scholarly journals Effects of Cholecystokinin in the Supraoptic Nucleus and Paraventricular Nucleus are Negatively Modulated by Leptin in 24-h Fasted Lean Male Rats

2010 ◽  
Vol 22 (5) ◽  
pp. 446-452 ◽  
Author(s):  
C. Caquineau ◽  
A . J. Douglas ◽  
G. Leng
Keyword(s):  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Male Rats

Release of oxytocin and vasopressin by magnocellular nuclei in vitro: specific facilitatory effect of oxytocin on its own release

1984 ◽  
Vol 102 (1) ◽  
pp. 63-NP ◽  
Author(s):  
F. Moos ◽  
M. J. Freund-Mercier ◽  
Y. Guerné ◽  
J. M. Guerné ◽  
M. E. Stoeckel ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Male Rats ◽  
Facilitatory Effect ◽  
Vasopressin Release ◽  
Paraventricular Nuclei ◽  
Magnocellular Nuclei ◽  
Oxytocin Release ◽  
Supraoptic Nuclei

ABSTRACT The release of endogenous oxytocin and vasopressin by rat paraventricular and supraoptic nuclei in vitro during a 10-min period, 30 min after beginning the incubation, was measured radioimmunologically. Mean basal hormone release per 10 min and per pair of nuclei was: 128·4 ± 12·4 (s.e.m.) pg vasopressin (n = 15) and 39·0 ± 3·0 pg oxytocin (n = 66) for supraoptic nuclei from male rats; 273·9 ± 42·6 pg vasopressin (n = 11) and 34·2 ± 3·5 pg oxytocin (n = 15) for supraoptic nuclei from lactating rats; 70·0 ± 8·6 pg vasopressin (n = 52) and 21·8 ± 1·3 pg oxytocin (n = 68) for paraventricular nuclei from male rats; 59·1 ± 8·6 pg vasopressin (n = 10) and 27·0 ± 4·6 pg oxytocin (n = 16) for paraventricular nuclei from lactating rats. In male and lactating rats, both nuclei contained and released more vasopressin than oxytocin. For oxytocin alone, the paraventricular nucleus of male rats contained and released significantly less hormone than the supraoptic nucleus. This difference was not apparent in lactating rats. For vasopressin alone, the paraventricular nucleus contained and released significantly less hormone than the supraoptic nucleus in both male and lactating rats. When the hormone released was calculated as a percentage of the total tissue content the release was about 0·9% for oxytocin from both nuclei in male and lactating rats and also for vasopressin in lactating rats, but was only about 0·5% for vasopressin from both nuclei in male rats. The influence of oxytocin and analogues of oxytocin (including one antagonist) upon the release of oxytocin and vasopressin was studied. Adding oxytocin to the incubation medium (0·4–4 nmol/l solution) induced a dose-dependent rise in oxytocin release from both nuclei of male or lactating rats. A 4 nmol/l solution of isotocin had a similar effect to a 0·4 nmol/l solution of oxytocin, but arginine-vasopressin never affected basal release of oxytocin. In no case was vasopressin release modified. An oxytocin antagonist (1 μmol/l solution) significantly reduced basal oxytocin release and blocked the stimulatory effect normally induced by exogenous oxytocin, as did gallopamil hydrochloride (D600, 10 μmol/l solution), a Ca2+ channel blocker, or incubation in a Ca2+-free medium. These findings are discussed in relation to the literature on the central effects of neurohypophysial peptides. It may be concluded that the regulatory role of endogenous oxytocin in the hypothalamus on the milk-ejection reflex could result from its local release in the extracellular spaces of magnocellular nuclei. J. Endocr. (1984) 102, 63–72

THE RELATION BETWEEN THE HYPOTHALAMIC NEUROSECRETION AND THE CORTICOTROPHIN RELEASE IN EXPERIMENTAL CONDITIONS

1960 ◽  
Vol XXXIV (I) ◽  
pp. 8-18 ◽  
Author(s):  
E. Kivalo ◽  
U. K. Rinne
Keyword(s):  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Supraoptic Nucleus ◽  
Acute Stress ◽  
Neurosecretory Material ◽  
Experimental Conditions ◽  
Hypothalamic Cells ◽  
The One ◽  
Hypophysial Portal ◽  
Acth Release

ABSTRACT Acute stress, chronic stress plus hydration, cortisone treatment, cortisone treatment plus dehydration were used as methods of investigation and the relation between the neurosecretory activity of the hypothalamic supraoptic nucleus and paraventricular nucleus and the neurosecretory material around the hypophysial portal vessels of the median eminence on the one hand and the corticotrophin release on the other hand, has been studied in the rat. Whereas stress stimulates both the activity of the above mentioned cells of the hypothalamus and the ACTH release, stress plus hydration causes a depression of these hypothalamic cells but nevertheless causes a marked ACTH release. Cortisone inhibits the activity of the cells in the supraoptic nucleus and the paraventricular nucleus as well as the ACTH release whereas cortisone plus dehydration causes stimulation but inhibits the ACTH release. In some stress and cortisone treatment groups the variations of the neurosecretory material around the hypophysial portal vessels and of the ACTH release were found to show a correlation. It is concluded that the activity of the cells of the supraoptic nucleus and the paraventricular nucleus and the ACTH release do not seem to have any definite connection, whereas some observations indicate that the neurosecretory material in the region of the median eminence around the hypophysial portal vessels may have some significance in ACTH release.

