Behavior In Syrian Hamsters Research Articles

Tamoxifen antagonizes the effects of estradiol on energy balance and estrous behavior in Syrian hamsters.

Ovariectomized Syrian hamsters were treated with estradiol benzoate (5 micrograms/day for 4 wk), tamoxifen (500 micrograms/day), an antiestrogen that competes with estradiol for central and peripheral estrogen receptors, or both estradiol benzoate and tamoxifen. As expected, estradiol treatment caused significant decreases in body weight and fat content without affecting food intake. Given alone, tamoxifen had no effect on body weight or composition, but when given concurrently, tamoxifen significantly attenuated the effects of estradiol. These results stand in contrast to findings in rats where nonsteroidal antiestrogens, including tamoxifen, mimic the effects of estradiol on body weight and energy metabolism and are completely devoid of any antiestrogenic actions. As in rats, tamoxifen was a potent inhibitor of estrous behavior, whether induced with estradiol alone or with sequential treatment with estradiol and progesterone. Again, as in rats, tamoxifen acted as an antagonist and a weak estrogen agonist on uterine weight. These findings support the notion that the relative agonistic and antagonistic actions of tamoxifen, and other antiestrogens, vary with species and with the estrogen-sensitive endpoint being investigated.

Decreased availability of metabolic fuels suppresses estrous behavior in Syrian hamsters.

The availability of oxidizable metabolic fuels affects reproductive physiology and behaviors in female mammals. In Syrian hamsters, 48 h of food deprivation is sufficient to suppress secretion of gonadotropins and ovarian steroids and to prevent the occurrence of ovulation and estrous behavior. These experiments attempted to determine whether the deprivation-induced suppression of lordosis is entirely due to the disruption of ovarian steroid secretion or whether there are also changes in behavioral responsiveness to estradiol and/or progesterone (P). Estrous behavior was induced in ovariectomized hamsters with sequential injections of 5 micrograms of estradiol benzoate (EB) and 200 micrograms P. Food deprivation for 48 h, either before or just after EB treatment, significantly suppressed the amount of time females spent in lordosis during a 5-min test with a sexually experienced male. Treatment with an inhibitor of glycolysis (2-deoxy-D-glucose) in combination with an inhibitor of fatty acid oxidation (methyl palmoxirate) for 48 h mimicked the effects of food deprivation and suppressed the amount of time spent in lordosis after treatment with EB+P. Given alone, neither metabolic inhibitor had an effect on lordosis. These findings indicate that suppression of hamster estrous behavior by metabolic fuel deprivation is at least in part due to a reduced responsiveness to estradiol and/or progesterone. Furthermore, estrous behavior is responsive to metabolic fuels in general. This is unlike hamster ovulatory cycles, which are primarily responsive to glucose availability.

Availability of metabolic fuels controls estrous cyclicity of Syrian hamsters.

Food deprivation and weight loss inhibit ovulation and estrous behavior in Syrian hamsters. In the present experiments, lean hamsters were more susceptible to starvation-induced anestrus than fat hamsters. However, anestrus was not caused by changes in any dimension of body size per se, but instead by the availability of metabolic fuels. Simultaneous pharmacological blockade of both fatty acid oxidation and glycolysis inhibited reproduction, but, as long as one of these metabolic pathways could be used, estrous cycles continued. Thus, reproduction in female Syrian hamsters is sensitive to the general availability of oxidizable metabolic fuels.

Abdominal vagus and regulation of ingestive behavior and body weight in golden hamsters.

A series of experiments was undertaken to examine the role of the vagus nerve in body weight regulation and the control of ingestive behavior in Syrian hamsters. Body weight, food and water intake, and feeding responsiveness to the putative satiety hormone cholecystokinin (CCK) were studied in hamsters with total subdiaphragmatic or selective gastric vagotomy. Body weight and food intake during ad libitum feeding were unaffected by either type of vagotomy. However, hamsters with total subdiaphragmatic or gastric vagotomy could better maintain body weight during intermittent food access. Vagotomy blocked feeding suppression after low-dose (4.0 micrograms/kg) systemic injections of CCK octapeptide (CCK-8). This blocking effect was specific to feeding suppression in response to CCK-8, because vagotomized hamsters remained responsive to other putative satiety hormones (bombesin, calcitonin, and thyrotropin-releasing hormone). Hamsters with either type of vagotomy were, however, responsive to high doses (greater than or equal to 8.0 micrograms/kg) of CCK-8, thus indicating that extravagal (possibly central nervous system) sites of CCK action may also be relevant to the control of feeding. The results are discussed in relation to normal vagal function in hamsters and vagal control of ingestive behavior in other species.

Effects of the hepatocarcinogen, aflatoxin, on open-field behaviors in Syrian hamsters

For 35 days male Syrian hamsters were exposed to food treated with aflatoxin, copper acetate, aflatoxin plus copper acetate, or a control diet. When tested in an open-field, the copper acetate and the control groups showed normal decreases in rears, squares entered, and escape attempts across trials. The two aflatoxin-treated groups, however, did not show a decrease across trials on these measures. In fact, the aflatoxin plus copper acetate group showed significant increases in rears and escape attempts. There seems to be a lack of habituation in all animals receiving aflatoxin, and concurrent copper treatment failed to alter this response. Thus, the open-field test revealed behavioral changes while the hamsters were still in a precancerous stage.