Inhibition of lordosis in female hamsters and rats by 8-OH-DPAT treatment.

In the present experiments, the ability of the 5-HT1A agonist, 8-OH-DPAT, to inhibit lordosis was determined in ovariectomized hamsters and rats under various hormonal conditions. Systemic administration of 8-OH-DPAT (0.25 mg/kg) significantly inhibited lordosis duration in ovariectomized hamsters treated on 3 consecutive wk with estradiol benzoate (3 or 10 micrograms) and progesterone (500 micrograms). Similarly, systemic administration of 8-OH-DPAT (0.25 mg/kg) significantly inhibited lordosis frequency in ovariectomized rats treated on 3 consecutive wk with estradiol benzoate (0.25, 0.5, or 25 micrograms for 3 days) and progesterone (500 micrograms), although females treated with the higher doses of estrogen were slightly less inhibited on the second and third wk of testing. Results indicate that the 5-HT1A agonist, 8-OH-DPAT, effectively inhibited lordosis in female hamsters, as well as female rats, under varied hormonal conditions.

Androgenic-anabolic steroids modify beta-endorphin immunoreactivity in the rat brain.

Immunocytochemical localization of beta-endorphin in the brains of intact and castrated male rats was conducted after the administration of high levels of androgenic-anabolic steroids (AAS; 14 daily injections of sesame oil or a cocktail of 2 mg/kg testosterone cypionate, 2 mg/kg nandrolone decanoate, and 1 mg/kg boldenone undecylenate) at doses commonly self-administered by athletes who are considered 'heavy abusers'. In normal intact oil-treated males, cytoplasmic immunoreactivity was prevalent throughout the arcuate nucleus while intense fiber tract immunoreactivity was most prevalent in the bed nucleus of the stria terminalis and the paraventricular hypothalamic nucleus. Administration of AAS significantly decreased the number of neurons exhibiting cytoplasmic immunoreactivity only in the rostral region of the arcuate nucleus. AAS treatment had no effect on beta-endorphin immunoreactivity in the middle or caudal aspects of the arcuate nucleus.

Estrogen dependence of cholinergic systems that regulate lordosis in cycling female rats.

Previous evidence indicated that physostigmine, an acetylcholinesterase inhibitor, facilitated lordosis behavior when administered intraventricularly to cycling female rats on proestrus prior to the onset of natural sexual receptivity, but not when administered to rats on mid-diestrus or diestrus II. In the present experiments, intraventricular infusion of physostigmine (10 micrograms bilaterally) facilitated lordosis on mid-diestrus and diestrus II if females were primed with two injections of estradiol (0.2, 0.1, or 0.05 micrograms) administered 20 h and 32 h prior to infusion of physostigmine. Despite unequal levels of endogenous progesterone, physostigmine facilitated lordosis equally on mid-diestrus and diestrus II following estradiol priming. Finally, intraventricular infusion of the muscarinic receptor blocker scopolamine (20 micrograms bilaterally) reduced the incidence of lordosis in females that displayed lordosis on mid-diestrus following estrogen priming. Results confirm that cholinergic mechanisms influence sexual behavior displayed by cycling female rats. Data further indicate that sufficient estrogen stimulation is necessary for cholinergic neurons to facilitate lordosis. However, progesterone does not play a major role in the regulation of lordosis by cholinergic systems.

Effects of a muscarinic antagonist on various components of female sexual behavior in the rat.

The effects of the muscarinic antagonist scopolamine on lordosis, solicitation, pacing, approach, attractivity, and activity were evaluated in ovariectomized rats brought into sexual receptivity with estrogen and progesterone. Systemic (1 mg/rat) or intraventricular (10 micrograms bilaterally) administration of scopolamine significantly reduced the incidence of lordosis and solicitation behaviors and disrupted typical pacing of sexual contacts with a stimulus male. In addition, females avoided contact with a stimulus male, but not a stimulus female, following intraventricular infusion of scopolamine. The levels of general activity and frequencies of sexual contacts were similar in females treated intraventricularly with scopolamine and vehicle solutions. Consequently, scopolamine disrupted various components of sexual behavior, including lordosis, solicitation, pacing, and approach, without altering female attractivity or general activity.

Up-regulation of androgen receptor immunoreactivity in the rat brain by androgenic-anabolic steroids.

