Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The excitatory neurotransmitter glutamate is involved in the control of most, perhaps all, neuroendocrine systems, yet the sites of glutamatergic neurons and their processes are unknown. Here, we used in situ hybridization and immunohistochemistry for the neuron-specific vesicular glutamate transporter-2 (VGLUT2) to identify the neurons in female rats that synthesize the neurotransmitter glutamate as well as their projections throughout the septum-hypothalamus. The results show that glutamatergic neurons are present in the septum-diagonal band complex and throughout the hypothalamus. The preoptic area and ventromedial and dorsomedial nuclei are particularly rich in glutamatergic neurons, followed by the supraoptic, paraventricular, and arcuate nuclei, whereas the suprachiasmatic nucleus does not express detectable amounts of VGLUT2 mRNA. Immunoreactive neurites are seen in very high densities in all regions analyzed, particularly in the preoptic region, followed by the ventromedial, dorsomedial, and arcuate nuclei as well as the external layer of the median eminence, whereas the mammillary complex does not exhibit VGLUT2 immunoreactivity. Many VGLUT2 immunoreactive fibers also contained synaptophysin, suggesting that the transporter is indeed localized to presynaptic terminals. Together, the results identify glutamatergic cell bodies throughout the septum-hypothalamus in region-specific patterns and show that glutamatergic nerve terminals are present in very large numbers such that most neurons in these brain regions can receive glutamatergic input. We examined the GnRH system as an example of a typical neuroendocrine system and could show that the GnRH perikarya are closely apposed by many VGLUT2-immunoreactive boutons, some of which also contained synaptophysin. The presence of VGLUT2 mRNA-containing cells in specific nuclei of the hypothalamus indicates that many neuroendocrine neurons coexpress glutamate as neurotransmitter, in addition to neuropeptides. These systems include the oxytocin, vasopressin, or CRH neurons as well as many others in the periventricular and mediobasal hypothalamus. The presence of VGLUT2 mRNA in steroid-sensitive regions of the hypothalamus, such as the anteroventral periventricular, paraventricular, or ventromedial nuclei indicates that gonadal and adrenal steroid can directly alter the functions of these glutamatergic neurons.
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PMID:Distribution of vesicular glutamate transporter-2 messenger ribonucleic Acid and protein in the septum-hypothalamus of the rat. 1253 29

The functional significance of the novel estrogen receptor beta in brain areas that exclusively contain the ERbeta receptor subtype such as the paraventricular (PVN) and the supraoptic (SON) nuclei of the hypothalamus is not yet fully understood. The present study attempts to characterize the peptidergic nature of the ERbeta-containing neuronal population in the PVN and the SON using the double in situ histochemistry method in the female rat. Using this method, the ERbeta mRNA coexpressions with the novel opioid neuropeptide (orphanin FQ and its receptor ORL1) mRNA in addition to the previously reported neuropeptide (arginine vasopressin-AVP, oxytocin-OXY, corticotropin releasing hormone-CRH, enkephalin-ENK) mRNAs were assessed. In the PVN, roughly half of the ERbeta expression was colocalized with the prepro-orphanin FQ mRNA, which was comparable to the colocalization observed between the ERbeta and AVP mRNAs in the same region. In addition, there was 20% overlap between the ERbeta and ORL1 receptor mRNAs, and 10% overlap between the ERbeta and OXY mRNAs in the PVN. By contrast, the coexpression between the prepro-orphanin FQ and ERbeta mRNAs was less striking in the SON. Potential interactions between the ERbeta and the well-characterized AVP-OXY neurosecretory system as well as the novel OFQ-ORL1 opioid neuropeptide system may provide new leads for the functional significance of ERbeta, specifically in stress/autonomic responses.
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PMID:Colocalization of estrogen beta-receptor messenger RNA with orphanin FQ, vasopressin and oxytocin in the rat hypothalamic paraventricular and supraoptic nuclei. 1269 Apr 47

In the period before and after parturition, i.e., in pregnancy and lactation, a variety of neuroendocrine alterations occur that are accompanied by marked behavioral changes, including emotional responsiveness to external challenging situations. On the one hand, activation of neuroendocrine systems (oxytocin, prolactin) ensures reproduction-related physiological processes, but in a synergistic manner also ensures accompanying behaviors necessary for the survival of the offspring. On the other hand, there is a dramatic reduction in the responsiveness of neuroendocrine systems to stimuli not relevant for reproduction, such as the hypothalamo-pituitary-adrenal (HPA) axis responses to physical or emotional stimuli in both pregnant and lactating rats. With CRH being the main regulator of the HPA axis, downregulation of the brain CRH system may result in various behavioral, in particular emotional, adaptations of the maternal organisms, including changes in anxiety-related behavior. In support of this, the lactating rat becomes less emotionally responsive to novel situations, demonstrating reduced anxiety, and shows a higher degree of aggressive behavior in the test for agonistic behavior as well as in the maternal defense test. These changes in emotionality are independent of the innate (pre-lactation) level of anxiety and are seen in both rats bred for high as well as low levels of anxiety. Both brain oxytocin and prolactin, highly activated at this time, play a significant role in these behavioral and possibly also neuroendocrine adaptations in the peripartum period.
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PMID:Brain mechanisms underlying emotional alterations in the peripartum period in rats. 1276 45

