Inactivation of the medial preoptic area/anterior hypothalamus by lidocaine reduces male sexual behavior and sexual incentive motivation in male rats.

Permanent bilateral lesions of the medial preoptic area anterior hypothalamus (MPOA/AH) produce a drastic inhibition of male sexual behavior in all species studied to date. The present experiment was designed to evaluate if temporal inactivation of the MPOA/AH by infusions of lidocaine also inhibits sexual behavior in male rats. This would allow us to rule out the possibility that the behavioral effects observed after damage of the MPOA/AH could be associated with plastic changes induced by the lesion in other brain regions. We also evaluated sexual incentive motivation in males after the infusion of lidocaine in a test in which copulation is not possible but where males maintain approach behavior to the estrous females despite repeated testing. The percentage of animals displaying mounts, intromissions and ejaculation was significantly reduced while mount and intromission latency were prolonged after infusion of lidocaine. No changes were observed in sexual behavior after infusion of lidocaine in animals with cannulae outside the MPOA/AH suggesting that the inhibitory effects are specific to this brain region. Sexual incentive motivation was also affected by administration of lidocaine. Males consistently showed a clear preference for the sexually receptive female except when infused with lidocaine. After the infusion of the compound a significant reduction in the time spent in the incentive zone of the stimulus female was observed. These results support the hypothesis that neurons of the MPOA/AH are involved in the control of male sexual motivation.

GABA Receptors in the Medial Preoptic Area Modulate the Onset of Oestradiol-Induced Maternal Behaviour in Hysterectomised-Ovariectomised, Pregnant Rats.

We studied the participation of GABA neurotransmission in the medial preoptic area (mPOA) with respect to the onset of the pup retrieval response and nest building. Pregnant female rats were implanted with bilateral cannulae in the mPOA on day 12 of pregnancy and, on day 16, the females were hysterectomised and ovariectomised and given 200 µg/kg of oestradiol benzoate. Two days later, the females received one of the following intracerebral drug treatments: GABAB agonist baclofen (200 ng); GABAB antagonist phaclofen (1 µg); GABAA antagonist bicuculline (60 ng); or physiological saline. Five minutes after intracerebral infusion, three foster pups were introduced into the females' home cage. The subjects were observed for pup grouping (retrieval) during 15 min, after which the pups were left with the female. During the next 12 h, an observation was made every 1 h to determine whether the pups had been grouped (retrieved) or not. The GABAB agonist baclofen reduced the proportion of females retrieving pups from 4 to 8 h following pup introduction. By contrast, both the GABAA antagonist bicuculline and the GABAB antagonist phaclofen enhanced the proportion of females retrieving pups during the first 3 h of observation. The latency to pup retrieval in subjects treated with the GABAB agonist baclofen was significantly longer than that in subjects given any of the antagonists. All females built a nest but baclofen reduced nest quality. These data show that activation of GABAB receptors in the mPOA has an inhibitory effect on basic maternal behaviours, whereas blockade of either the GABAA or GABAB receptor facilitates pup retrieval. It is possible that reduced GABAergic tone in the mPOA is a key element in the initiation of maternal behaviours in postparturient rats.

Role of Oestrogen α Receptors in Sociosexual Behaviour in Female Rats Housed in a Seminatural Environment.

The present study investigated the role of oestrogen receptor (ER)α in the ventromedial nucleus of the hypothalamus (VMN), the preoptic area (POA), the medial amygdala (MePD) and the bed nucleus of stria terminalis (BNST) in sociosexual behaviour in female rats. This was conducted in two sets of experiments, with the VMN and POA investigated in the first set, and the MePD and BNST in the second set. The VMN and POA received intense projections from the MePD and BNST. We used a short hairpin RNA encoded within an adeno-associated viral vector directed against the gene for ERα to reduce the number of ERα in the VMN or POA (first set of experiments) or in the BNST or MePD (second set of experiments) in female rats. The rats were housed in groups of four ovariectomised females and three males in a seminatural environment for 8 days. Compared with traditional test set-ups, the seminatural environment provides an arena in which the rats can express their full behavioural repertoire, which allowed us to investigate multiple aspects of social and sexual behaviour in groups of rats. Behavioural observation was performed after oestrogen and progesterone injections. A reduction of ERα expression in the VMN or POA diminished the display of paracopulatory behaviours and lordosis responses compared to controls, whereas the lordosis quotient remained unaffected. This suggests that ERα in the VMN and POA play an important role in intrinsic sexual motivation. The reduction in ERα did not affect the social behaviour of the females, although the males sniffed and pursued the females with reduced ERα less than the controls. This suggests that the ERα in the VMN and POA is involved in the regulation of sexual attractiveness of females. The ERα in the MePD and BNST, on the other hand, plays no role in sociosexual behaviour.

