Oxytocin in the central nervous system and sexual behaviour in male rats

1987 ◽  
Vol 414 (1) ◽  
pp. 133-137 ◽  
Author(s):  
Andy M. Hughes ◽  
Barry J. Everitt ◽  
Stafford L. Lightman ◽  
Kathryn Todd
Reproduction ◽  
2001 ◽  
pp. 915-924 ◽  
Author(s):  
L Pinilla ◽  
LC Gonzalez ◽  
F Gaytan ◽  
M Tena-Sempere ◽  
E Aguilar

Selective oestrogen receptor modulators constitute a family of drugs that are used increasingly in the management of oestrogen-associated pathology. Raloxifene is a selective oestrogen receptor modulator that is used to treat and prevent osteoporosis in post-menopausal women. The actions of raloxifene on bone, breast, uterus and serum cholesterol concentrations have been widely analysed, but very few studies have investigated the possible actions of this drug on the central nervous system. The central nervous system of the newborn rat is very sensitive to oestrogen action. In this study a series of experiments was conducted to analyse the effects of different doses of raloxifene (50, 100, 250 or 500 microg per rat per day) administered to neonatal rats on days 1-5 of age. Female rats treated with raloxifene showed decreased gonadotrophin secretion, hyperprolactinaemia, advanced vaginal opening, decreased body weight, persistent presence of cornified epithelial cells in vaginal smears, anovulation, inhibition of positive feedback between oestradiol and LH, and infertility. Male rats showed delayed balanopreputial separation, reduced body weight and hyperprolactinaemia. All these changes resemble those obtained after neonatal administration of oestradiol benzoate, thus indicating, for the first time, that raloxifene exerts an oestrogenic action on the hypothalamic-pituitary structures controlling reproductive function in rats.


2009 ◽  
Vol 181 (4S) ◽  
pp. 81-82
Author(s):  
Yoshiji Miwa ◽  
Keiko Nagase ◽  
Taisei Kaneda ◽  
Nobuyuki Oyama ◽  
Hironobu Akino ◽  
...  

1951 ◽  
Vol 7 (3) ◽  
pp. 271-279 ◽  
Author(s):  
J. T. EAYRS

The growth of the body and central nervous system and the emergence of stereotyped behaviour have been studied in male and female rats during the first 24 days of life. The effects of daily injections of equine gonadotrophin on these measures have also been investigated. The weight of the body and of the central nervous system was significantly less in the female than in the male. The daily administration of 10 i.u. of equine gonadotrophin was without effect on either. The movements of the trunk and limbs concerned in the body-righting reflex became coordinated more slowly in the gonadotrophin-injected animals than in their litter-mate controls. At 15 days old, male rats were able to right in mid-air more successfully than litter-mate females. The placing reflex appeared earlier in the male than in the female. Its appearance was accelerated in the females given gonadotrophin, but not in the males. In the ventral funiculus of the spinal cord of 24-day-old experimental animals, the axis cylinders occupied more space relative to that occupied by myelin than did those of the controls. The total amount of myelin present was unchanged. There was no sex difference in the progress of myelination in the spinal cord. The significance of these findings in relation to the secretion of sex hormones is discussed. It is suggested that the secretion of androgen may be responsible for an acceleration of nervous maturation.


2021 ◽  
Author(s):  
Yoshimitsu Kanai ◽  
Takao Ito ◽  
Yuta Yamamoto ◽  
Naoko Yamagishi

Abstract The central nervous system receives body energy information and controls feeding behavior and lipogenesis1. Ghrelin, insulin, leptin and vagal afferents transmit the status of fasting, blood glucose, body fat, and food intake, respectively2-5. Estrogen, which is secreted from adipocytes and gastric parietal cells and from the ovaries in females, also acts upon the central nervous system and liver to inhibit feeding behavior and lipogenesis6-9. How blood triglyceride levels are monitored and how estrogen levels are regulated from the perspective of the lipid homeostasis is not well understood. Using male rats, we show that gastric parietal cells secrete estrogen in response to blood triglyceride levels. Parietal cells predominantly use fatty acid as an energy source. When male rats are administered olive oil or glucose, blood estrogen levels increase as the blood triglyceride, but not glucose, levels rise. Estrogen levels in stomach tissues increase as the blood triglyceride levels rise, and blood triglyceride level-dependent increases of blood estrogen levels are cancelled in gastrectomized rats. We therefore propose that in males, parietal cells in the stomach act as a sensor for the blood triglyceride levels and can secrete estrogen to inhibit the hepatic lipogenesis and feeding behavior when blood triglyceride levels are high.


Author(s):  
Julia Zaccarelli-Magalhães ◽  
Thaisa Meira Sandini ◽  
André Rinaldi Fukushima ◽  
Helenice De Souza Spinosa

Varenicline is a medication used for smoking treatment that acts as a partial agonist for nicotinic cholinergic receptors α4β2 and α3β4 and as a total agonist of receptor α7 in the central nervous system. Pharmacokinetic is important information for medications that acts in the central nervous system. This kind of assay is commonly done by expensive and complex analytical techniques. Therefore, the aim of this study was to evaluate the possibility of using the open field test as a pharmacokinetic model for varenicline in male rats exposed to a single dose of varenicline. Male rats received a single dose orally (gavage) of three different concentrations of varenicline: 0.03 (therapeutic dose for humans), 0.1 and 0.3 mg/kg or water (control group). The open field observations were recorded 30 min, 1, 2, 4, 6, 24, 48, 72 h and 7 days after the administration of varenicline or water. The results showed alterations in locomotion and rearing frequencies, as well as in immobility time observed in open field, which is consistent with this drug’s plasma peak. Consequently, this behavioral test apparently can be considerate as a model for pharmacokinetic evaluation of varenicline.


2020 ◽  
Vol 6 ◽  
pp. 205951312093944
Author(s):  
Desmond D Mascarenhas

Introduction: Survivors of severe burns suffer lifetime neuroinflammatory consequences manifested by higher incidence of major depression and neurodegenerative disease. In a scald model, nephrilin peptide has previously been shown to protect rats from loss of lean body mass, kidney function and glycaemic control, complications that have also been shown to endure in burn patient populations. Nephrilin’s mechanism of action has been suggested to involve protection from excessive oxidative stress. Methods: Using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) amplification of transcripts in total RNA extracted from dorsal root ganglia of male rats 14 days after exposure to thermal insult, we query the relative levels of expression of 34 genes believed to be associated with oxidative stress biology in the central nervous system (CNS). We use these data to explore the central role of oxidative stress in astrogliosis, immunosuppression and mitochondrial homeostasis. Results and Discussion: Rats that received nephrilin treatment (4 mg/kg by subcutaneous bolus injection once daily for seven days after scald injury) showed significantly reduced elevations in gene expression of some key genes such as NOX2, GFAP, AQP4 and RAC1, but not of others such as NOX4, STEAP4, ARG1 and CCL2. Conclusion: The implications of these data with reference to nephrilin’s potential clinical utility for mitigating the enduring effects of burn trauma on the CNS are discussed. Nephrilin reduces the expression of some genes implicated in neurodegeneration after burn insult. Lay Summary Nephrilin peptide is a novel treatment for short- and long-term systemic effects of burn trauma. This study measures the capability of nephrilin to address post-traumatic neurodegenerative disease by looking at the expression of genes in the central nervous system, in a rat scald model. Nephrilin appears to have beneficial effects by reducing the expression of some key genes known to be relevant in neurodegenerative processes, but not others.


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