109 Chemogenetic silencing of corticotropin releasing factor neurons in the paraventricular nucleus: the effect on post-stress sleep

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A45-A45
Author(s):  
Irma Gvilia ◽  
Sunil Kumar ◽  
Dennis McGinty ◽  
Ronald Szymusiak
Keyword(s):  
Paraventricular Nucleus ◽  
Nrem Sleep ◽  
Corticotropin Releasing Factor ◽  
Male Rats ◽  
Male Rat ◽  
Sleep Onset Latency ◽  
Post Surgery ◽  
Crf Neurons ◽  
Emg Electrodes ◽  
Post Stress

Abstract Introduction We have previously shown that pharmacological elevation of corticotropin releasing factor (CRF) signaling in the brain results in exacerbation of sleep disturbances evoked by the exposure of rats to an acute stressor, the dirty cage of a male rat. In the present study we (1) assessed wake-sleep behavior of mice after the exposure to the dirty cage stress paradigm, and (2) examined the effect of chemogenetic silencing of CRF neurons in the hypothalamic paraventricular nucleus (PVN) on sleep occurring following the exposure to this stressor. Methods First, a group of mice (n=12) was implanted with EEG/EMG electrodes. In two weeks, post-surgery, six mice were transferred to dirty cages of male rats and recorded for 24 hours. Control mice were transferred to clean cages. In the second study, a group of CRF-ires-cre mice (n=8) received bilateral injections of AAV-hSyn-DIO-hM4Di-mCherry targeting the PVN. The other group of CRF-ires-cre mice (n=8) was injected AAV-hSyn-DIO-mCherry (control vector). All mice were implanted with EEG/EMG electrodes. Dirty cage experiments were started following a 4-week postsurgical period to allow gene recombination and expression. Mice were subjected to intraperitoneal (IP) administration of clozapine-n-oxide (CNO; 3 mg/kg) at ZT1, placed into dirty cages, and recorded for post-stress sleep. Results: Results In mice expressing hM4Di inhibitory DREADDs (designer receptors activated by designer drugs) versus mice injected with control AAV, IP CNO (3 mg/kg) resulted in a significant decrease of post-stress sleep onset latency, decrease of time spent in wakefulness (first hour, 74±5.3 vs. 89±11.0, second hour, 37.2±10.3% vs. 81.3±9.3%; third hour, 40.1±3.3% vs. 47.1±14.3%; fourth hour, 44.4±6.0 vs. 55.5±9.9), and increase in non-rapid eye movement (NREM) sleep time (26.0±5.4% vs. 11.0±11.1%; 62.8%±9.8 vs. 18.7 ± 9.6%; 59.9±3.2% vs. 52.9±14.5%; 55.6±6.2 vs. 44.5±10.0). The hM4Di expressing mice exhibited longer episodes of NREM sleep, compared to mice injected with control AAV (first hour, 133.3±80.1sec vs. 21±1.7sec; second hour, 43256±83.4sec vs. 73.5±44.1sec; third hour, 459.2±139.8sec vs. 139±80.6sec; fourth hour, 233.1±82.6sec vs. 190±72.3sec). Conclusion Chemogenetic silencing of CRF neurons in the PVN attenuates acute stress-induced sleep disturbance in mice. Support (if any) Supported by Department of Veterans Affairs Merit Review Grant # BX00155605 and SRNSF (Georgia) grant FR-18-12533

Effect of different types of stressors on peptide messenger ribonucleic acids in the hypothalamic paraventricular nucleus

1993 ◽  
Vol 128 (6) ◽  
pp. 485-492 ◽  
Author(s):  
Sandra Ceccatelli ◽  
Catello Orazzo
Keyword(s):  
Paraventricular Nucleus ◽  
Immobilization Stress ◽  
Thyrotropin Releasing Hormone ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Ribonucleic Acids ◽  
Releasing Hormone ◽  
Different Types

Using in situ hybridization we have studied the effects of different types of stressors, such as ether, immobilization, cold and swimming, on the expression of several peptide messenger ribonucleic acids (mRNAs) in the hypothalamic paraventricular nucleus of adult male rats. Paraventricular nucleus sections were hybridized using synthetic oligonucleotide probes complementary to mRNA for corticotropin-releasing hormone, neurotensin, enkephalin and thyrotropin-releasing hormone. A clear upregulation of neurotensin mRNA was seen after ether and, to a lesser extent, after immobilization stress, whereas after the two other stressors neurotensin mRNA was undetectable, as in control rats. An increase in enkephalin mRNA was observed in a selective region of the dorsal part of the medioparvocellular subdivision of the paraventricular nucleus only after ether and immobilization stress. No significant changes were seen in corticotropin-releasing hormone and thyrotropin-releasing hormone mRNA levels in any of the experimental paradigms. The present results show selective changes for various peptide mRNAs in the paraventricular nucleus after various types of stress. Significant effects could be demonstrated only on neurotensin and enkephalin mRNA after ether and immobilization stress. This suggests that adaptive changes in the rate of synthesis, processing and transport of the peptide may develop over a longer period of time.