Neuropeptides play an important role in the regulation of feeding behavior and obesity. The mechanisms for controlling food intake involve a complicated interplay between peripheral systems (including gustatory stimulation, gastrointestinal peptide secretion, and vagal afferent nerve responses) and central nervous system (CNS) neuropeptides and/or monoamines. These neuronal systems include neuropeptides (CRH, opioids, neuropeptide-Y (NPY) and peptide YY (PYY), vasopressin and oxytocin, CCK, and leptin) and monamines (serotonin, dopamine, norepinephrine). In addition to regulating eating behavior, a number of CNS neuropeptides participate in the regulation of neuroendocrine pathways. Thus, clinical studies have evaluated the possibility that CNS neuropeptide alterations may contribute to dysregulated secretion of the gonadal hormones, cortisol, thyroid hormones and growth hormone in the eating disorders. Most of the neuroendocrine and neuropeptide alterations apparent during symptomatic episodes of AN and BN tend to normalize after recovery. This observation suggests that most of the disturbances are consequences rather than causes of malnutrition, weight loss and/or altered meal patterns. Still, an understanding of these neuropeptide disturbances may shed light on why many people with AN or BN cannot easily "reverse" their illness and even after weight gain and normalized eating patterns, many individuals who have recovered from AN or BN have physiological, behavioral and psychological symptoms that persist for extended periods of time.
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PMID:A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa. 1276 12

Anorexia and Bulimia Nervosa are disorders of unknown etiology that invariably begin during adolescence and near in time to puberty in young women. These disorders are associated with aberrant eating behaviors, body image distortions, impulse and mood disturbances, as well as characteristic temperament and personality traits. It is well known that malnutrition produces changes in neuroendocrine function. More recently, disturbances in neuronal systems have been found to play a role in the modulation of feeding, mood, and impulse control. These neuronal systems include neuropeptides (CRH, opioids, neuropeptide-Y (NPY) and peptide YY (PYY), vasopressin and oxytocin, CCK, and leptin) and monoamines (serotonin, dopamine, norepinephrine). Disturbances of most of these neuronal systems have been found when people are ill with an eating disorder, but it was not certain whether they were a cause or consequence of symptoms. In order to address these questions, a growing number of studies have investigated whether neuromodulatory disturbances persist after recovery. Studies from several centers tend to show altered serotonin activity persists after prolonged normalization of weight, nutrition, and menstrual function, as do anxiety, obsessionality, and perfectionism. While there are fewer data, there may be persistent alterations of dopamine or some neuropeptides in some subjects in a recovered state. The inaccessibility of the central nervous system has made it difficult to understand brain and behavior. In the past decade, new tools, such as brain imaging, have offered the possibility of better characterization of complex neuronal function and behavior. Such studies have tended to consistently find that alterations of brain regions, such as the temporal lobe, occur in people who are ill with anorexia nervosa and appear to persist after some degree of weight gain and recovery. New imaging technology, that marries Positron Emission Tomography (PET) imaging with selective neurotransmitter radioligands, confirms that altered serotonin neuronal pathway activity persists after recovery from an eating disorder and supports the possibility that these psychobiological alterations might contribute to traits, such as increased anxiety or extremes of impulse control, that, in turn, may contribute to a vulnerability to the development of an eating disorder. In summary, studies of pathophysiology are starting to nominate new candidates for treatment leading to the possibility of finding effective treatments for this often chronic or fatal disorder.
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PMID:Neurotransmitter and imaging studies in anorexia nervosa: new targets for treatment. 1276 13

Oxytocin released within the brain under basal conditions and in response to stress is differentially involved in the regulation of the hypothalamo-pituitary-adrenal (HPA) axis. Because the HPA axis plays an important role in the regulation of wakefulness, central oxytocin may modulate sleep-wake behaviour. In the present vehicle-controlled study, we assessed the influence of a selective oxytocin receptor antagonist (des-Gly-NH2d(CH2)5 [Tyr(Me)2,Thr4] OVT; 0.75 microg/5 microl) or of synthetic oxytocin (0.1 microg and 1 microg/5 microl), infused into the lateral ventricle (i.c.v.), on the sleep pattern in male Wistar rats (n=7). Compared to vehicle, the oxytocin antagonist slightly but persistently increased wakefulness at the expense of all sleep states. This finding indicates that endogenous brain oxytocin promotes sleep. However, acute icv infusion of oxytocin delayed sleep onset latency, which resulted in a transient reduction of non-REMS and REMS, and augmented high-frequency activity in the electroencephalogram (EEG) within non-REMS. These observations agree with previous reports that icv oxytocin induces a state of arousal. Based on these findings, we postulate that oxytocin has a dual mechanism of action in dependence of the physiological state. Under basal, stress-free conditions, endogenous oxytocin may promote sleep. Conversely, the high brain levels of oxytocin after central oxytocin infusion may reflect a condition of stress accompanied by behavioural arousal and, possibly via an excitatory action on the CRH system, increase vigilance.
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PMID:Intracerebral oxytocin modulates sleep-wake behaviour in male rats. 1283 3

