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Biomedical subjects

L G Clemens

Publications and source records attributed to L G Clemens.

At least 55 records · Page 3Linked to original sources
PubMed1983

Gonadal hormone activation of male courtship ultrasonic vocalizations and male copulatory behavior in castrated male deer mice (Peromyscus maniculatus bairdi).

The influence of testosterone (T), a 5 alpha-reduced metabolite of T, dihydrotestosterone, and an aromatized metabolite of T, estradiol, on 35-kHz ultrasonic calling and male copulatory behavior by male deer mice (Peromyscus maniculatus bairdi) was examined. Daily treatment with testosterone propionate (TP), dihydrotestosterone propionate (DHTP), or estradiol benzoate (EB) restored male ultrasonic calling in long-term castrated males. Both TP and DHTP restored male copulatory behavior, but EB was ineffective in facilitating copulation. Synergism of EB and DHTP action was observed; when subthreshold doses of EB (1 microgram/day) and DHTP (50 micrograms/day) were administered in combination, male ultrasonic calling and male copulatory behavior were activated. In relation to other comparative findings, these results indicate that the degree to which male sexual behavior is facilitated by 5 alpha-reduced androgens and/or estrogens is influenced by the species and the particular pattern of masculine behavior under consideration.

Animals↗
PubMed1982

Alteration of muscarinic binding in specific brain areas following estrogen treatment.

Systemic administration of estradiol benzoate (EB) to ovariectomized female rats significantly altered cholinergic muscarinic binding of [3H]quinuclidinyl benzilate in discrete brain regions. Specifically, EB increased muscarinic binding in the medial basal hypothalamus (MBH) and decreased muscarinic binding in the medial preoptic area (POA). These alterations were dose-dependent and appeared to reflect changes in the number of muscarinic binding sites. Treatment with EB failed to significantly affect binding in several control areas in females or in the MBH and POA of males.

Amygdala↗
PubMed1982

Development of feminine sexual behavior in the rat: androgenic and temporal influences.

The contributions of prenatal and postnatal androgen exposure upon the development of sexual behavior in rats were examined by prenatal treatment of pups with an androgen antagonist (flutamide) and postnatal androgenization or castration. Male and female rats were exposed to the androgen receptor-blocker flutamide (FLU) in utero via prenatal injections to the mother on Days 10 through 22 of gestation. At birth (Day 1) males were castrated. Both males and females were injected with either 100 micrograms testosterone propionate (TP) or oil on Day 1. In adulthood all gonadectomized animals were tested for the display of feminine sexual behavior (lordosis) in response to a range of estrogen dosages. Prenatal exposure to FLU enhanced lordosis in both sexes when compared to vehicle-treated controls. Postnatal TP treatment decreased lordotic potential as expected. However, in animals given TP postnatally, those receiving prenatal flutamide had higher lordosis quotients than animals receiving vehicle treatment. These data confirm (1) that the development of feminine sexual behavior is inhibited by androgen exposure, (2) that such exposure occurs prenatally, (3) that the potential for feminine behavioral differentiation occurs prenatally as well as postnatally, and (4) that androgen acts perinatally to affect estrogen sensitivity in adulthood.

Aging↗
PubMed1982

Testosterone acts as a prohormone to stimulate male copulatory behavior in male deer mice (peromyscus maniculatus bairdi).

In order to determine the importance of reduced and aromatized metabolites of testosterone for male sexual behavior in Peromyscus maniculatus bairdi, castrated males were treated with 5 alpha-reductase and aromatase inhibitors. In the first experiment, testosterone propionate (TP) activation of male copulatory behavior was blocked by the administration of the 5 alpha-reductase inhibitor 4-androsten-3-one-17-beta carboxylic acid (17 beta C). These treatments also prevented TP stimulation of seminal vesicles and ventral prostate gland weight. The inhibitory effects of 17 beta C were specific to testosterone, since 17 beta C did not prevent dihydrotestosterone propionate (DHTP) induction of male sexual behavior or seminal vesicles and ventral prostate gland weight increases. In the second experiment, TP activation of male copulatory behavior was prevented by the administration of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD). The ATD did not interfere with DHTP activation of male reproductive behavior. Also, TP and DHTP stimulation of accessory sex organ weight was not blocked by ATD. On the basis of these data, it is suggested that metabolism of testosterone to both 5 alpha-reduced androgens and estrogens is obligatory for testosterone to reliably stimulate male sexual behavior in castrated male deer mice.