GABA and behavior: the role of receptor subtypes.

The discovery of different GABA receptor subtypes has stimulated research relating this neurotransmitter to a variety of behavioral functions and clinical disorders. The development of new and specific GABAergic compounds has made it possible to try to identify the specific functions of these receptors. The purpose of the present review is to evaluate the data regarding the functions of the GABA receptor subtypes in different behaviors such as motor function, reproduction, learning and memory, and aggressive-defensive behaviors. A description of GABAergic functions (stress, peripheral effects, thermoregulation) that might directly or indirectly affect behavior is also included. The possible involvement of GABA in different neurological and psychiatric disorders is also discussed. Although much research has been done trying to identify the possible role of GABA in different behaviors, the role of receptor subtypes has only recently attracted attention, and only preliminary data are available at present. It is therefore evident that still much work has to be done before a clear picture of the behavioral significance of these receptor subtypes can be obtained. Nevertheless, existing data are sufficient to justify the prediction that GABAergic agents, in the near future, will be much used in the field of behavioral pharmacology. It is hoped that the present review will contribute to this. Some specific suggestions concerning the most efficient way to pursue future research are also made.

Impaired discrimination of and aversion to parasitized male odors by female oxytocin knockout mice.

A major cost of social behavior is the increased risk of exposure to parasites, with animals utilizing social information to recognize and avoid infected conspecifics. In mice, females can discriminate between infected and uninfected males on the basis of social cues, displaying aversive responses to the odors of infected males. In the present study, using female mice whose gene for oxytocin (OT) has been selectively deleted (OT knockout mice (OTKO)), we show that at least one normal allele for OT is required for the mediation of the recognition and avoidance of parasitized males. Female wild type (OTWT) and heterozygous (OTHZ) mice distinguished between the odors of individual males infected with the louse, Polyplax serrata, and uninfected males while the KO mice did not. Exposure to the odors of infected males induced analgesia in OTWT and OTHZ females, with OTKO females displaying attenuated analgesia. OTWT and OTHZ females, but not the OTKO females, also distinguished between the odors of novel and familiar infected males and modulated their analgesic responses on the basis of prior familiarity. In an odor choice test, OTWT and OTHZ females displayed a marked initial choice for the odors of uninfected males, whereas the OTKO females showed no consistent choice. This impairment was specific to the odors of infected males. OTKO females displayed normal analgesic responses to another aversive social odor, that of a stressed male, and an aversive non-social odor, that of a cat. The OTKOs had normal non-social olfactory memory, but were impaired in their social odor memory. These findings indicate that a normal OT gene comprises an essential part of the central recognition mechanism whereby females can both reduce the transmission of parasites to themselves and select for parasite-free males.

Oxytocin and estrogen receptor alpha and beta knockout mice provide discriminably different odor cues in behavioral assays.

Social behavior involves both the recognition and pro-duction of social cues. Mice with selective deletion(knockout) of either the gene for oxytocin (OT) or genes for the estrogen receptor (ER) -c or -B display impaired social recognition. In this study we demonstrate that these gene knockout mice also provide discriminably different social stimuli in behavioral assays. In an odor choice test, which is a measure of social interest and discrimination, outbred female Swiss-Webster mice discriminated the urine odors of male knock-outs IKO: OTKO, alphaERKO, betaERKO) from the odors of their wildtype littermates (WT: OTWT, alphaERWT, betaERWT). Females showed marked initial choices of the urine odors of OTWT and betaERWT males over those of OTKOand PERKO males, and alphaERKO males over alphaERWT males. The odors of OTKO and betaERKO males also induced aversive, analgesic responses, with the odors of WTs having no significant effects. Odors of both the alphaERWT andalphaERKO males induced aversive, analgesic responses,with the odors of the WT inducing significantly greater analgesia. The odors of restraint stressed WT and KO males also elicited analgesia with, again, females dis-playing significantly greater responses to the odors of stressed OTKO and betaERKO males than their WTs, and significantly lower analgesia to the odors of stressedalphaERKO than alphaERWT males. These findings show that the KO mice are discriminated from their WTs on the basis of odor and that the various KOs differ in the relative attractiveness/aversiveness of their odors. Therefore, in behavioral assays one causal route by which gene inactivation alters the social behavior of knockout mice may be mediated through the partners'modified responses to their odors.

