Effects of Chronic Oestradiol, Progesterone and Medroxyprogesterone Acetate on Hippocampal Neurogenesis and Adrenal Mass in Adult Female Rats

2014 ◽  
Vol 26 (6) ◽  
pp. 386-399 ◽  
Author(s):  
M. Chan ◽  
C. Chow ◽  
D. K. Hamson ◽  
S. E. Lieblich ◽  
L. A. M. Galea
2007 ◽  
Vol 25 (8) ◽  
pp. 2473-2482 ◽  
Author(s):  
Melissa J. Glenn ◽  
Erin M. Gibson ◽  
Elizabeth D. Kirby ◽  
Tiffany J. Mellott ◽  
Jan K. Blusztajn ◽  
...  

2019 ◽  
Vol 28 (4) ◽  
pp. 352-360 ◽  
Author(s):  
Abdeslam Mouihate ◽  
Samah Kalakh ◽  
Rawan AlMutairi ◽  
Abdelrahman Alashqar

Background/Aims: Prenatal exposure to lipopolysaccharide (LPS) dampens hippocampal neurogenesis. This effect is associated with increased anxiety-like behavior in adult offspring. Furthermore, blocking serotonin transporters (SERT) promotes adult neurogenesis. Previous studies were performed largely in males. Therefore, we explored the impact of prenatal LPS on neurogenesis, SERT expression in the hippocampus, and anxiety-like behavior in female rats during prepubertal and adulthood stages. Materials and Methods: Timed pregnant rats were injected with either saline or LPS (100 µg/kg, i.p.) on gestational days 15, 17, and 19. Newly born neurons were monitored by immunohistochemistry, and anxiety-like behavior was monitored using the elevated plus maze and open-field test. SERT expression in the hippocampus was assessed by Western blot and immunofluorescence. Results: Prenatal LPS led to reduced hippocampal neurogenesis in adult but not in prepubertal female offspring. This reduced neurogenesis was associated with enhanced hippocampal expression of SERT protein. However, there was no significant impact of prenatal LPS on anxiety-like behavior. Conclusions: Prenatal LPS-induced reduction in neurogenesis was dissociated from anxiety-like behavior in adult female rats. Furthermore, the long-lasting impact of prenatal LPS on neurogenesis in female offspring was age-dependent.


2018 ◽  
Author(s):  
Wansu Qiu ◽  
Aarthi R. Gobinath ◽  
Yanhua Wen ◽  
Jehannine Austin ◽  
Liisa A.M. Galea

ABSTRACTFolate is an important regulator of hippocampal neurogenesis, and in utero spinal cord development. Both high levels of folic acid and low levels of folate can be harmful to health, as low levels of folate have been linked to several diseases while high folic acid supplements can mask a vitamin B12 deficiency. Depressed patients exhibit folate deficiencies, lower levels of hippocampal neurogenesis, elevated levels of homocysteine, and elevated levels of the stress hormone, cortisol, which may be inter-related. Here, we are interested in whether different doses of natural folate or synthetic folic acid diets can influence neurogenesis in the hippocampus, levels of plasma homocysteine, and serum corticosterone in adult female rats. Adult female Sprague-Dawley rats underwent dietary interventions for 29 days. Animals were randomly assigned to six different dietary groups: folate deficient + succinylsulfathiazole (SST), low 5-methyltetrahydrofolate (5-MTHF), low 5-MTHF + (SST), high 5-MTHF + SST, low folic acid, and high folic acid. SST was added to a subset of the 5-MTHF diets to eliminate folic acid production in the gut. Before and after dietary treatment, blood samples were collected for corticosterone and homocysteine analysis, and brain tissue was collected for neurogenesis analysis. High folic acid and low 5-MTHF without SST increased the number of immature neurons (doublecortin-expressing cells) within the ventral hippocampus compared to folate deficient controls. Low 5-MTHF without SST significantly increased the number of immature neurons compared to low and high 5-MTHF + SST, indicating that SST interfered with elevations in neurogenesis. Low folic acid and high 5-MTHF+SST reduced plasma homocysteine levels compared to controls, but there was no significant effect of diet on serum corticosterone levels. Low folic acid and high 5-MTHF+SST reduced the number of mature new neurons in the ventral hippocampus (BrdU/NeuN-positive cells) compared to folate deficient controls. Overall, folic acid dose-dependently influenced neurogenesis, with low levels decreasing but high levels increasing, neurogenesis in the ventral hippocampus, suggesting this region, which is important for regulating stress, is particularly sensitive to folic acid in diets. Furthermore, the addition of SST negated the effects of 5-MTHF to increase neurogenesis in the ventral hippocampus.