To characterize central nervous system changes that occur with anabolic steroid abuse in humans, immunocytochemical localization of androgen receptors in the brains of 10 intact and 10 castrated male rats was conducted after the administration of high levels of androgenic-anabolic steroids (AAS; 14 daily injections of sesame oil or a cocktail of 2 mg/kg testosterone cypionate, 2 mg/kg nandrolone decanoate, and 1 mg/kg boldenone undecylenate). In normal intact oil-treated males, nuclear androgen receptor immunoreactivity was present in many 'classical' and 'non-classical' androgen target sites in the brain. Administration of AAS increased the intensity of immunoreactivity in most classical androgen target sites and increased both the intensity of immunoreactivity and number of immunoreactive cells in most non-classical androgen target sites. These results may suggest that androgen receptors in the brain are up-regulated by AAS. The simultaneous androgen receptor up-regulation in these regions by AAS may account for the complex anabolic steroid abuse syndrome. Consistently, androgen receptor immunoreactivity in most brain regions was reduced or absent after castration, suggesting that endogenous androgen levels are necessary for normal androgen receptor immunoreactivity. These results identify the distribution of one central nervous system mechanism modified by AAS.

The effect of estrogen treatment on scopolamine inhibition of lordosis.

Previous evidence indicates that the cholinergic muscarinic antagonist, scopolamine, inhibits lordosis in female rats. In the experiments reported here, the effects of various doses and repeated administrations of estrogen on the scopolamine inhibition of lordosis were examined. In the first experiment, intraperitoneal injections of scopolamine (1 mg/rat) completely inhibited lordosis in ovariectomized rats primed with low doses of estradiol benzoate (0.25 or 0.5 micrograms for 3 days) and progesterone (500 micrograms). However, scopolamine was significantly less effective in inhibiting lordosis in females primed with a higher dose of estradiol benzoate (25 micrograms for 3 days) and progesterone (500 micrograms). When hormone priming was repeated on subsequent weeks, scopolamine continued to inhibit lordosis in females that received 0.25 micrograms estradiol benzoate but was less effective in females primed with 0.5 micrograms. Scopolamine failed to inhibit lordosis in females treated with 25 micrograms estradiol benzoate on these later tests. In the second experiment, various doses of scopolamine (1, 2, or 4 mg/rat) were administered intraperitoneally to females primed with the highest dose of estradiol benzoate (25 micrograms) and progesterone (500 micrograms). Lordosis was inhibited equally by all scopolamine doses during the first week. As in the first experiment, scopolamine failed to inhibit lordosis at all doses on subsequent weeks of testing. These results indicate that the ability of scopolamine to inhibit lordosis is reduced by increasing the dose or the number of estrogen exposures. Because higher doses of scopolamine failed to restore its inhibitory effect on lordosis an upregulation of muscarinic receptors by estrogen cannot account for the reduced effectiveness of scopolamine.

Physostigmine facilitation of lordosis in naturally cycling female rats.

Both systemic and intracerebral administrations of the cholinergic muscarinic antagonist, scopolamine, have been shown to inhibit naturally occurring sexual behavior in intact, cycling female rats. The present study examined the facilitative effects of the acetylcholinesterase inhibitor, physostigmine (eserine), on sexual behavior in intact, cycling female rats. Cycling was determined by daily monitoring of sexual behavior and vaginal cytology. When administered during either early proestrus or proestrus, physostigmine activated lordosis 15 min and 1 hr after intraventricular infusion (10 micrograms bilaterally). However, infusion of physostigmine failed to facilitate lordosis 15 min after administration during either diestrus I, mid-diestrus, or diestrus II. The administration of this cholinergic agent did not interrupt cyclicity patterns. Because estrogen levels are highest during proestrus and cholinergic facilitation appears to be limited to this time, it is suggested that estrogen priming of central cholinergic systems is necessary for the cholinergic regulation of sexual behavior in intact, cycling female rats.

Scopolamine inhibition of lordosis in naturally cycling female rats.

Cholinergic antagonists, such as scopolamine, atropine, and hemicholinium-3, have been found previously to inhibit lordosis in ovariectomized rats primed with estrogen and progesterone. The present study further examined this effect using intact cycling female rats. Cycling was determined by daily monitoring of sexual behavior and vaginal cytology. In the first experiment, intraventricular administration of the muscarinic receptor blocker, scopolamine, was found to significantly inhibit lordosis behavior during natural estrus (10 or 20 micrograms bilaterally). In the second experiment, systemic administration of scopolamine was also found to significantly inhibit lordosis behavior during natural estrus (4 mg/kg, IP). Administration of the cholinergic antagonist did not significantly interrupt cyclicity patterns. These results indicate that central cholinergic muscarinic systems contribute to the regulation of lordosis during natural behavioral estrus in intact female rats.