UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used in situ hybridization and radio-immunoassay to compare temporal dynamics of components in the hypothalamo-pituitary limb of the hypothalamo-pituitary-adrenal axis during sustained hypovolemic stress in adrenalectomized (ADX) rats to those previously reported in intact animals. We asked three questions: first, does corticotropin-releasing hormone (CRH) gene transcription occur in neuroendocrine neurones of the hypothalamic paraventricular nucleus (PVH) of ADX rats, and if so, how is it temporally organized; second, what is the expression pattern of the vasopressin and other genes known to be colocalized in these neuroendocrine neurones; third, if adrenocorticotropin hormone (ACTH) secretion occurs, what is its temporal profile? We found that sustained hypovolemia evoked a brief episode of CRH gene transcription in ADX rats that occurred earlier than in intact rats. However, in contrast to saline-injected controls, this activation was not maintained because declines in CRH hnRNA and mRNA were seen as the stress continued. Although increased vasopressin gene transcription was not seen in intact hypovolemic rats, robust increases were measured throughout in ADX rats, suggesting that in the absence of corticosterone the vasopressin gene is transcribed preferentially to the CRH gene during sustained hypovolemia. c-fos and preproenkephalin mRNA profiles also exhibited earlier onsets compared to intact rats. Finally, the onset and duration of ACTH secretion was the same in ADX rats as previously reported in intact rats. Collectively, these data support two hypotheses regarding the actions of corticosterone. First, that it provides some form of facilitatory signal allowing neuroendocrine CRH transcriptional mechanisms to remain active during sustained hypovolemia. Second, that it strongly inhibits the response of the vasopressin gene to hypovolemic stress.
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PMID:Adrenalectomy dramatically modifies the dynamics of neuropeptide and c-fos gene responses to stress in the hypothalamic paraventricular nucleus. 1092 82

The 5-HT(2A/2C) agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI) stimulates hypothalamic neurons to increase the secretion of several hormones. This study addressed two questions: 1) are the neuroendocrine effects of DOI mediated via activation of 5-HT(2A) receptors; and 2) which neurons are activated by 5-HT(2A) receptors. The 5-HT(2A) antagonist (+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol (MDL 100,907; 0.001, 0.01, or 0.1 mg/kg, s.c.) was administered before rats were challenged with DOI (2.5 mg/kg, i.p.). MDL 100,907 produced a dose-dependent inhibition (ED(50) congruent with 0.001 mg/kg) of the effect of DOI on plasma levels of ACTH, corticosterone, oxytocin, prolactin, and renin without altering basal hormone levels. Complete blockade of the effect of DOI was achieved for all hormones at MDL 100,907 doses of 0.01-0.1 mg/kg. In a parallel experiment, DOI was injected 2 hr before killing to determine its effects on the expression of Fos, the product of the immediate early gene c-fos. DOI induced an increase in Fos immunoreactivity in corticotropin-releasing factor (CRF) and in oxytocin-expressing neurons but not in vasopressin-containing neurons in the hypothalamic paraventricular nucleus or CRF cells in the amygdala. Pretreatment with MDL 100,907 (0.1 mg/kg, s.c.) blocked the DOI-induced increase in Fos expression in all regions including the hypothalamus, amygdala (central and corticomedial), bed nucleus of the stria terminalis, and prefrontal cortical regions. The combined neuroanatomical and pharmacological observations suggest that the neuroendocrine responses to DOI are mediated by activation of neurons in the hypothalamic paraventricular nucleus and associated circuitry. Furthermore, selective activation of 5-HT(2A) receptors mediates the hormonal and Fos-inducing effects of DOI.
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PMID:5-HT2A receptors stimulate ACTH, corticosterone, oxytocin, renin, and prolactin release and activate hypothalamic CRF and oxytocin-expressing cells. 1133 86

