Precocious ovarian stimulation following hypothalamic and amygdaloid lesions in rats

1960 ◽  
Vol 198 (2) ◽  
pp. 381-385 ◽  
Author(s):  
Mildred Elwers ◽  
Vaughn Critchlow

The effects of neural lesions on the functional development of the reproductive system were studied in prepubertal female rats. Small electrolytic lesions were placed bilaterally in 66 female rats at 18–20 days of age; 42 littermates served as controls, and 7 rats were blank-operated. All animals were weighed two to three times a week and examined daily for vaginal opening. At 33 days of age the uteri, ovaries and adrenals were weighed and prepared for histological study. All brains were examined histologically for lesion localization. Lesions in the anterior hypothalamus or in the medial portion of the amygdaloid complex were associated with precocious ovarian stimulation. With the exception of one lesion in the basal septum and one in caudate-putamen, bilaterally symmetrical lesions in other parts of the brain and asymmetrical lesions have been ineffective. These results are compatible with an anterior hypothalamic mechanism involved in the inhibition of gonadotropin secretion and suggest the inclusion of the medial portion of the amygdaloid complex in this mechanism.

2020 ◽  
Vol 10 (3-s) ◽  
pp. 37-42
Author(s):  
Hadjer Bekhedda ◽  
Norredine Menadi ◽  
Abbassia Demmouche ◽  
Abdelaziz Ghani ◽  
Hicham Mai

Introduction: Aluminum (Al) has the potential to be neurotoxic in human and animals, is present everywhere in the environment, many manufactured foods and medicines and is also added to drinking water for purification purposes and tooth paste cosmetic products They accumulate in living organisms and disrupt balances, and accumulate in the body biological systems, causing toxic effects (They may affect the nervous system, kidney, liver, respiratory or other functions). Nervous system is a vulnerable target for toxicants due to critical voltages which must be maintained in the cells and the all responses when voltages reach threshold levels. Objective This study aimed to expose the impact of aluminum chloride (AlCl3) on brain architecture. Methods: In our study, twenty healthy female rats were intraperitoneal administered of aluminum chloride (ALCL3) at 10 mg / kg body weight with consecutively for 15 day Result. The results showed a highly significant reduction in body weight (p<0.0001).  This is because aluminum has an anorectic effect contrariwise, there is no significant impact of aluminium exposure has been observed with respect to brain weight and relative brain weight respectively (p<0.912), (p<0.45). The histological study describes the alterations in the brain marked tissue necrosis and cytoplasmic vacuolations and karyopyknosis of neuronal cells of the brain. Conclusion; Aluminum is a toxic heavy metal and a ubiquitous environmental pollutant. It can alter the permeability of the blood-brain barrier and enter the brain, severely affecting the functioning of the nervous system. Keywords: Toxicity, brain, Aluminium chloride, Rats female, necrosis.


1962 ◽  
Vol 41 (2) ◽  
pp. 301-313 ◽  
Author(s):  
S. Horowitz ◽  
J. J. Van der Werff ten Bosch

ABSTRACT Electrolytic lesions were placed in the anterior hypothalamus of 3–4 day-old female rats; vaginal opening was hastened in comparison with blank-operated littermates in 12 of 17 rats bearing a lesion in the basal supra-and post-chiasmatic area. In the animals with the earliest vaginal opening, lesions reached upward towards the region of the anterior commissure and the paraventricular nuclei. The degree of advancement of puberty in rats operated at the age of 3 or 4 days was similar to that caused by lesions made at 10, 14 or 15 days. This finding suggests that the effect of a lesion upon gonadotrophin secretion does not begin to take place until after the age of at least two weeks.


1979 ◽  
Vol 90 (3) ◽  
pp. 385-393 ◽  
Author(s):  
José Borrell ◽  
Flavio Piva ◽  
Luciano Martini

ABSTRACT Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.


1960 ◽  
Vol XXXV (II) ◽  
pp. 225-234 ◽  
Author(s):  
R. Bourrillon ◽  
R. Got ◽  
R. Marcy

ABSTRACT A new method for preparation of Human Menopausal Gonadotrophin involves successively alcoholic precipitation, kaolin adsorption and chromatography on ion exchangers. A highly active material is obtained which corresponds to 1 mg per litre of urine and has an activity of 1 mouse uterus unit at a dose of 0.003 mg. This gonadotrophin possesses both follicle stimulating and luteinizing activities in hypophysectomized female rats, by histological study. It contains 13 % hexose, 10% hexosamine and 8.5 % sialic acid. A further purification, by zone electrophoresis on starch, gives a final product, biologically active at 0.001 mg, which behaves as an homogenous substance in free electrophoresis with mobility −4.76 × 10−5 at pH 8.6.


