Biomedical subjects

L G Clemens

Publications and source records attributed to L G Clemens.

At least 37 records · Page 2Linked to original sources

PubMed1989

Anatomical organization of the sexually dimorphic perineal neuromuscular system in the house mouse.

The anatomy of the sexually dimorphic motoneuron nuclei of the bulbocavernosus (BC) and ischiocavernosus (IC) muscles, as well as the non-sexually dimorphic external and sphincter (EAS), was examined in hybrid B6D2F1 mice using the retrograde tracer, cholera toxin-bound horseradish peroxidase. Motoneurons innervating the BC were located in the dorsomedial nucleus (DM), as well as in the ventral nucleus (V) and in the mid-region of the ventral horn (MVH). Following injections restricted to the IC, labelled neurons were found in the dorsolateral nucleus (DL), as well as in V, DM and MVH. Cells innervating the EAS in both males and females were located in the DM, as well as in the V and MVH. An elaborate network of dendrites extended between all labelled nuclei. The present results demonstrate that the anatomical specificity of the sexually dimorphic neuromuscular system of the mouse differs from that observed in other species.

Animals↗

PubMed1989

Environmental influences on masculine sexual behavior in mice.

Retention of masculine copulatory behaviors following castration varies among B6D2F1 male mice. In the present study, we examined the effect of test environment and the amount of behavioral testing after castration, on retention of copulatory responses in castrated B6D2F1 male mice. Results showed that weekly behavioral testing after castration was not necessary for the retention of ejaculatory reflexes. However, the test environment had a major effect. Following castration, 26% of the males completely stopped showing ejaculatory responses when tested in the test arenas. When these males were tested in their home cages, 75% achieved at least one ejaculatory response in four home cage tests. Castrated males that continued to copulate in the test arena situation also achieved ejaculatory reflexes in their home cages. These results indicate that for some B6D2F1 males, the retention of sexual behaviors after castration is influenced by environmental factors.

Animals↗

PubMed1989

Cholinergic regulation of female sexual behavior in rats demonstrated by manipulation of endogenous acetylcholine.

Infusions of the cholinesterase inhibitor, eserine, into the lateral ventricle of the brain facilitated lordosis in ovariectomized, estrogen primed female rats. Lordosis was also facilitated by infusions of 5 or 10 micrograms acetylcholine when this was accompanied by a low dose of eserine. Systemic treatment with the muscarinic antagonist, atropine (2 mg), completely blocked the facilitative effects of eserine and acetylcholine. In female rats made highly receptive by treatment with estrogen and progesterone, lordosis was inhibited by infusion of scopolamine into the lateral ventricles. These results agree with previous findings that sexual receptivity is regulated in part by endogenous cholinergic activity.

Acetylcholine↗

PubMed1989

Perinatal modification of a sexually dimorphic motor nucleus in the spinal cord of the B6D2F1 house mouse.

The sexually dimorphic dorsomedial nucleus (DM) of the spinal cord of mice is affected by gonadal steroids in adulthood and these effects are dependent upon genotype. Following castration of adult mice there is a decrease in DM cell size in DBA/2J and hybrid B6D2F1 strains and a decrease in the number of cells staining with thionin in C57B1/6J and B6D2F1 strains. The effects of androgens on development of the DM nucleus were examined in B6D2F1 mice, which exhibit both characteristics in adulthood. Testosterone propionate (TP) administered to females pre- or postnatally resulted in a significantly larger number of motoneurons in the region of the DM when compared to administration of the vehicle alone, while soma area remained unchanged. Adult males castrated on the day of birth had significantly fewer cells in the DM than did intact males. Differences in cell size between shams and castrates were dependent upon age.

Aging↗

PubMed1988

Retention of masculine sexual behavior following castration in male B6D2F1 mice.

The reduction of masculine sexual behavior following castration varies widely among genotypes. In contrast to the loss of sexual behavior by castrated males of other strains, males of the B6D2F1 genotype retain the ejaculatory reflex for many weeks after castration. The present study examined this retention phenomenon. Masculine sexual behaviors were measured before and after castration or sham operation in male C57BL/6J, DBA/2J, and B6D2F1 mice. Castrated C57BL/6J and DBA/2J males showed a rapid decline in copulatory behavior. In contrast, 30% of the B6D2F1 males continued to ejaculate 25 weeks after castration. Regardless of whether or not sexual behaviors were retained, levels of plasma testosterone and hypothalamic nuclear estrogen receptors were reduced by castration. These results suggest that the intra- and inter-strain differences in the retention of sexual behavior following castration are not due to differences in levels of steroid hormones. Further, some B6D2F1 males retain the ability to copulate in the absence of gonadal hormone levels required for the maintenance of sexual behavior in other genotypes.

Animals↗

PubMed1988

Hormonal restoration of masculine sexual behavior in long-term castrated B6D2F1 mice.

