Sexual behavior in animals

The present study investigated the role of brain serotonin activity in the mediation of masculine sexual behavior in the intact male rat. The results of previous studies suggest a dissociation of the effects of gonadal hormones on central serotonin metabolism and sexual behavior in the male rat. However, serotonin activity was measured some 24 hours after the last test of sexual activity. In the present experiment, animals were assigned to one of five groups, and were sacrificed by decapitation immediately after meeting their respective behavioral criterion. High performance liquid chromatography (HPLC) was used to measure concentrations of serotonin and its metabolite, 5-hydroxyindoleacetic acid, in the hypothalamus-preoptic area. Analyses of variance revealed no significant differences in brain serotonin activity as a function of sexual behavior. Results are discussed in the context of the role of biogenic amines in the mediation of masculine sexual behavior in the male rat.

Forty-eight adult Long-Evans male rats were tested
following castration for male and female sex behavior.
Following baseline test Ss received 200 mug injections of estradiol daily except on days of female tests when
20 mug of progesterone were given. Tests for male and female
behavior were alternated every third day. Significant
increases in mean lordosis and male behavior occurred
following hormone treatment. After hormone tests eight Ss received anterior lesions and five Ss received preoptic lesions. Afer recovery Ss were placed on the same schedule of hormones and tests as for the previous condition. No
significant changes in mean lordosis or male behavior occurred
following either lesion. It was concluded that estrogen is
effective in restoring male behavior and producing female
sex behavior in castrated males. While no significant changes
occurred following the lesions, it was determined that repetition and extension of the work is justified.

Performance on three preoperative and three postoperative
copulation tests was compared for male rats given dorsal
hippocampal, dorsal hippocampal plus cortical, other lesion,
and sham lesions. Dorsal hippocampal lesions produced
statistically significant changes in the temporal pacing
of some components of sexual behavior, i.e. the post-ejaculatory interval, intercopulatory interval, and total
test time decreased. Hippocampal plus cortical lesions
had no effect on sexual behavior. The results are interpreted
as supporting a model of inhibition in which a
sexual inhibitory process is built up concomitantly with
the sexual arousal process.

Twenty-six 75-day-old, ovariectomized Long-Evans female
rats were randomly divided into two groups of ten and one
group of six animals. The ten Group I Ss received, in consecutive
treatment periods, 2 mg progesterone (P-2) daily,
2 mg testosterone propiorate (TP-2) daily, TP-2 daily plus
P-2 every fourth day, and P-2 every fourth day. The ten Group
II Ss received, in consecutive treatment periods, P-2 every
fourth day, and 4 mg dihydrotestosterone (DHT-4) daily plus
P-2 every fourth day. Both Groups I and II were tested for
female sexual behavior. A significant increase in the lordosis
response was observed only in Group I Ss after receiving TP-2
plus P-2 every fourth day. Group III Ss were tested for male
sexual behavior after receiving DHT-4 daily. Male sexual
behavior increased significantly after DHT-4 treatments. It
was concluded that progesterone exerts a facilitatory effect
on female sexual behavior only when the Ss have been previously
primed with an aromatizable androgen and that dihydrotestosterone
is capable of inducing male sexual behavior in female rats.

Fourteen 75-day-old female rats of the Long-Evans strain
were ovariectomized and divided into two groups of seven.
Group I received daily injections of 2mg testosterone propionate
(TP) and was tested for male sexual behavior. Group
II, in addition to daily injections of TP, also received injections
of 1mg progesterone on five of the ten test days.
This group was tested for female sexual behavior. TP was
found to exert a facilitory effect on both male and female
sexual behavior. Female sexual behavior was enhanced
further when progesterone was administered 4 to 6 hours
prior to testing. Progesterone, when injected alone, was
found to induce lordosis. It was concluded that TP was
first being converted to estrogen and it was the estrogen
which was responsible for the increase in female sexual
behavior. The fact that progesterone, which enhances
estrogen-induced lordosis, also enhances testosterone-induced
lordosis supports this position.