2006 ◽  
Vol 291 (1) ◽  
pp. R155-R162 ◽  
Author(s):  
Stephanie A. Dean ◽  
Junhui Tan ◽  
Roselyn White ◽  
Edward R. O’Brien ◽  
Frans H. H. Leenen

The present study tested the hypothesis that 17β-estradiol (E2) inhibits increases in angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (AT1R) in the brain and heart after myocardial infarction (MI) and, thereby, inhibits development of left ventricular (LV) dysfunction after MI. Age-matched female Wistar rats were treated as follows: 1) no surgery (ovary intact), 2) ovariectomy + subcutaneous vehicle treatment (OVX + Veh), or 3) OVX + subcutaneous administration of a high dose of E2 (OVX + high-E2). After 2 wk, rats were randomly assigned to coronary artery ligation (MI) and sham operation groups and studied after 3 wk. E2 status did not affect LV function in sham rats. At 2–3 wk after MI, impairment of LV function was similar across MI groups, as measured by echocardiography and direct LV catheterization. LV ACE mRNA abundance and activity were increased severalfold in all MI groups compared with respective sham animals and to similar levels across MI groups. In most brain nuclei, ACE and AT1R densities increased after MI. Unexpectedly, compared with the respective sham groups the relative increase was clearest (20–40%) in OVX + high-E2 MI rats, somewhat less (10–15%) in ovary-intact MI rats, and least (<10–15%) in OVX + Veh MI rats. However, because in the sham group brain ACE and AT1R densities increased in the OVX + Veh rats and decreased in the OVX + high-E2 rats compared with the ovary-intact rats, actual ACE and AT1R densities in most brain nuclei were modestly higher (<20%) in OVX + Veh MI rats than in the other two MI groups. Thus E2 does not inhibit upregulation of ACE in the LV after MI and amplifies the percent increases in ACE and AT1R densities in brain nuclei after MI, despite E2-induced downregulation in sham rats. Consistent with these minor variations in the tissue renin-angiotensin system, during the initial post-MI phase, E2 appears not to enhance or hinder the development of LV dysfunction.


2009 ◽  
Vol 55 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Kazuyo TUJIOKA ◽  
Miho OHSUMI ◽  
Kenji HORIE ◽  
Mujo KIM ◽  
Kazutoshi HAYASE ◽  
...  

2018 ◽  
pp. 80-88
Author(s):  
V. L. Karbovskyy ◽  
I. A. Shevchuk ◽  
O. V. Kurkina ◽  
T. Ye. Makovska

One of the critical steps in development of safe and efficient drugs during their pre-clinical trials are toxicity studies. Therefore, the aim of our work was to study PEG-Filstim toxic effects on animal internal organs and tissues. Toxicity study of PEG-Filstim was performed in 50 white wild-type rats of both sexes with body weight of 170 to 230 g on daily (28 days) subcutaneous administration in the doses of 0.5, 1.0 and 2.0 mg/kg. In all groups of animals, after completing the experiment careful pathomorphologic and histological examination was performed. PEG-Filstim has been shown to possess no toxic effects on internal organs of laboratory rats and does not cause specific changes in the heart, kidneys and mucous coat of stomach on daily subcutaneous administration in the doses of 0.5, 1.0, and 2.0 mg/kg within 28 days. In the maximum applied dose of 2.0 mg/kg, the studied drug causes pronounced acute splenic hyperplasia, related to hyper-proliferation of the reticular tissue, leads to functional strain of the liver due to formation of hematopoietic foci in it, as well as impaired integrity of the respiratory epithelium and congestive signs in the lungs, swelling of the brain tissues, abnormalities in the gray matter structure and hyperemia of the brain vessels. These effects were not observed in the animals, to which the drug was administered in the doses of 0.5 and 1.0 mg/kg. Administration of PEG-Filstim (in all studied doses) results in increasing the size of the ankle joint in rats, which is related to hyper-proliferation of the reticular tissue, leading to bone defect formation in the form of perforation with subsequent filling the periosteum with reticular tissue and formation of hematopoietic foci within its boundaries.


2008 ◽  
Vol 294 (6) ◽  
pp. E1088-E1096 ◽  
Author(s):  
J. Roa ◽  
E. Vigo ◽  
D. García-Galiano ◽  
J. M. Castellano ◽  
V. M. Navarro ◽  
...  

Kisspeptins have emerged as potent elicitors of gonadotropin secretion and, therefore, putative targets for pharmacological intervention. In this context, desensitization of gonadotropin responses to continuous administration of kisspeptins has begun to be characterized, but information so far available is mostly restricted to LH responses in males, whereas the similar phenomenon in females, of obvious therapeutic interest, remains virtually unexplored. We report herein LH and FSH responses to continuous intracerebral administration of kisspeptin in female rats at different developmental and metabolic states. Infusion of kisspeptin-10 to adult female rats induced a transient elevation in serum LH concentrations, followed by a precipitous drop and normalization of LH levels thereafter. Elevation of LH after kisspeptin infusion was prolonged in underfed animals; a phenomenon mimicked by leptin administration. Conversely, FSH levels were persistently heightened along continuous kisspeptin infusion, but duration of this response was shortened by undernutrition. In pubertal females, LH and FSH levels remained elevated at the end of a 7-day infusion of kisspeptin; responses whose magnitude was augmented by subnutrition but not mimicked by leptin. In all settings, terminal gonadotropin-releasing hormone responses were fully preserved, suggesting that eventual desensitization must occur upstream from the pituitary. In summary, our current data document the pharmacological consequences of continuous administration of kisspeptin to female rats, with remarkable differences being detected between LH and FSH responses, in different developmental and metabolic states. These observations of potential pharmacological interest might help also to delineate the physiological roles of kisspeptins in the dynamic regulation of gonadotropin secretion in the female.


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