR with the use of TaqMan probes and primers. Serum hormones (leptin, ghrelin, adiponectin, visfatin and insulin) were assayed by specific RIAs . RESULTS: During the experimental period SHF rats had the same body weight gain and caloric intake as CN rats. At the age of 8 weeks SHF rats showed increased epididymal fat mass and adipocyte volume, impaired glucose tolerance, normal basal fasting insulin, visfatin, and ghrelin level, but decreased adiponectin and high leptin level. In the ARC, the SHF rats showed increased expression of mRNA for orexigenic neuropeptide Y (NPY), agouti-related protein (AgRP) and anorexigenic pro-inflammatory cytokine IL-6. In the PVN, the SHF rats showed increased expression of mRNA for anorexigenic melanocortin 4 receptor (MC4R) and IL-6. CONCLUSION: Overexpression of orexigenic NPY and AgRP in the ARC indicates leptin resistance in SHF rats. The increased expression of MC4R in PVN points to the activation of melanocortin anorexigenic system which, along with increased hypothalamic IL-6, might prevent the animals from overfeeding. Higher adiposity in these rats results from the high fat-diet composition and not from increased caloric intake. Furthermore, enhanced leptin production appears the main factor indicating the predisposition to autoimmunity in these overfed rats.

• MeSH
• Adiponectin blood   MeSH
• Adiposity MeSH
• Agouti-Related Protein genetics   metabolism   MeSH
• Analysis of Variance MeSH
• Adipose Tissue, White cytology   MeSH
• Adipocytes, White MeSH
• Dietary Fats administration & dosage   MeSH
• Energy Intake MeSH
• Gene Expression MeSH
• Ghrelin blood   MeSH
• Interleukin-6 genetics   metabolism   MeSH
• Insulin blood   MeSH
• Rats MeSH
• Leptin blood   MeSH
• RNA, Messenger metabolism   MeSH
• Neuropeptide Y genetics   metabolism   MeSH
• Nicotinamide Phosphoribosyltransferase blood   MeSH
• Arcuate Nucleus of Hypothalamus metabolism   MeSH
• Paraventricular Hypothalamic Nucleus metabolism   MeSH
• Obesity genetics   metabolism   MeSH
• Area Under Curve MeSH
• Glucose Intolerance MeSH
• Rats, Inbred Lew MeSH
• Receptor, Melanocortin, Type 4 genetics   metabolism   MeSH
• Appetite Regulation physiology   MeSH
• Aging MeSH
• Feeding Behavior MeSH
• Body Weight MeSH
• Cell Size MeSH
• Litter Size MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Adiponectin MeSH
• Agouti-Related Protein MeSH
• Dietary Fats MeSH
• Ghrelin MeSH
• Interleukin-6 MeSH
• Insulin MeSH
• Leptin MeSH
• RNA, Messenger MeSH
• Neuropeptide Y MeSH
• Nicotinamide Phosphoribosyltransferase MeSH
• Receptor, Melanocortin, Type 4 MeSH

BACKGROUND: CART (cocaine- and amphetamine-regulated transcript) peptide and cholecystokinin (CCK) are neuromodulators involved in feeding behavior. This study is based on previously found synergistic effect of leptin and CCK on food intake and our hypothesis on a co-operation of the CART peptide and CCK in food intake regulation and Fos activation in their common targets, the nucleus tractus solitarii of the brainstem (NTS), the paraventricular nucleus (PVN), and the dorsomedial nucleus (DMH) of the hypothalamus. RESULTS: In fasted C57BL/6 mice, the anorexigenic effect of CART(61-102) in the doses of 0.1 or 0.5 microg/mouse was significantly enhanced by low doses of CCK-8 of 0.4 or 4 microg/kg, while 1 mg/kg dose of CCK-A receptor antagonist devazepide blocked the effect of CART(61-102) on food intake. After simultaneous administration of 0.1 microg/mouse CART(61-102) and of 4 microg/kg of CCK-8, the number of Fos-positive neurons in NTS, PVN, and DMH was significantly higher than after administration of each particular peptide. Besides, CART(61-102) and CCK-8 showed an additive effect on inhibition of the locomotor activity of mice in an open field test. CONCLUSION: The synergistic and long-lasting effect of the CART peptide and CCK on food intake and their additive effect on Fos immunoreactivity in their common targets suggest a co-operative action of CART peptide and CCK which could be related to synergistic effect of leptin on CCK satiety.