In contrast to the facilitative effects reported for other rodents, testosterone treatment at the time of castration previously was reported to inhibit masculine sexual behavior in male B6D2F1 mice. Males of this genotype vary in their behavioral response to castration. Some castrates retain sexual behaviors for many weeks after surgery, whereas others do not. In the present study, we sought to determine the effects of exogenous steroid hormone treatment on castrated B6D2F1 mice that had ceased to show copulatory behavior. Testosterone propionate and estradiol benzoate restored copulatory behavior to precastration levels in B6D2F1 males that did not retain sexual behaviors after castration.

Animals↗

PubMed1988

Brain localization of cholinergic influence on male sex behavior in rats: agonists.

Cholinergic agonists were microinjected into either the lateral ventricle or the preoptic area of sexually experienced male rats. In Experiment 1 carbachol, injected into the lateral ventricles, delayed the initiation of sexual behavior. When injected into the preoptic area, carbachol again delayed the onset of copulation, but these delays were shorter than after ventricular injections. In addition, preoptic injections reduced the number of intromissions preceding ejaculation. In Experiment 2 ventricular injections of the muscarinic agonist oxotremorine again delayed initiation of sexual behavior and also slowed its rate. However, oxotremorine injections into the preoptic area, through cannulae angled to miss all ventricles, only decreased the number of intromissions preceding ejaculation. These data suggest that cholinergic synapses in proximity to the ventricles may decrease sexual arousal, while cholinergic mechanisms in or near the preoptic area may reduce ejaculatory threshold.

Animals↗

PubMed1988

Brain localization of cholinergic influence on male sex behavior in rats: antagonists.

The muscarinic receptor antagonist scopolamine was microinjected into either the preoptic area or the lateral ventricle, preceding sexual behavior tests. In Experiment 1 unilateral ventricular injections of scopolamine delayed the initiation of copulation, while unilateral preoptic injections had no effect. In Experiment 2 bilateral injections into the preoptic area produced dose-related decreases in the percentages of animals intromitting and ejaculating. In Experiment 3 scopolamine, injected alone into the preoptic area, again decreased the percentages of animals mounting, intromitting, and ejaculating. The muscarinic agonist oxotremorine, injected alone into the preoptic area, decreased ejaculatory threshold (i.e., decreased the number of intromissions preceding ejaculation) as previously reported. Concurrent oxotremorine and scopolamine injections into the preoptic area were not different from vehicle; thus, scopolamine blocked oxotremorine's effect. These data suggest that some cholinergic activation of the preoptic area is critical for normal copulation, since bilateral blockade of muscarinic receptors there dramatically decreased the number of animals copulating. However, increased cholinergic activity there only reduced ejaculation threshold.

Animals↗

PubMed1987

Characteristics of the spinal nucleus of the bulbocavernosus are influenced by genotype in the house mouse.

Sex differences and differences related to genotype have been observed in the nervous system. These observations provide the opportunity to relate differences in neural structure to functional differences. The spinal nucleus of the bulbocavernosus (SNB) was examined in castrated and gonadally intact male house mice from the following 3 genotypes: C57B1/6J, DBA/2J, and the B6D2F1 (F1) hybrid (resulting from a cross between a C57B1/6J female and a DBA/2J male). The number and size of SNB neurons were determined from thionin-stained thick sections from spinal cords of these mice. The gonadally intact DBA males had significantly fewer SNB motoneurons than either the C57 or F1 males, but no strain differences were observed for the size of SNB cells. Castration of adults significantly reduced SNB neuronal number, but not somatic area, in the C57s (the maternal strain) and reduced somatic area, but not neuronal number, in the DBAs (the paternal strain). Both characteristics of the SNB were reduced by castration in the F1 hybrid. Thus, the size and number of SNB neurons appear to be inherited independently and the influence of gonadal hormones on these traits varies with genotype.

Animals↗

PubMed1987

A prenatal source for defeminization of female rats is the maternal ovary.

Sexual behavior in laboratory rats is influenced by a variety of factors in the perinatal environment. Male rats are masculinized and defeminized in response to circulating testosterone perinatally. Females undergo a process of feminization but in some cases are exposed to testosterone. Previous work has shown that during prenatal development female rats normally undergo a partial masculinization and defeminization of sexual behavior as reflected by altered responsiveness to gonadal hormones in adulthood. In the present study we investigated whether the maternal ovary influences adult females' responsiveness to gonadal hormones. Pregnant rats were ovariectomized on Day 10 of pregnancy and their offspring tested for sexual behavior in adulthood. Following ovariectomy pregnancies were maintained by administration of systemic progesterone. In addition the ovariectomized pregnant rats were given one of three daily treatments (Days 10-21): 0.2 microgram estradiol benzoate in sesame oil and 0.1 cc propylene glycol, 5 mg of the aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) in 0.1 cc propylene glycol, or 0.1 cc propylene glycol. A control group was generated from SHAM operated mothers given daily control injections of propylene glycol and sesame oil. Offspring were ovariectomized in adulthood and tested for display of feminine sexual behavior in response to estradiol benzoate and progesterone or estradiol benzoate alone. Masculine sexual behavior was measured in response to testosterone propionate (TP). Feminine sexual behavior was enhanced in offspring from ovariectomized mothers given only progesterone replacement during pregnancy. Offspring from mothers treated with ATD displayed the greatest elevations in feminine sexual behavior. Estradiol treatments of ovariectomized mothers prevented the increase in feminine potential seen in offspring in the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstatrienes↗

