Progestin Receptor-Mediated Reduction of Anxiety-Like Behavior in Male Rats

BACKGROUND: It is well known progesterone can have anxiolytic-like effects in animals in a number of different behavioral testing paradigms. Although progesterone is known to influence physiology and behavior by binding to classical intracellular progestin receptors, progesterone's anxiety reducing effects have solely been attributed to its rapid non-genomic effects at the GABA A receptor. This modulation occurs following the bioconversion of progesterone to allopregnanolone. Seemingly paradoxical results from some studies suggested that the function of progesterone to reduce anxiety-like behavior may not be entirely clear; therefore, we hypothesized that progesterone might also act upon progestin receptors to regulate anxiety. METHODOLOGY/PRINCIPAL FINDINGS: To test this, we examined the anxiolytic-like effects of progesterone in male rats using the elevated plus maze, a validated test of anxiety, and the light/dark chamber in the presence or absence of a progestin receptor antagonist, RU 486. Here we present evidence suggesting that the anxiolytic-like effects of progesterone in male rats can be mediated, in part, by progestin receptors, as these effects are blocked by prior treatment with a progestin receptor antagonist. CONCLUSION/SIGNIFICANCE: This indicates that progesterone can act upon progestin receptors to regulate anxiety-like behavior in the male rat brain

Mediation of rat postejaculatory 22 kHz ultrasonic vocalization by dopamine D2 receptors

We investigated the role of dopamine receptor subtypes in the regulation of ultrasonic vocalization and masculine copulatory behavior. Intact sexually experienced male Long-Evans rats were treated with saline, selective dopamine D1 (SKF 38393) and D2 (LY 171555) receptor agonists and with selective dopamine D1 (SCH 23390) and D2 (raclopride) receptor antagonists 15 and 30 min before the 30-min test session, respectively. Mating stimuli were ovariectomized female rats injected SC with estradiol benzoate (8 micrograms/0.1 ml/rat) and progesterone (200 micrograms/0.1 ml/rat), 48 and 4 hr before the test session, respectively. We found a decrease in the number of intromissions required to reach ejaculation in animals treated with SKF 38393 (10 mg/kg/IP), LY 171555 (doses ranging from 0.01 to 0.5 mg/kg/SC) and with raclopride (0.1 mg/kg/SC). LY 171555 reduced the postejaculatory vocalization (PEV) in a dose-dependent fashion with complete suppression at the highest dose. No other parameters of sexual behavior were affected by this treatment. Raclopride, a dopamine D2 receptor antagonist, antagonized the suppressive effects of the D2 agonist LY 171555 on the PEV (and also decreased the number of intromissions to reach ejaculation), whereas SCH 23390, a dopamine D1 receptor antagonist, did not. Raclopride, given alone at the dose of 0.5 mg/kg/SC, almost completely suppressed all behavioral activity, whereas the lower dose (0.1 mg/kg) decreased intromission frequency and increased the length of the 22 kHz PEV. Therefore, we suggest that 22 kHz PEV is under the control of dopamine D2 receptor

Subtle behavioural changes produced in rat pups by in utero exposure to haloperidol

Prenatal exposure to a dopamine receptor blocking agent such as haloperidol (given to the mother at a dose of 0.5 mg/kg s.c. from day 4 to day 15 of gestation) produced subtle behavioural changes in rat pups. Haloperidol decreased the rate of ultrasonic vocalization in 4-day-old male pups removed from the nest. The changes in ultrasonic emission elicited by in utero exposure to this neuroleptic were markedly different from those produced by its administration during the early postnatal period. Moreover, adult male rats treated prenatally with haloperidol exhibited a significant increase in the intensity of ultrasonic 22 kHz post-ejaculatory calls emitted during sexual behaviour. The duration of the period of the 22 kHz calls emission was also significantly increased by haloperidol treatment. These results confirm that ultrasonic vocalization in rats is a sensitive indicator of subtle changes in adverse treatments administered during development