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N G Simon

Publications and source records attributed to N G Simon.

31 records · Page 2Linked to original sources
PubMed1984

Endocrine induction of intermale aggression in mice: a comparison of hormonal regimens and their relationship to naturally occurring behavior.

The level of intermale-like fighting behavior induced in female mice by various regimens of gonadal hormones known to establish aggression was compared. Regardless of whether the animals were exposed to testosterone propionate on the day of birth, the highest aggression scores were observed following chronic testosterone exposure in adult life. Females so treated also exhibited significantly more aggression than intact males. The least effective regimen was neonatal exposure to estradiol benzoate followed by long-term exposure of the adult to testosterone. Lastly, while castrated adult males were less likely to display aggressive behavior, those that fought did so at a level comparable to that of intact males.

Aggression↗
PubMed1980

Prenatal exposure to prednisone permanently alters fighting behavior of female mice.

Female mice born of mothers administered 100 microgram prednisone on Days 13-18 of gestation attacked a stimulus male significantly sooner following the commencement of testosterone treatment in adult life than did mice born of control mothers. In a second ed postpartum aggression as compared to controls. In both experiments females of the 100 microgram prednisone group showed a reduction in birth weight relative to controls. The effect on body weight did not persist since no differences were observed on Day 21 of life. The data show that prenatal exposure to prednisone permanently modifies the later intraspecific fighting behavior of female mice.

Aggression↗
PubMed1979

Prenatal exposure to testosterone and its precursors influences morphology and later behavioral responsiveness to testosterone of female mice.

Prenatal exposure to testosterone (T), dehydroepiandrosterone or progesterone significantly increased ano-genital distance of female mice. In addition, prenatal exposure to T or pregnenolone significantly reduced the duration of T exposure during adult life required to induce intraspecific fighting behavior. However, the most masculinized females, those exposed to T prenatally, still had significantly shorter ano-genital distances and required a longer exposure period to T in order to establish fighting than did prenatally oil-exposed male mice. Additional experiments revealed that pregnenolone augments later responsiveness to the aggression-promoting property of T only if it is administered during the prenatal period of development.

Aggression↗
PubMed1978

Prenatal exposure to prednisone in humans and animals retards intrauterine growth.

Prednisone treatment for infertility and subsequent pregnancy maintenance in humans resulted in a significant decrease in the birth weight of full-term infants and a marked increase in the percentage of newborn infants weighing 2500 grams or less, that is, "light for dates" in comparison to control offspring. A parallel experiment with mice indicated that the reduction of birth weight was caused by exposure to corticosteroids rather than to maternal disease or malfunction.

Animals↗
PubMed1978

Spontaneous pup-killing by mice in response to large litters.

Primiparous lactating nice mice whose young were removed on the day of parturition were presented with foster litters of either 12 or 16 day-old young. The adults spontaneously killed young during Day 3-7 of the lactation period, killing more in the 16-pup than in the 12-pup litter. The lactating animal appeared to select the young to be killed on the basis of body weight. It killed significantly more young that were in the bottom half than in the top half of the weight range for its particular litter.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

Androgens and estrogens modulate 5-HT1A and 5-HT1B agonist effects on aggression.

Intermale offensive aggressive behavior is facilitated by gonadal steroids and inhibited by serotonin (5-HT), presumably through its effects at 5-HT1A and 5-HT1B receptor sites. To examine the interaction between these neuroendocrine and neurochemical regulatory systems, CF-1 male mice were gonadectomized and implanted with silastic capsules containing either diethylstilbestrol (DES, a synthetic estrogen), the nonaromatizable androgens methyltrienolone (R1881) or dihydrotestosterone (DHT), or testosterone (T). Two weeks later, they were given 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, a 5-HT1A agonist; 0.1 or 1.0 mg/kg), CGS12066B (a 5-HT1B agonist; 4.0 or 8.0 mg/kg), 0.1 or 1.0 mg/kg 8-OH-DPAT + 4.0 mg/kg CGS12066B, or vehicle, and tested for aggression. In the presence of DES, the higher 8-OH-DPAT dose given in combination with CGS attenuated aggression in comparison to vehicle controls. When given nonaromatizable androgen (R1881 or DHT), all drug treatments except 0.1 mg/kg 8-OH-DPAT significantly reduced offensive attack behavior. In the presence of T, which provides estrogenic and androgenic stimulation, aggression scores were significantly reduced when males were given the high dose of 8-OH-DPAT or CGS12066B, as well as in the 1.0 mg/kg 8-OH-DPAT + CGS12066B condition. Assessments of changes in motor behavior showed significant impairment when 8.0 mg/kg CGS12066B was administered across all hormonal conditions, indicating that reductions in offensive aggression in these treatment groups were nonspecific. The results demonstrate differential effects of the steroidal environment on the ability of 5-HT1A and 5-HT1B agonists to modulate aggression, with estrogens producing a more restrictive environment than androgens for serotonergic inhibition of male-typical aggressive behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