The role of subtypes of the opioid receptor in the anxiolytic action of chlordiazepoxide.

Previous studies have shown that the opiate antagonist naloxone blocks the anxiolytic-like effects of benzodiazepines in several models of anxiety, including the elevated plus-maze. Although naloxone preferentially binds to the mu opioid receptor, its selectivity is rather low. The opioid receptor subtype important for anxiolytic-like actions of benzodiazepines in the plus-maze remains, therefore, unknown. In the present experiments, the ability of antagonists selective for subtypes of the opioid receptor to block the anxiolytic-like effects of chlordiazepoxide in the elevated plus-maze was evaluated in Swiss mice. Chlordiazepoxide, 5 mg/kg, increased the proportion as well as the number of open arms entries without modifying closed arms entries. Lower doses of the benzodiazepine were ineffective. The mu receptor antagonist beta-funaltrexamine, 10 and 20 mg/kg, the delta antagonist naltrindole, 10 mg/kg, and the kappa antagonist nor-binaltorphimine, 2.5 and 5 mg/kg, were then combined with chlordiazepoxide, 5 mg/kg. beta-funaltrexamine, 10 mg/kg, reduced the effects of the benzodiazepine while the dose of 20 mg/kg completely blocked the effects. Nor-binaltorphimine was ineffective at a dose of 2.5 mg/kg, but completely inhibited the actions of chlordiazepoxide when the dose was 5 mg/kg. Naltrindole was ineffective. None of the antagonists affected plus-maze behavior when administered alone. It was concluded that the mu and kappa receptors are important for the anxiolytic-like actions of chlordiazepoxide in the elevated plus maze.

Sexual behaviour in castrated rabbits treated with testosterone, oestradiol, dihydrotestosterone or oestradiol in combination with dihydrotestosterone.

Sexual behaviour and the function of the accessory sexual glands were studied in castrated rabbits injected with testosterone benzoate (TB), oestradiol benzoate (OEB), dihydrotestosterone benzoate (DHTB) or OEB in combination with DHTB. Testosterone benzoate (1 mg daily for 90 days) stimulated the sexual behaviour more than any of the other steroids. The combination of OEB (0-33 mg) and DHTB (1 mg) was no more effective than either of these steroids given alone. The function of the accessory sexual glands was stimulated to a level comparable to that of intact animals given TB. Dihydrotestosterone benzoate was, however, not very effective in this respect. Oestradiol benzoate alone or in combination with DHTB caused hypertrophy and very low secretory activity of the seminal vesicles. These results suggest that testosterone itself is active both in the brain and in the accessory sexual glands in rabbits. This is in contrast to the rat, in which aromatization to oestradiol in the brain and reduction to DHT in the periphery seems to be important.

Sexual reinforcement is blocked by infusion of naloxone into the medial preoptic area.

The present experiment was designed to determine whether infusions of naloxone into specific brain sites can block sexual reinforcement as evaluated with the conditioned place preference procedure. Methylnaloxonium (5 micrograms/cannula) was infused bilaterally either into the medial preoptic area (MPOA) or into the nucleus accumbens (NAC) of sexually experienced male rats. We chose the MPOA because it is important for sexual behavior, and several opioid peptides have been shown to modify sexual behavior when infused there. The NAC appears to be a critical structure for drug-induced reward. Methylnaloxonium blocked place preference produced by ejaculation after infusion into the MPOA without affecting sexual behavior. Infusion of the antagonist into the NAC did not reduce the reinforcing properties of ejaculation. These data suggest that the MPOA may be a site where sexual reward is produced.

Reinforcing properties of ejaculation in the male rat: role of opioids and dopamine.