1965 ◽  
Vol 48 (2) ◽  
pp. 263-271 ◽  
Author(s):  
Herbert Schriefers ◽  
Gerlinde Scharlau ◽  
Franzis Pohl

ABSTRACT After the administration of anabolic steroids to adult female rats in daily doses of 1 mg per animal for 14 days, the following parameters were investigated: the rate of the Δ4-5α-hydrogenase-catalyzed cortisone reduction in liver slices and microsomal fractions, the adrenal weight and the in vitro corticosterone production rate. Among the steroids tested, only 17α-methyl-testosterone and 17α-ethyl-19-nor-testosterone were effective in lowering significantly cortisone reduction rate by liver slices with concomitant decreases in microsomal Δ4-5α-hydrogenase-activity. Testosterone, 19-nor-testosterone, 17α-ethinyl-19-nor-testosterone, 17α-methyl-17β-hydroxy-androsta-1,4-dien-3-one and 1-methyl-17β-hydroxy-androst-1-en-3-one were ineffective or only slightly effective. Adrenal weight and absolute corticosterone production rate (μg/60 min per animal) were decreased after treatment with 17α-methyl-testosterone, 17α-ethyl-19-nor-testosterone and 1-methyl-17β-hydroxy-androst-1-en-3-one. Corticosterone production was decreased with 17α-ethinyl-19-nor-testosterone in spite of an unchanged adrenal weight. The relative corticosterone production rate (μg/60 min · 100 mg adrenal) was in any cases unaffected. According to these results there exists – with the exception of 17α-ethinyl-19-nor-testosterone – a strict parallelism between corticosteroid turnover and corticosterone production rate: unchanged turnover is correlated with unchanged corticosterone production rate, while a decreased turnover is correlated with decreased adrenal activity. The protein-anabolic effect of certain anabolic steroids may be partly due to an anti-catabolic action of these compounds resulting from a decreased corticosteroid inactivation and production rate. Possible mechanisms by which anabolic steroids may affect corticosteroid-balance are discussed.


1963 ◽  
Vol 42 (2) ◽  
pp. 254-262 ◽  
Author(s):  
J. J. van der Werff ten Bosch ◽  
H. E. Swanson

ABSTRACT Adult female rats were given a normal diet, or a diet which contained 0.15% propylthiouracil. At the beginning of the experiment one half of the rats were left intact, whilst the others received an electrolytic basal midline lesion in the anterior hypothalamus. Of each of the four groups of rats, one half was killed after 14 days, the others after 28 days. It was found (both after 14 and after 28 days) that the presence of a lesion reduced the thyroid weight to approximately 75% of the value in intact rats on the same diet, which might be normal or contain propylthiouracil. Propylthiouracil caused thyroid enlargement (to 278% after 14 days and 352–360% after 28 days) in intact rats as compared with intact rats on a normal diet, and in lesioned rats as compared with lesioned rats on a normal diet. It is concluded that lesions cause a lowered steady state of the thyroid-pituitary feed-back system, but that this system responds normally to the alteration of the steady state caused by the propylthiouracil-induced block in thyroid hormone output.


1959 ◽  
Vol XXXII (II) ◽  
pp. 167-176 ◽  
Author(s):  
Walter Schätzle

ABSTRACT In normal adult female rats a single injection of 5 IU corticotrophin was followed by a retention of glucoproteid material in the anterior lobe of the hypophysis and by impairment of the luteinization. In spayed adult female rats the same corticotrophin administration caused stratification and mucification of the vaginal epithelium.


Author(s):  
Bita Barghi ◽  
Majid Shokoohi ◽  
Amir Afshin Khaki ◽  
Arash Khaki ◽  
Maryam Moghimian ◽  
...  

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