PubMed1987

Nicotinic cholinergic influences on sexual receptivity in female rats.

Drugs which alter nicotinic cholinergic transmission were administered to female rats to examine the neurochemical regulation of feminine sexual behavior. Nicotine (50, 100 or 200 micrograms/kg, IP) facilitated lordosis behavior 5 minutes after injection in estrogen-primed ovariectomized (OVX) rats. Pretreatment with the nicotinic antagonist, mecamylamine (MECA, 2.5 or 10 mg/kg) prevented this effect, while atropine pretreatment (30 mg/kg) reduced it. Mecamylamine pretreatment also reduced lordotic behavior induced by bilateral intracerebroventricular (ICV) injection of the cholinesterase inhibitor, eserine (5 micrograms/cannula). However, MECA treatment (5 or 10 micrograms/cannula, bilaterally, ICV, or 5 or 10 mg/kg, IP) did not reduce sexual receptivity in OVX rats made highly receptive with estrogen plus progesterone priming. By comparison with previously published results, MECA is apparently less effective than muscarinic antagonists in disrupting sexual receptivity in several paradigms. There appears to be a critical muscarinic link in the neural circuit for sexual receptivity, but there does not appear to be a comparable nicotinic link. In fact, the lordosis-facilitating effect of nicotine may be a pharmacological effect unrelated to the normal neurochemical regulation of sexual receptivity.

Animals↗

PubMed1986

Cholinergic mediation of feminine sexual receptivity: demonstration of progesterone independence using a progestin receptor antagonist.

Feminine sexual receptivity can be elicited by the intracerebral administration of muscarinic cholinergic substances in ovariectomized female rats treated with small amounts of estrogen. These experiments were designed to investigate whether this facilitative cholinergic mechanism is dependent upon progesterone. In the first experiment, estrogen-primed animals were injected with RU 38486, a progestin receptor antagonist, 1 h before progesterone or vehicle injection. Injection of RU and progesterone on Day 1 of testing produced animals which were sexually unreceptive. Furthermore, injection of the antagonist without concomitant progesterone produced animals which were unresponsive to progesterone given 24 h later. Thus, RU 38486 itself may be binding to progestin receptors in critical brain regions, preventing progesterone from binding to these same receptors. In Experiment 2, animals made sexually unreceptive by treatment with RU 38486 subsequently became receptive when injected intracerebrally with oxotremorine, a muscarinic agonist. Therefore, activation of progestin receptors does not appear necessary for the cholinergic mediation of sexual receptivity. As in Experiment 1, animals receiving progesterone on Day 1 showed a diminished response to a second progesterone injection 24 h later; an even greater decrease in this response was observed in animals that also received the antagonist on Day 1.

Animals↗

PubMed1986

Norepinephrine infusions into the medial preoptic area inhibit lordosis behavior.

Neurotransmitters, including norepinephrine, have been implicated in the mediation of ovarian steroid induced lordosis behavior in ovariectomized rats. In this study we have found that norepinephrine (NE) infusions into the medial preoptic area (MPOA) reduced lordosis frequencies of estrogen-progesterone treated (0.5 micrograms estradiol benzoate for three days followed by 500 micrograms progesterone 4-5 hours before testing) receptive rats. Norepinephrine doses of 2 micrograms or more per animal infused into the MPOA significantly reduced lordosis levels within five minutes. Infusions of 10 and 20 micrograms doses of NE suppressed lordosis levels for 15 minutes after infusion. At the lowest inhibitory dose (2 micrograms/animal) simultaneous infusion of 5 micrograms/microliter of the noradrenergic antagonist yohimbine, but not of phentolamine or propranolol, blocked the reduction in lordosis resulting from NE infusion. Preoptic infusions of epinephrine and clonidine were also effective in reducing lordosis quotients, while methoxamine, phenylephrine and isoproterenol did not alter receptivity. These findings are consistent with the conclusion that the direct effect of norepinephrine infusions into the MPOA is inhibition of lordosis responding. There is some evidence that this inhibitory influence is mediated by alpha 2-noradrenergic receptors.