Ejaculation-induced reward in the male rat was evaluated by the conditioned place-preference paradigm. It was supposed that ejaculation induces a reward state such that it can be conditioned to environmental stimuli. Males were allowed to ejaculate once and were then immediately transferred to a place-preference cage. One ejaculation produced place preference. Naloxone (16 mg/kg) not only blocked this place preference but also induced a place aversion. Naloxone by itself had no effect on place preference. It is suggested that release of endogenous opioids renders ejaculation rewarding. Pimozide, in a dose of 1 mg/kg, had no effect on ejaculation-induced reward. Dopamine thus seems to be of slight importance for that effect of copulation. Perhaps compulsive sexual activity obeys the same mechanisms as compulsive drug use in opiate addicts.

Cholinergic mechanisms and sexual behavior in the male rabbit.

The effects of cholinolytic as well as of cholinomimetic agents on sexual behavior in male rabbits were investigated. Castrated animals, injected with a supramaximal testosterone dose, were used. Scopolamine or methylscopolamine, 0.1 mg/kg, inhibited sexual activity. A dose of 0.02 mg had no effects. The muscarinic receptor-stimulating drug, pilocarpine, completely inhibited sexual activity at doses of 2, 10, and 50 mg/kg. A subeffective dose of methylscopolamine completely antagonized the effects of pilocarpine 2 mg/kg, partly the effect of pilocarpine 10 mg/kg, and not at all the effect of pilocarpine 50 mg/kg. Scopolamine completely antagonized the effects of pilocarpine 2 and 10 mg/kg, and not at all the effects of pilocarpine 50 mg/kg. The data indicate that the peripheral effects of both the receptor-blocking and stimulating agents is most important for the effects on sexual behavior, although a central site of action of pilocarpine cannot be ruled out.

GABAergic drugs and sexual motivation, receptivity and exploratory behaviors in the female rat.

Female rats were allowed to pace sexual interactions in a bilevel chamber, where a sexually vigorous male was tethered to the bottom level. Exploratory behaviors (sniffing, rearing), locomotor activity (expressed as number of level changes and periods of inactivity) as well as items of sexual motivation (latency to descend to the male's level, approaches towards the male and genital exploration) were recorded. In addition, sexual receptivity was evaluated in a non-paced situation. A test for motor impairment was also performed. The GABA transaminase inhibitor gamma-acetylene GABA reduced exploratory behaviors at doses much lower than those needed to reduce receptivity. The GABA reuptake inhibitor SKF 100330A did not affect any behavior category at doses of 15 and 30 mg/kg, but had a sedative action at 60 mg/kg. This was shown as impaired motor coordination and an almost total absence of activity in the bilevel chamber. Receptivity was not impaired, however. The mixed GABAA/ GABAB agonist progabide reduced exploratory behaviors and receptivity without producing motor impairment at a dose of 400 mg/kg. The GABAA agonist THIP impaired motor coordination and reduced receptivity and exploratory behaviors at a dose of 10 mg/kg. A larger dose, 20 mg/kg, had a strong sedative action. Only a small proportion of the animals descended to the males level. The GABAB agonist baclofen reduced receptivity at a dose that had no effect on motor coordination or exploratory behaviors. None of the drugs had a specific effect on sexual motivation. Whenever behaviors reflecting motivation were reduced, there were also other behavioral effects indicative of sedation. These data show that GABA receptor agonists, particularly the GABAB agonist baclofen, reduce sexual receptivity at doses that have only slight effect on motor functions or exploratory behaviors. In contrast, non-specific enhancement of GABAergic activity by a transaminase or reuptake inhibitor have effects on motor functions and exploratory behaviors at doses much lower than those needed to reduce receptivity.

The locomotor-reducing effects of GABAergic drugs do not depend on the GABAA receptor.

The locomotion-reducing effect of the GABAB agonist baclofen was compared with that of the GABAA agonists, aminopropanesulfonic acid (APSA) and THIP. It was found that baclofen was more potent than the other drugs. After intraventricular injection, baclofen induced almost complete immobility, whereas APSA did not affect locomotor activity. THIP had an intermediate effect. The GABA transaminase inhibitor gamma-acetylenic GABA (GAG) provoked a dose-dependent reduction of locomotion. Neither the effects of THIP nor those of GAG could be blocked by concurrent administration of bicuculline. The antagonist itself did not affect locomotor activity. It is concluded that the GABAA receptor is not important for the locomotion-reducing effects of GABAergic drugs.