We have previously proposed the existence of ultrashort loop-positive feedback regulation of corticotropin-releasing hormone (CRH) in the hypothalamus. To gain a better understanding of this effect, we performed double-label in situ hybridization to identify the neurons in the paraventricular nucleus (PVN) that express CRH type 1 receptor (CRH-R1) following stress. We also conducted immunohistochemistry to determine whether CRH-R1 mRNA was translated to CRH-R1 protein in the PVN. Thirty-minute restraint stress given to male Wistar rats increased c-fos mRNA expression primarily in the CRH-producing neurons of the parvocellular PVN. Small numbers of vasopressin and oxytoxin-producing cells were also labeled by c-fos probes. Approximately 70% of CRH-R1 positive neurons exhibited CRH mRNA 2 h after the beginning of stress, while only a small percentage of the vasopressin and oxytocin-producing cells coexpressed CRH-R1 mRNA. CRH-R1 immunoreactivity, which was detected in the perikarya and fibers of PVN neurons, appeared to increase in response to stress, though this was not statistically significant. Pretreatment with a selective CRH-R1 antagonist, CP-154,526, significantly attenuated stress-induced corticotropin (ACTH) secretion as well as c-fos mRNA expression in the PVN. These results demonstrate that acute stress increases neuronal activation and CRH-R1 mRNA expression primarily in CRH-producing neurons of the parvocellular PVN, that CRH-R1 message is translated to CRH-R1 protein, and that PVN neurons are activated at least in part through CRH-R1 under acute stress. The data further support the possibility of feedback regulation of CRH itself in CRH-producing neurons.
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PMID:Expression of corticotropin-releasing hormone type 1 receptor in paraventricular nucleus after acute stress. 1139 2

This issue of Peptides was inspired by a gathering of CCK researchers at the first Neuronal Cholecsytokinin Gordon Conference. The papers in this issue reflect the diversity of CCK research and demonstrate how the field has matured. Reviews describe the regulation of CCK gene expression and CCK release, the nature of the hormone binding site of the CCK A receptor, interaction of CCK, dopamine and GABA, the role of CCK in thermoregulation, sexual behavior and satiety in rodents and humans. The research articles document features of cardiovascular regulation, reduced cocaine sensitization and decreased satiety in rats that lack the CCK A receptor. Pro CCK processing in neuroblastoma cells and the elevation of CCK levels in CSF in a model of chronic pain are detailed in other articles. Three articles using different behavioral paradigms in rat and sheep examine CCK in learning and memory. Two articles that examine CCK in different behaviors that have a dopaminergic component are included. Other articles describe the interaction between a 5HT(3) antagonist and CCK-induced satiety and c-fos activation and document secretion of oxytocin and vasopressin in female patients and controls in response to CCK 4 administration. There is good reason to believe that the future is bright for research on CCK. With the organization of national and international meetings, CCK researchers have a forum for communication. Opportunities for cooperation and collaboration have never been better. The easy integration of academic basic and clinical science with industrial science bodes very well for the advancement of our understanding of the multiple roles that CCK plays in the brain and for the future development of CCK-based therapies.
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PMID:An introduction to neuronal cholecystokinin. 1145 11

The drinking behavior and the c-fos expression in rat brain induced by electrical stimulation of the subfornical organ (SFO) were examined. SFO stimulation induced stable and significant drinking behavior and Fos protein expression in 8 areas of the forebrain (organum vasculosum of the lamina terminalis, median preoptic nucleus, paraventricular nucleus, supraoptic nucleus, lateral hypothalamic area, perifornical dorsal area, substantia innominata and thalamic reunions nucleus), and in 3 areas of the hindbrain (area postrema, solitary tract nucleus and lateral parabrachial nucleus). In certain neurons of paraventricular and supraoptic nuclei, co-expression of Fos protein and vasopressin was induced by SFO stimulation. Intracerebroventricular injection of atropine partly blocked the SFO stimulation-induced drinking behavior and the Fos protein expression in the brain, suggesting that an M-cholinergic mechanism may be involved.
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PMID:[Cholinergic mechanism in the drinking behavior and c-fos expression in brain induced by subfornical organ stimulation in rats]. 1147 Dec 22