Prostaglandins have long been thought to play important roles in the mechanism of parturition. Here we review the involvement of prostaglandins in myometrial and cervical functions with emphasis on human labor and birth. In addition, the cellular sources of prostaglandins as well as their interactions with various other endocrine, paracrine and physical factors, such as oxytocin, corticotropin releasing hormone, nitric oxide, platelet activating factor, cytokines, endothelin and stretch are also addressed together with their potential role in the molecular reorganization of cervical structure associated with labor and delivery. Finally, the premier role of progesterone in pregnancy maintenance and parturition is juxtaposed with the proposed "fine-tuning", modulatory role of prostaglandins and the above listed factors in the regulation of parturition.
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PMID:Prostaglandins and the myometrium and cervix. 1468 94

Paraventricular (PVN) and supraoptic nuclei of the hypothalamus maintain homeostasis by modulating pituitary hormonal output. PVN and supraoptic nuclei contain five major cell types: oxytocin-, vasopressin-, CRH-, somatostatin-, and TRH-secreting neurons. Sim1, Arnt2, and Otp genes are essential for terminal differentiation of these neurons. One of their common downstream genes, Brn2, is necessary for oxytocin, vasopressin, and CRH cell differentiation. Here we show that Sim2, a paralog of Sim1, contributes to the expression of Trh and Ss genes in the dorsal preoptic area, anterior-periventricular nucleus, and PVN. Sim2 expression overlaps with Trh- and Ss-expressing cells, and Sim2 mutants contain reduced numbers of Trh and Ss cells. Genetically, Sim1 acts upstream of Sim2 and partially compensates for the loss of Sim2. Comparative expression studies at the anterior hypothalamus at early stages reveal that there are separate pools of Trh cells with distinctive molecular codes defined by Sim1 and Sim2 expression. Together with previous reports, our results demonstrate that Sim1 and Otp utilize two common downstream genes, Brn2 and Sim2, to mediate distinctive sets of neuroendocrine hormone gene expression.
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PMID:Sim2 contributes to neuroendocrine hormone gene expression in the anterior hypothalamus. 1498 28

Nociceptin/orphanin FQ (N/OFQ), a peptide closely related to dynorphin A, is the endogenous agonist of the NOP receptor that moderately increases food intake under various conditions. Its orexigenic properties are mediated by the brain circuitry. In the present review, we focus on discussing the nature of hyperphagic effects of N/OFQ with special emphasis on its function within feeding-related neural networks. Although some of N/OFQ's orexigenic effects resemble those induced by opioids, reward-dependent feeding appears to be affected in a different manner by agonists of the NOP and classical opioid receptors. Also, data suggest that N/OFQ may not only promote feeding initiation, but rather its role may be to inhibit signaling responsible for inhibition of consummatory behavior. Central systems involved in termination of feeding that seem to be influenced by N/OFQ encompass oxytocin, alpha-MSH, and CRH.
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PMID:Minireview: Characterization of influence of central nociceptin/orphanin FQ on consummatory behavior. 1504 61

Regulation of myometrial functions during gestation, labor and birth are in the forefront of research in reproductive sciences. The complexity of the problem is reflected by our scant understanding of the intimate cellular and molecular events underlying these phenomena, despite extensive efforts spanning several decades. Unlike other smooth muscles, the myometrium is, to a large extent, under hormonal control. Of these, the steroid hormones, progesterone and estrogen, play dominant roles in terms of uterine growth, the maintenance of quiescence during gestation and the preparation of the uterus for labor and delivery. In addition to steroid hormones, there are a number of factors that modulate myometrial contractility (oxytocin, prostaglandins, endothelin, platelet activating factor) and relaxation (corticotropin releasing hormone, prostacyclin, nitric oxide). Although notable advances have been made towards understanding some of the key steps in receptor signaling that define the actions of these factors, a good deal of new information is needed to fully understand this fundamental life process. Pharmaceutical agents have been used extensively to induce labor or to prolong pregnancy in the case of preterm labor that represents the major cause of perinatal morbidity and mortality. Because preterm labor is a syndrome of multiple etiologies, pharmacologic agents will have to be targeted accordingly. This review attempts to present a critical overview of these topics.
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PMID:Regulation of myometrial smooth muscle functions. 1532 Jul 59


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