Naloxone blocks anxiolytic-like effects of benzodiazepines in Swiss but not in Balb/c mice.

The ability of naloxone to block the effects of the benzodiazepines chlordiazepoxide and diazepam was evaluated in Swiss and Balb/c mice subjected to the light/dark choice test of anxiety or to a choice paradigm for measuring spontaneous exploratory behaviour. In Swiss mice, naloxone (5 or 10 mg/kg) completely or partially suppressed the anxiolytic-like effects of chlordiazepoxide (5 mg/kg) and diazepam (1 mg/kg) in the light/dark test. Naloxone alone was ineffective. None of these compounds affected locomotion in the free exploratory test. In Balb/c mice, naloxone did not reduce the anxiolytic-like action of benzodiazepines in the light/dark test. Moreover, naloxone did not antagonize the decrease in neophobia observed after anxiolytic treatment in Balb/c mice in the free exploratory paradigm. In this strain, benzodiazepines produced an increase of locomotor activity, whereas naloxone decreased it. The stimulant effects of benzodiazepines on locomotor activity were abolished by naloxone. As naloxone (2 mg/kg) reversed the morphine-induced hyperthermia both in Swiss and in Balb/c mice, differences in possible pharmacokinetic factors between the two strains can be ruled out as an explanation for the failure of naloxone to antagonize anxiolytic-like effects in Balb/c mice. Therefore, the ability of naloxone to reverse anxiolytic effects does not hold for all strains of mice.

Stereospecific actions of baclofen on sociosexual behavior, locomotor activity and motor execution.

The behavior effects of racemic baclofen and the R and S enantiomers were studied in order to determine whether the stereospecificity found in receptor binding studies also applies to the behavioral actions of the drug. Racemic and R-baclofen inhibited sexual behavior, locomotor activity and motor execution at relatively low doses while s-baclofen was completely inactive even when a dose 40 times higher than the minimum effective dose of R-baclofen was used. The R enantiomer seems to be twice as active as racemic baclofen. These data strongly suggest that the behavioral effects of baclofen are the result of an action at the GABA-B receptor. In order to differentiate the effects of baclofen on sexual interactions from those on nonspecific social interactions, the sociosexual behavior was observed with a castrated male or a receptive female as stimulus animal. R, S-baclofen had effects only upon sociosexual interaction with a receptive female. Moreover, the inhibitory effects of baclofen were restricted to behavioral items related to sexual interactions, primarily those constituting precopulatory behaviors. Since no effect was observed in social interactions with a castrated male, it is suggested that the inhibition of sociosexual behavior is not a consequence of impairment of motor execution. Rather it appears that baclofen has a specific inhibitory effect on behaviors associated with the initiation of copulatory activity. Therefore, once initiated, sexual behavior was not significantly modified by baclofen.

Inhibitory effect of opiates on male rat sexual behavior may be mediated by opiate receptors outside the central nervous system.

The importance of opiate receptors outside the central nervous system for the inhibitory actions of morphine on male rat sexual behavior was evaluated. Morphine (10 mg/kg) produced an almost complete inhibition of sexual behavior. This inhibition was antagonized by naloxone at a dose of 1 mg/kg but not at a dose of 0.25 mg/kg. The quaternary opioid antagonist methylnaloxone effectively blocked the inhibitory actions of morphine at a dose of 20 mg/kg but not at a dose of 5 mg/kg. Since the affinity of methylnaloxone for opiate receptors is about 5% of that of naloxone, it may be concluded that both antagonists were about equally effective in inhibiting the effects of morphine. Furthermore, the opiate-like drug loperamide was found to inhibit sexual behavior. This drug acts mainly outside the central nervous system. Its effect was blocked by both naloxone and methylnaloxone, suggesting that opiate receptors are involved. It was also shown that methylnaloxone is unable to block the reinforcing effects of morphine in the conditioned place preference procedure. Because the reinforcing effects of opiates seem to be localized to the central nervous system, it may be proposed that methylnaloxone does not antagonize morphine's central effects. Moreover, loperamide had no effect in the place preference procedure, suggesting that this drug does not act at central opioid receptors. Taken together, these data show that peripheral opioid receptors are responsible for at least some of the inhibitory actions of morphine on male sexual behavior. After treatment with morphine + methylnaloxone, ejaculatory mechanisms were facilitated, reflected in a reduced number of preejaculatory intromissions and a shortened ejaculation latency.(ABSTRACT TRUNCATED AT 250 WORDS)

Naloxone blocks the antianxiety but not the motor effects of benzodiazepines and pentobarbital: experimental studies and literature review.