The subfornical organ (SFO) has been suggested to be important for water intake and secretion of vasopressin (AVP). However, the role of the SFO cholinergic mechanism in the control of body fluid regulation is not clear. This study determined the effects of local cholinergic stimulation in the SFO produced by administration of physostigmine on drinking and cellular excitation in the anterior third ventricle (AV3V) region and in the supraoptic and paraventricular nuclei (SON and PVN). The results showed that injection of physostigmine into the SFO induced water intake and c-fos expression in the AV3V area as well as in the AVP containing neurons in the hypothalamus. Pretreatment of the SFO with mecamylamine, a nicotinic receptor antagonist, had no effect on physostigmine induced behavioral and c-fos responses. The muscarinic receptor blocker atropine, however, abolished both drinking and cellular activation after injection of physostigmine into the SFO. Immunostaining experiments demonstrated positive acetyltransferase (ChAT) in the SFO. Intensive ChAT immunoreactivity was located in the cholinergic fibers in the SFO. Together, the results indicate that SFO cholinergic mechanisms are important in co-operation with the AV3V and hypothalamic neurons in the control of thirst and AVP-mediated body fluid homeostasis.
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PMID:Functional relationship between subfornical organ cholinergic stimulation and cellular activation in the hypothalamus and AV3V region. 1174 49

The suprachiasmatic nuclei (SCN) contain a master clock driving the majority of circadian rhythms in mammals. It is believed that the SCN confers circadian rhythmicity as well as light responsiveness to pineal melatonin secretion via a direct projection to the paraventricular nucleus of the hypothalamus (PVN). Neurons in the SCN respond to light during subjective night with an expression of the immediate early gene c-fos. The number and distribution of c-Fos protein-containing neurons depend on the zeitgeber time (ZT) at which the light stimulus is presented. To investigate whether this phase-dependent activity is present in the SCN output neurons targeting the PVN, we combined retrograde cholera toxin subunit B (ChB) tracing from the PVN with c-Fos immunohistochemistry. Male golden hamsters were injected iontophoretically with ChB into the PVN area and 7 days later given a 1.5-hr light stimulus at either ZT 14 or ZT 19 followed by vascular fixation. Light stimulation at ZT 19 gave rise to more c-Fos containing neurons in the SCN than light presented at ZT 14. Double immunostaining for ChB and c-Fos revealed that light stimulation at ZT 14 induced c-Fos expression in 26.6% +/- 2.8% of the retrogradely filled perikarya, whereas light-stimulation at ZT 19 increased this fraction to 40.7% +/- 1.9%. This demonstrates the presence of a phase-dependent c-Fos induction in the suprachiasmatic-paraventricular projection system. Triple immunohistochemistry showed that light-activated output neurons contained both gastrin-releasing peptide and vasoactive intestinal polypeptide and to a lesser extent vasopressin. The present findings provide functional evidence of light activation of central pathways involved in the regulation of circadian output rhythms.
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PMID:Light-induced c-Fos expression in suprachiasmatic nuclei neurons targeting the paraventricular nucleus of the hamster hypothalamus: phase dependence and immunochemical identification. 1175 66

The present study was conducted to investigate the pattern of neuronal activation and corticotropin-releasing hormone (CRH) expression in fed, food deprived and refed lean (Fa/?) and obese (fa/fa) Zucker rats. The pattern of neuronal activation was studied by measuring the expression of the immediate-early gene c-fos. Expression of c-fos and CRH mRNA was determined by in situ hybridization histochemistry. In both lean and obese rats, one hour of refeeding led to a transient increase in c-fos mRNA levels which was detected in the paraventricular hypothalamic nucleus (PVH), the dorsomedial hypothalamic nucleus, the supraoptic nucleus, the paraventricular thalamic nucleus, the central nucleus of amygdala (CeA), the lateral and medial parabrachial nuclei, the nucleus of the solitary tract, and the area postrema. In addition, refeeding led to strong activation of the arginine-vasopressin neurons located in the magnocellular part of the PVH. Following 24 h of food deprivation, CRH expression in the parvocellular division of the PVH was significantly higher in obese rats compared to lean animals. During refeeding, PVH CRH mRNA levels in obese rats decreased to reach control values. The decrease in CRH expression in obese rats was accompanied by the alleviation of the hypercorticosteronemia that characterized obese Zucker rats. CRH mRNA levels in the central nucleus of the amygdala were significantly higher in lean rats than in obese animals, when the rats were fed ad libitum During food deprivation, CeA CRH mRNA levels decreased in lean rats and gradually returned to predeprivation values during refeeding. In refed obese rats, CeA levels of CRH mRNA were higher than those of ad libitum fed or food-deprived obese mutants. In the perifornical region of the lateral hypothalamic area (LHA), the expression of CRH mRNA rose significantly in response to refeeding in lean rats, but not in obese animals. Following the first hour of refeeding, the number of neurons expressing CRH mRNA in the LHA in lean rats almost doubled. The present results demonstrate that refeeding has a stimulating effect in obese Zucker rats in a pattern of activation similar to that seen in lean Fa/? rats. They also demonstrate differences in CRH expression between Fa/? and fa/fa rats after refeeding. The most apparent of these differences was seen in the lateral hypothalamus in which refeeding failed to up-regulate CRH expression in obese rats.
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PMID:Neuronal activation and corticotropin-releasing hormone expression in the brain of obese (fa/fa) and lean (fa/?) Zucker rats in response to refeeding. 1191 62