Animals↗

PubMed1986

Evidence for involvement of midbrain central gray in cholinergic mediation of female sexual receptivity in rats.

Experiments were designed to determine the role of the midbrain central gray (MCG) in facilitation of lordosis by cholinergic agonists. In Experiment 1, estradiol-treated female rats received microinjections of carbachol into the MCG and showed a dose-related behavioral facilitation to the agonist. In Experiment 2, MCG injections of oxotremorine (OXO), a selective muscarinic receptor agonist, yielded a dose-related facilitation; this was blocked by systemic pretreatment with scopolamine (SCOP), a muscarinic antagonist. In Experiment 3, MCG-lesion animals were injected unilaterally with OXO intraventricularly following contralateral injection of SCOP or vehicle. Females with MCG damage displayed significantly less facilitation than sham-lesion animals. Pretreatment with SCOP abolished lordosis facilitation in both groups. In addition, after treatment with estradiol and progesterone, sham-lesion females showed more receptivity than MCG-lesion females. Systemic injection of SCOP produced a significant decline in lordosis for both groups. On the basis of these data, it is suggested that the MCG plays an important role in the cholinergic mediation of female sexual receptivity.

Animals↗

PubMed1985

A microcomputer-based system for recording and analyzing behavioral data regarding the sexual activity of male rodents.

A microcomputer (TRS-80 Model 4P) based system has been developed to aid in the collection and analysis of behavioral data regarding sexual activity in male rodents. Its capabilities include the recording of events, the online calculation of frequency and latency measures, the monitoring of temporal intervals as demanded by experimental protocols, and the prompting of experimenter activities at prescribed times.

Animals↗

PubMed1985

Prenatal antiandrogen feminizes behavioral but not neurochemical response to estrogen.

In ovariectomized female rats, estrogen activates high levels of female sexual behavior and induces an increase in the number of cholinergic muscarinic binding sites in the medial basal hypothalamus, an area known to regulate this behavior. Male rats normally show low levels of female sexual behavior and no alteration in muscarinic binding in response to estrogen treatment. An experiment was conducted to determine if a prenatal treatment that feminizes the sexual behavior of male rats would also establish the potential for estrogen to increase muscarinic binding in the male hypothalamus. Results indicate that prenatal exposure to the antiandrogen, flutamide, enhanced estrogen-activated female sexual behavior in male rats but failed to reverse the inability of estrogen to increase muscarinic binding in the medial basal hypothalamus.

Androgen Antagonists↗

PubMed1984

Pharmacological and anatomical aspects of cholinergic activation of female sexual behavior.

Forebrain infusion of cholinergic agonists activated the sexual response, lordosis, in ovariectomized female rats that had been primed with a low dose of estrogen. Carbachol, an agonist with both muscarinic and nicotinic properties, and oxotremorine, an agonist with a primarily muscarinic action, produced dose-related increases in the frequency of lordosis elicited by stimulus male rats. This facilitation of lordosis was prevented when females were pretreated systemically with atropine or scopolamine, two muscarinic receptor antagonists. These results indicate that the effect of carbachol and oxotremorine on lordosis is mediated by cholinergic muscarinic receptors. The location of these receptors within the brain has not been identified. Ventricular infusion of carbachol was as effective as infusion directly into the medial preoptic area (POA) and more effective than infusion directly into the ventromedial hypothalamus (VMH). Furthermore, when carbachol or oxotremorine was delivered to the POA through cannulae angled to avoid traversing the lateral ventricles, no facilitation of lordosis was observed. These data suggest that muscarinic receptors stimulated by central infusion of cholinergic agonists may not be located in either the POA or the VMH, two regions traditionally implicated in the regulation of lordosis.

Animals↗

PubMed1983

Inhibition of estrogen-activated sexual behavior by androgens.

Experiments to determine the potential of androgen to inhibit estrogen-activated female sexual behavior in rats were conducted. Treatment with either testosterone propionate (0.8 or 1.6 mg/day) or dihydrotestosterone propionate (0.2, 0.4, or 0.8 mg/day) significantly reduced the incidence of lordosis in ovariectomized females receiving estradiol benzoate (1 microgram/day). A similar suppression of estrogen-activated lordosis by testosterone was observed in castrated male rats. Flutamide, an androgen-receptor blocker, prevented the inhibition of lordosis by testosterone in females, indicating that the interaction of testosterone or a metabolite with an androgen receptor may be an important feature of this inhibition. Furthermore, the ability of dihydrotestosterone to inhibit lordosis at lower doses than testosterone suggests that the conversion of testosterone to dihydrotestosterone may also be necessary. These experiments demonstrate the potential of testosterone to inhibit the occurrence of female sexual behavior in rats, in contrast to its established facilitative effect on this behavior.

Androgens↗