Gonadal Steroid Influence Upon Sexual and Aggressive Behavior of Female Rats

1988 ◽  
Vol 41 (3-4) ◽  
pp. 271-286 ◽  
Author(s):  
N. E. Van De Poll ◽  
M. S. Taminiau ◽  
E. Endert ◽  
A. L. Louwerse
1972 ◽  
Vol 53 (1) ◽  
pp. 47-57 ◽  
Author(s):  
C. M. TAPPER ◽  
F. NAFTOLIN ◽  
K. BROWN-GRANT

SUMMARY The changes in plasma luteinizing hormone (LH) concentration during the first few days after ovariectomy in the rat differ according to the stage of the cycle at which the operation is performed. When carried out at oestrus there was no increase in LH concentration in the first 4 days. After operation at metoestrus the concentration was increased at 3 days but not earlier. Ovariectomy at dioestrus resulted in an immediate increase after 8 h, a subsequent fall, though not to basal levels, and a fairly steady rise thereafter. Ovariectomy at pro-oestrus produced a very large initial rise in plasma LH which probably represents an accelerated release of the ovulatory surge of LH rather than a specific response to ovariectomy. At 24 h after ovariectomy at pro-oestrus levels were below normal and did not increase again for a further 3 days. In contrast, male rats showed a rapid and sustained rise in plasma LH concentration after castration. It is suggested that the different patterns seen in the female may be related to the time that elapsed since the hypothalamo—pituitary system was exposed to high levels of circulating oestradiol. The changes in plasma LH concentration observed after ovariectomy in neonatally androgen-treated rats, rats in persistent oestrus due to exposure to constant light, and rats in early pregnancy are consistent with this hypothesis. Differing responses to the administration of sodium pentobarbitone between male and female rats even 21 days after gonadectomy suggest that there may also be differences in this negative feedback system between the two sexes that are independent of the nature of the gonadal steroid secreted.


1984 ◽  
Vol 247 (2) ◽  
pp. E258-E264 ◽  
Author(s):  
L. J. Cambotti ◽  
F. E. Cole ◽  
A. A. Gerall ◽  
E. D. Frohlich ◽  
A. A. MacPhee

In rats, gonadal steroid hormones present during the neonatal period produce permanent or "organizational" effects that play a role in the sexual differentiation of the brain and sexually dimorphic patterns of behavior. Because there exists a sexually dimorphic pattern in the development of hypertension in the spontaneously hypertensive rat (SHR), we examined the influence of neonatal gonadal hormones on arterial pressure and body weight in these rats. Male SHR rats were castrated or sham-operated (controls) on their day of birth. Female rats received 1.25 mg testosterone propionate (TP) or sesame oil vehicle on their 2nd day of life. Sham-operated males and TP and oil females were gonadectomized at 81 days of age. To examine the transient or "activational" effects of gonadal steroid hormones, testosterone implants were placed subcutaneously in all rats at 128 days of age and were removed at 170 days of age. The rats were killed at 202 days of age, and selected organ weights were determined. During the original treatment, days 44-79, blood pressure in castrated males was comparable to that of control females, whereas blood pressure in neonatal TP females was not different from that of control males. When exposed to testosterone in adulthood, blood pressure increased more in neonatal TP female rats than in control females. Partial correlation analysis indicated that differences in body weights among the groups could not account for their variances in blood pressure. These data suggest that the neonatal gonadal hormone milieu contributes significantly to the sexually dimorphic pattern of hypertension development in the SHR.


1989 ◽  
Vol 257 (5) ◽  
pp. R1040-R1045 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share

Central adrenoreceptor-mediated regulation of vasopressin secretion and cardiovascular function was studied in male rats and female rats in specific estrous cycle phases. In conscious, unrestrained rats with intracerebroventricular (icv) cannulas and femoral artery and vein catheters, plasma arginine vasopressin concentration (PAVP), mean arterial blood pressure (MABP), and heart rate (HR) were determined before and 5 and 15 min after icv injection of 10 micrograms norepinephrine or 50 micrograms phenylephrine. Norepinephrine (icv) increased PAVP in proestrus and metestrus four and three times (P less than 0.01 and 0.05, respectively) more than in males. Norepinephrine induced similar MABP elevations (P less than 0.01) in males and females in all cycle phases; HR decreased only in proestrus, estrus, and metestrus (P less than 0.01). The increase in PAVP after icv phenylephrine was four and three times greater in proestrous and diestrous females (P less than 0.01 and 0.05, respectively) than in males. The proestrous MABP rise was three times that in males (P less than 0.05); HR decreased similarly in diestrus, proestrus, and males. These results suggest gonadal steroid hormones influence adrenoreceptor-mediated control of vasopressin secretion, MABP, and HR.