• MeSH
• Hormone Antagonists pharmacology   MeSH
• Benzodiazepinones pharmacology   MeSH
• Devazepide pharmacology   MeSH
• Phenylurea Compounds pharmacology   MeSH
• Thinness * MeSH
• Injections, Intraperitoneal MeSH
• Injections, Intraventricular MeSH
• Cocaine- and Amphetamine-Regulated Transcript Protein MeSH
• Mice, Inbred C57BL MeSH
• Mice MeSH
• Neurons drug effects   metabolism   MeSH
• Dorsomedial Hypothalamic Nucleus drug effects   physiology   MeSH
• Paraventricular Hypothalamic Nucleus drug effects   physiology   MeSH
• Solitary Nucleus drug effects   physiology   MeSH
• Exploratory Behavior drug effects   physiology   MeSH
• Peptide Fragments pharmacology   MeSH
• Nerve Tissue Proteins pharmacology   MeSH
• Proto-Oncogene Proteins c-fos metabolism   MeSH
• Receptor, Cholecystokinin A antagonists & inhibitors   MeSH
• Receptor, Cholecystokinin B antagonists & inhibitors   MeSH
• Appetite Regulation drug effects   physiology   MeSH
• Sincalide pharmacology   MeSH
• Drug Synergism MeSH
• Dose-Response Relationship, Drug MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Hormone Antagonists MeSH
• Benzodiazepinones MeSH
• Devazepide MeSH
• Phenylurea Compounds MeSH
• Cocaine- and Amphetamine-Regulated Transcript Protein MeSH
• L 365260 MeSH Browser
• Peptide Fragments MeSH
• Nerve Tissue Proteins MeSH
• Proto-Oncogene Proteins c-fos MeSH
• Receptor, Cholecystokinin A MeSH
• Receptor, Cholecystokinin B MeSH
• Sincalide MeSH

Cerebellum is a profound structure of the central nervous system. Human cerebellum weighs about 150 g which represents around 10% of the total weight of the brain. It receives main input from sensory systems but the cerebellum functions as a part of the motor system. The cerebellum contributes by only few direct connections to motoneurons (therefore it cannot initiate any motor activity) but it projects profusely to all major motor control regions of the cerebral cortex. The cerebellum acts as a controller and coordinator. It compares movement intention with, performance and coordinates the equilibrium, posture and muscle tone necessary for the smooth coordinated motor activity. The number of input projections which exceed considerably the output ones (40:1) speaks out of an enormous analytical and synthetic capacity of the cerebellum. Interneuronal transmission of informations and carriage of afferent and efferent signals are provided by wide variety of chemical messengers (amino acids, biogenic amines and neuropeptides) of the local origin or delivered from the precerebellar nuclei. Direct and reciprocal connections between the hypothalamus and cerebellum have anatomically been well documented but monosynaptic contacts between the cerebellum and the hypothalamic paraventricular nucleus have not been approved yet. Cerebellum can respond to stress, however, this response may not be related only to the primary effect of the stressor but also to its consequences.

• MeSH
• Afferent Pathways MeSH
• Efferent Pathways MeSH
• Stress, Physiological metabolism   physiopathology   MeSH
• Humans MeSH
• Cerebellum anatomy & histology   metabolism   physiology   physiopathology   MeSH
• Cerebellar Nuclei anatomy & histology   MeSH
• Neurotransmitter Agents metabolism   MeSH
• Paraventricular Hypothalamic Nucleus anatomy & histology   physiology   MeSH
• Receptors, Neurotransmitter metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• English Abstract MeSH
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Neurotransmitter Agents MeSH
• Receptors, Neurotransmitter MeSH

Daily rhythm of arginine vasopressin (AVP) mRNA levels in the suprachiasmatic nucleus (SCN) of rats maintained under a short, LD 8:16 photoperiod differed from that of rats maintained under a long, LD 16:8 photoperiod: under the short photoperiod the morning AVP rise occurred significantly later than under the long one. Daily profiles of AVP mRNA in the supraoptic and paraventricular nuclei were not rhythmic and AVP mRNA levels under LD 8:16 did not differ from those under LD 16:8. The data indicate that photoperiod affects selectively the clock driven AVP gene expression in the SCN.