Androstatrienes↗
PubMed1981

Fluoxymesterone and the development of sexual behavior in the golden hamster.

Male hamsters castrated at birth and female hamsters were treated on postnatal Days 2-4 with 100 microgram of testosterone. 100 microgram of fluoxymesterone, or the hormone vehicle. As adults, mounting behavior and lordosis were measured following exogenous hormone treatment. Although the degree of penile or clitoral virilization did not appear to differ between testosterone- and fluoxymesterone-treated animals, behavioral differences occurred. Neonatal treatment with fluoxymesterone failed to "masculinize" or defeminize" behavior; neonatal testosterone treatment induced mounting in males and females and intromission in males. These results, along with those of others, indicate that fluoxymesterone has little or no central neural effect on sexual behavior in the hamster.

Animals↗
PubMed1981

Cholinergic influences on estrogen-dependent sexual behavior in female rats.

The ability of cholinergic agents to influence hormone-dependent sexual behavior in female rats was examined. In the first experiment, female sexual behavior, indicated by the incidence of lordosis, was significantly increased in estrogen-treated female rats following bilateral infusion of a cholinergic receptor agonist, carbachol (.5 microgram/cannula), into the medial preoptic area of the brain. Infusion of an artificial cerebrospinal fluid vehicle failed to facilitate lordosis. The incidence of lordosis was normally highest 15 min after carbachol infusion, began to wane by 45 min, and had returned to control levels by 90 min. Further, centrally administered carbachol activated lordosis at lower levels of estrogen priming than did systemically administered progesterone. In a second experiment, female rats, brought into sexual receptivity by administration of estrogen and progesterone, received preoptic infusions of an acetylcholine synthesis inhibitor, hemicholinium-3. Significant reductions in the incidence of lordosis were observed following bilateral infusion of hemicholinium-3 (1.25 microgram/cannula). This inhibition of lordosis was prevented when carbachol (.5 microgram/cannula) was infused along with hemicholinium-3. Results confirm the importance of cholinergic influences on sexual behavior in female rats.

Acetylcholine↗
PubMed1980

Cholinergic brain mechanisms and the hormonal regulation of female sexual behavior in the rat.

Cholinergic muscarinic stimulation of the medial preoptic area or the mesencephalic reticular formation with carbachol or bethanechol facilitated lordosis in ovariectomized female rats treated with estrogen. Adrenalectomy did not abolish the facilitative influence of cholinergic stimulation in the preoptic area. Implants of carbachol in the neocortex failed to increase lordosis.

Animals↗
PubMed1980

Inhibition of lordotic behavior in female rats following intracerebral infusion of anticholinergic agents.

Cholinergic antagonists were bilaterally infused into forebrain areas of ovariectomized female rats brought into sexual receptivity by administration of estrogen and progesterone. Infusion of hemicholinium-3 (HG-3, 5 or 7.5 micrograms/cannula), an acetylcholine synthesis inhibitor believed to interfere with choline uptake, decreased the incidence of lordotic behavior displayed by females. This inhibition was prevented by infusion of choline chloride (120 micrograms/cannula) along with HC-3. Atropine sulfate, an acetylcholine receptor blocker, also reduced lordotic behavior in females following intracerebral infusion (20 micrograms/cannula). These results lend support to the suggestion that lordotic behavior is facilitated by central cholinergic activity.

Animals↗
PubMed1979

Neonatal treatment of hamsters with barbiturate alters adult sexual behavior.

Male and female hamsters were given 50 micrograms pentobarbital, 100 micrograms pentobarbital, or 100 micrograms d-amphetamine on postnatal Days 2-4. When tested for masculine sexual behavior in adulthood, males treated with 100 micrograms pentobarbital showed behavioral deficits when tested with testes intact as well as after castration and treatment with testosterone propionate. Deficits shown by 50 micrograms pentobarbital males were overcome by testosterone replacement. When tested for feminine sexual behavior, males treated with 50 micrograms pentobarbital showed enhanced lordotic responses whereas males treated with 100 micrograms d-amphetamine showed no differences from controls when tested for female sexual behavior or when tested for male sexual behavior. Drug treatments had no effect on adult masculine or feminine sexual behavior in neonatally treated females. The results of this study show that pentobarbital can inhibit normal masculinization of the male when given during behavioral sexual differentiation.

Animals↗