2014 ◽  
Vol 26 (1) ◽  
pp. 178
Author(s):  
C. Ahn ◽  
E. J. Hong ◽  
E. B. Jeung

The transient potential receptor (TRP) channels are membrane-binding proteins that are non-selectively permeable for cations, such as Ca2+ and Mg2+, in numerous mammalian cells. The extracellular or intracellular ions play key roles in physiological function, including muscle contraction, cytokine production, insulin release, and apoptosis. Although TRPM channels have been implicated in the brain, bone marrow, and spleen, the presence of TRPM2 has been reported in the endometrium of the uterus. To determine whether expression of the TRPM2 gene in the uterus is due to gonadal steroid hormones or a hormone-independent effect, the uterine TRPM2 gene was monitored in mature rats during the oestrous cycle and in immature rats after treatment with gonadal steroid oestrogen (E2), progesterone (P4) with/without their antagonist, ICI 182,780, and RU486. Dramatic induction of the level of TRPM2 mRNA occurs at proestrus, followed by a drop to baseline levels at metestrus, and its level is restored at diestrus. Furthermore, the immune-reactive TRPM2 is observed in stromal cells of the myometrium and endometrium, and changes during the oestrus cycle. In addition, E2-induced TRPM2 is inhibited by co-treatment with P4. Taken together, these results imply that TRPM2 expression levels in the uterus are regulated by gonadal steroid hormones E2 and P4. Results of this study suggest possible involvement of TRPM2 in reproductive function during the oestrous cycle in female rats.


2005 ◽  
Vol 288 (3) ◽  
pp. F513-F520 ◽  
Author(s):  
Hong Ji ◽  
Stefano Menini ◽  
Koby Mok ◽  
Wei Zheng ◽  
Carlo Pesce ◽  
...  

Renal injury is greater in male compared with female rats after renal wrap (RW) hypertension. We investigated the role of gonadal steroids in the sex differences in RW disease severity in male (M) and female (F), castrated (Cast), and ovariectomized (OVX) rats and after dihydrotestosterone (DHT) and 17β-estradiol (E2) treatment. Male castration attenuated the severity of RW-induced glomerulosclerosis (GS) [GS index (GSI): RW-M, 2.1 ± 0.2; RW-Cast, 1.3 ± 0.2; RW-Cast+DHT, 2.4 ± 0.4], mean glomerular volume (MGV; μm3 × 106: RW-M, 1.9 ± 0.1; RW-Cast, 1.45 ± 0.15; RW-Cast+DHT, 1.91 ± 0.15), tubular damage, and proteinuria (mg/day: RW-M, 130 ± 8; RW-Cast, 105 ± 5; RW-Cast+DHT, 142 ± 9), whereas DHT treatment abrogated these effects. Ovariectomy increased the GSI (RW-F, 0.69 ± 0.05; RW-OVX, 1.2 ± 0.1; RW-OVX+E2, 0.65 ± 0.05), tubular damage, and MGV (μm3 × 106: RW-F, 1.0 ± 0.06; RW-OVX, 1.5 ± 0.05; RW-OVX+E2, 0.96 ± 0.06), whereas E2 treatment prevented these effects. Furthermore, DHT treatment of RW-OVX animals exacerbated the GSI (1.9 ± 0.19), MGV (1.7 ± 0.2 × 106 μm3), and proteinuria (171 ± 21 mg/day) even further. Our data show that the lack of E2 and presence of androgens contribute to progressive renal disease induced by RW hypertension, suggesting that gonadal steroid status is an independent factor in the greater susceptibility men exhibit toward hypertension-associated renal disease compared with women.


2006 ◽  
Vol 28 (2) ◽  
pp. 130-134 ◽  
Author(s):  
Rosa Maria Martins de Almeida ◽  
Marcia Giovenardi ◽  
Simone Perroni da Silva ◽  
Verônica Paz de Oliveira ◽  
Dirson João Stein

OBJECTIVE: Much evidence supports the hypothesis that 5-hydroxytryptamine (5-HT) activation is related to the inhibition of aggression. We examined potentially pro- and anti-aggressive effects of the 5-HT2A/2C receptor agonist on specific brain sites. METHOD: Female Wistar rats on the 7th day postpartum were microinjected with the selective 5-HT2A/2C receptor agonist, alpha-methyl-5-hydroxytryptamine maleate (0.2 to 1.0 µg/0.2 µl) into the central amygdaloid nucleus and median preoptic nucleus. For each brain area studied, the frequency of the behaviors: locomotion, social investigation, lateral threat, attacks (frontal and lateral), and biting the intruder were compared among the various treatments by an Analysis of Variance, followed when appropriate, by Tukey's test. RESULTS: Microinjection of the selective 5-HT2A/2C receptor agonist, a-methyl-5-hydroxytryptamine maleate into central amygdaloid nucleus increased maternal aggression in the absence of concurrent changes in non-aggressive behavior. By contrast, microinjection of the selective 5-HT2A/2C receptor agonist at several dilutions into the median preoptic nucleusdid not alter aggressive behavior. CONCLUSIONS: The current and earlier data with pro- and anti-aggressive effects of the 5-HT2a/2c receptor agonist, when microinjected into the median preoptic nucleus relative to the central amygdaloid nucleus, medial septum and periaqueductal grey area in female rats point to functionally separate serotonin receptor populations in the amygdaloid-septal-hypothalamic and periaqueductal gray matter areas controlling aggressive behavior. It is possible that amygdaloid 5-HT2a/2c receptors may increase aggressive behavior in lactating females as a result of changes in fear.


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