Extra-cellular dopamine increases in the paraventricular nucleus of male rats during sexual activity

2003 ◽  
Vol 17 (6) ◽  
pp. 1266-1272 ◽  
Author(s):  
Maria Rosaria Melis ◽  
Salvatora Succu ◽  
Maria Stefania Mascia ◽  
Luca Cortis ◽  
Antonio Argiolas
Keyword(s):  
Sexual Activity ◽  
Paraventricular Nucleus ◽  
Male Rats

Hypothalamic paraventricular nucleus lesions do not prevent anorectic effect of exercise in male rats

1990 ◽  
Vol 259 (3) ◽  
pp. R579-R584 ◽  
Author(s):  
S. Rivest ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Paraventricular Nucleus ◽  
Wistar Rats ◽  
Energy Gain ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Serum Corticosterone ◽  
Male Wistar Rats

The effects of a hypothalamic paraventricular nucleus (PVN) lesion on energy balance were investigated in exercise-trained rats. Male Wistar rats weighing initially 250 g were divided into four groups. Two groups of rats underwent a bilateral PVN lesion, whereas the two remaining groups were sham operated. The PVN lesions were done electrolytically. One group from each surgical treatment was exercised, while the other group was kept in sedentary conditions. Rats were exercised on a rodent motor-driven treadmill at moderate intensity, 1 h/day for 21 consecutive days. Food intake and body weight were measured each day during the study. At the end of the treatment period, rats were killed, and carcasses were analyzed for their energy content. Serum corticosterone was measured by a competitive protein-binding assay. Energy gain and energy intake were lower in exercised rats than in sedentary controls, regardless of whether they were sham or PVN lesioned. Concurrently, there was no difference in the energy gain between PVN-lesioned and sham-operated rats, despite the fact that PVN-lesioned rats ended the experiment with a larger body weight than the sham-lesioned animals. Serum corticosterone levels were lower in PVN-lesioned rats than in sham-lesioned rats. In conclusion, the present results indicate that the PVN, the hypothalamic nucleus predominantly controlling the pituitary-adrenal axis activity, is not a prominent structure in the regulation of energy balance in exercised male Wistar rats.

scholarly journals LGR4 and Its Ligands, R-Spondin 1 and R-Spondin 3, Regulate Food Intake in the Hypothalamus of Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (2) ◽  
pp. 429-440 ◽  
Author(s):  
Ji-Yao Li ◽  
Biaoxin Chai ◽  
Weizhen Zhang ◽  
Danielle M. Fritze ◽  
Chao Zhang ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Energy Homeostasis ◽  
Male Rats ◽  
The Third ◽  
The Brain

The hypothalamus plays a key role in the regulation of feeding behavior. Several hypothalamic nuclei, including the arcuate nucleus (ARC), paraventricular nucleus, and ventromedial nucleus of the hypothalamus (VMH), are involved in energy homeostasis. Analysis of microarray data derived from ARC revealed that leucine-rich repeat-containing G protein-coupled receptor 4 (LGR4) is highly expressed. LGR4, LGR5, and LGR6 form a subfamily of closely related receptors. Recently, R-spondin (Rspo) family proteins were identified as ligands of the LGR4 subfamily. In the present study, we investigated the distribution and function of LGR4–LGR6 and Rspos (1–4) in the brain of male rat. In situ hybridization showed that LGR4 is expressed in the ARC, VMH, and median eminence of the hypothalamus. LGR4 colocalizes with neuropeptide Y, proopiomelanocortin, and brain-derived neurotrophic factor neurons. LGR5 is not detectable with in situ hybridization; LGR6 is only expressed in the epithelial lining of the lower portion of the third ventricle and median eminence. Rspo1 is expressed in the VMH and down-regulated with fasting. Rspo3 is expressed in the paraventricular nucleus and also down-regulated with fasting. Rspos 1 and 3 colocalize with the neuronal marker HuD, indicating that they are expressed by neurons. Injection of Rspo1 or Rspo3 into the third brain ventricle inhibited food intake. Rspo1 decreased neuropeptide Y and increased proopiomelanocortin expression in the ARC. Rspo1 and Rspo3 mRNA is up-regulated by insulin. These data indicate that Rspo1 and Rspo3 and their receptor LGR4 form novel circuits in the brain to regulate energy homeostasis.

Sign in / Sign up

Export Citation Format

Share Document