We sought to identify the areas that have altered neuronal activity within the hypothalamus of diabetic rats by mapping neuronal expression of c-fos protein (Fos) and Fos-related antigens. After a standard PAP immunocytochemical protocol, Fos-like immunoreactivity was observed in the paraventricular nucleus (PVN), supraoptic nucleus (SON), median preoptic area (MnPO), anterior hypothalamus (AH) and posterior hypothalamus (PH) of control (vehicle; n=6) and diabetic rats (Sprague-Dawley rats injected with STZ 65 mg/kg/ip 4 weeks prior to the experiment; n=6). Blood glucose levels were significantly elevated in the diabetic group (370+/-8 mg/dl) compared to control group (104+/-3 mg/dl). Diabetic rats had a significantly higher number of Fos-positive cells in PVN (2.5x), SON (7x) and MnPO (2x) compared to the control rats. However, diabetic rats had significantly fewer Fos-positive cells in the AH (0.3x) and no difference was observed in the PH between the diabetic and control rats. Despite the elevated number of Fos-positive cells in the diabetic rats, dehydration (water withdrawal for 24 h) or hypertonic challenge (1.5 ml of 0.1 M NaCl i.p. injection) produced a further increase in the number of Fos-positive cells in the PVN, SON and MnPO. Dehydration did not alter the number of Fos-positive cells in the AH or PH, but hypertonic challenge produced a significant increase in the Fos-positive cells in both the AH and PH of diabetic rats. This study demonstrates that: (1) there is increased basal neuronal activity in the PVN, SON and MnPO, a decrease in neuronal activity in the AH and no change in neuronal activity in the PH as indicated by Fos staining in diabetic rats; and (2) dehydration or hypertonic challenge produces a further increase in the number of Fos-positive cells in the PVN, SON, and MnPO which is comparable to control rats. These data support the conclusion that vasopressin producing neurons in the PVN and SON and autonomic areas within the lamina terminalis and hypothalamus are activated during diabetes and may contribute to the elevated levels of vasopressin and autonomic dysfunction during diabetes.
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PMID:Neuronal expression of fos protein in the forebrain of diabetic rats. 1244 95

The median preoptic nucleus (MePO) has been suggested to be an important area in the brain for the regulation of vasopressin (VP) release under the condition of osmotic stimulation. Fos immunoreactivity (Fos-ir), choline acetyltransferase (ChAT) immunoreactivity and retrograde labeling with fluoro-gold were used in this study to determine whether cholinergic neurons in the MePO can be activated by hypertonic NaCl, and to characterize the specific MePO cells that have anatomic projections to the supraoptic nuclei (SON). The results showed that c-fos expression specifically induced by hypertonic NaCl was found in the ChAT cells of the MePO. A retrograde tracing experiment demonstrated that the MePO neurons projecting to the SON were cholinergic. In addition, hypertonic saline-induced Fos-ir was colocalized with the MePO neurons back labeled with fluoro-gold from the SON. Together, these data provide evidence that the MePO cholinergic neurons are activated by osmotic stimulation, and suggest that cholinergic cells in the MePO are functionally important in the control of the SON neurons under the condition of hypertonic stimulation.
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PMID:Functional and anatomic relationship between cholinergic neurons in the median preoptic nucleus and the supraoptic cells. 1257 77

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