• MeSH
• Arginine Vasopressin genetics   MeSH
• Circadian Rhythm genetics   MeSH
• Photoperiod * MeSH
• Transcription, Genetic * MeSH
• Rats MeSH
• RNA, Messenger analysis   MeSH
• Paraventricular Hypothalamic Nucleus metabolism   MeSH
• Suprachiasmatic Nucleus metabolism   MeSH
• Supraoptic Nucleus metabolism   MeSH
• Rats, Wistar MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Arginine Vasopressin MeSH
• RNA, Messenger MeSH

The thyrotropin-releasing hormone (TRH) is a molecule with widespread distribution through many organ systems. The function of TRH is probably not identical in each system so that TRH synthesis and secretion may be unique for each system under specific experimental conditions. The present study was designed to explore the common and diverse features of the regulation of TRH encoded with the same gene in two different organs: hypophysiotropic hypothalamus and pancreatic islets. During in vitro incubation, the TRH content in hypothalamic structures remained stable while that in isolated pancreatic islets increased sharply. In contrast to the pancreatic islets, exposure to different concentrations of D-glucose did not affect TRH release from the hypothalamic paraventricular nucleus or median eminence. This divergence in the regulation of the hypophysiotropic and pancreatic TRH systems may be related to differences in the role of TRH produced in these tissues.

• MeSH
• Potassium Chloride pharmacology   MeSH
• Median Eminence drug effects   metabolism   MeSH
• Glucose pharmacology   MeSH
• Thyrotropin-Releasing Hormone metabolism   MeSH
• Hypothalamus drug effects   metabolism   MeSH
• Rats MeSH
• Cells, Cultured MeSH
• Islets of Langerhans drug effects   metabolism   MeSH
• Paraventricular Hypothalamic Nucleus drug effects   metabolism   MeSH
• Rats, Wistar MeSH
• Calcium pharmacology   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Potassium Chloride MeSH
• Glucose MeSH
• Thyrotropin-Releasing Hormone MeSH
• Calcium MeSH

New information has accrued from in vivo microdialysis studies about stress-related changes in norepinephrine concentrations in extracellular fluid of the paraventricular nucleus (PVN) and the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. Our data on the effects of lower brainstem hemisections show that paraventricular noradrenergic terminals are derived mainly from medullary A1 and A2 catecholaminergic cells. The activation of these cells contributes importantly to stress-induced noradrenergic activation in the paraventricular nucleus of conscious animals. The results from brainstem hemisection experiments also indicate that baseline levels and immobilization-induced increments in corticotropin-releasing hormone (CRH) mRNA expression in the PVN depend on ipsilaterally ascending medullary tract. Thus, the prevalent concept that stress-induced noradrenergic activation of the HPA axis depends mainly on activation of locus ceruleus noradrenergic neurons requires re-evaluation. Our new stress concepts favor stressor-specific activation of the HPA axis. The present data also suggest the existence of stressor-specific central pathways that differentially participate in the regulation of sympathoneuronal and adrenomedullary outflows as well as of the activity of the HPA axis. Furthermore, the results are inconsistent with a founding tenet of Selye's stress theory, the doctrine of nonspecificity, which defines stress as the nonspecific response of the body to any demand. We expect that future studies in this area will focus on further examination of the notion of stressor-specific patterns of central neurotransmitter release and elucidate the genetic bases of these patterns.

• MeSH
• Adrenocorticotropic Hormone metabolism   MeSH
• Stress, Physiological metabolism   physiopathology   MeSH
• Humans MeSH
• Neurosecretory Systems physiology   MeSH
• Norepinephrine metabolism   MeSH
• Paraventricular Hypothalamic Nucleus physiology   MeSH
• Pituitary-Adrenal System physiology   MeSH
• Hypothalamo-Hypophyseal System physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Adrenocorticotropic Hormone MeSH
• Norepinephrine MeSH