The role of opioid systems in the anticonflict effect of chlordiazepoxide, diazepam and pentobarbital was evaluated with a modified Vogel procedure. First, morphine, ineffective by itself, was combined with subeffective or marginally effective doses of the benzodiazepines in order to detect possible potentiation. However, the combined treatment reduced licking in the Vogel procedure as well as in a licking test where no shock was administered. Several doses of the benzodiazepines and pentobarbital were then administered in combination with several doses of the opiate antagonist naloxone. A dose-dependent inhibition of anticonflict effect was obtained. In an additional experiment, it was shown that naloxone blocked the effects of diazepam in the elevated plus-maze procedure. Motor deficiencies, as evaluated with a rotarod test, produced by the benzodiazepines and pentobarbital could not be antagonized by naloxone. It is concluded that opioids are important for the anticonflict but not for the motor effects of these drugs. An analysis of published studies concerning the interaction of opioids and benzodiazepines in several procedures supposed to reflect anxiolytic effects shows that the inhibition obtained with naloxone is reliable and not procedure specific. The mechanisms by which opiate antagonists produce this inhibition of anticonflict activity are not known. It is tentatively suggested that opioid activation associated with stress may be a necessary component of anxiolysis.

The inhibitory effects on sexual behavior and ambulatory activity of the mixed GABAA/GABAB agonist progabide are differentially blocked by GABA receptor antagonists.

Progabide inhibited male rat sexual behavior at a dose of 200 mg/kg. This dose had only modest effects on ambulatory activity and no effect at all on motor coordination as evaluated by a rotarod test. The GABAA antagonist bicuculline, at a dose of 1 mg/kg, blocked the effects of progabide on sex behavior. In contrast, the GABAB antagonist CGP 35348, at doses of 50 and 100 mg/kg, was ineffective. These doses have previously been shown to block the actions of baclofen on sexual behavior. It was concluded that the GABAA but not the GABAB receptor is important for the inhibitory effects of progabide on that behavior. The actions of progabide on ambulatory activity were not blocked by bicuculline or CGP 35348 at any of the doses used (up to 2 and 200 mg/kg, respectively). Even the combination of both antagonists was ineffective. This suggests that the motor effects of progabide are mediated by either a non-GABAergic receptor or by a subtype of the GABAA or the GABAB receptor that is not sensitive to the antagonists. Present results show that the effects of progabide on motor functions depend on mechanisms different from those involved in its effects on sexual behavior. They further suggest that the GABAA receptor may be important for drug actions on male sexual behavior.

Sexual motivation--an inquiry into events determining the occurrence of sexual behavior.

For the individual engaged in it, sexual behavior has no finality or purpose other than its own execution. Data are presented showing that the execution of sexual reflexes can promote learning, i.e. it functions as reinforcement. Furthermore, positive affect is generated. Based on these principles, a model of sexual motivation has been elaborated. The conceptual framework is the incentive motivation theory previously proposed by Bindra D, A motivational view of learning, performance, and behavior modification, Psychol Rev 1974: 81:199-213; A Theory of Intelligent Behavior, New York: Wiley, 1976; How adaptive behavior is produced: a perceptual-motivational alternative to response reinforcement, Behav Brain Sci 1978; 1:41-52. Although the model is intended for application to most mammals, the rat is used as example. Essentially, sexual approach behaviors are activated by appropriate incentives (conditioned in the male, unconditioned in the female). Approach is, in the inexperienced male, followed by the execution of copulatory reflexes as a consequence of accidentally obtained tactile stimulation of the perineal region. In the female, copulatory acts are activated by tactile stimulation of the flanks and hinds provided by the mounting male. The role of conditioning for the execution of copulatory reflexes and for the acquisition of incentive value of neutral stimuli is analyzed. It is also shown that the incentive properties of sexual acts are not substantially different from those of other incentives. Sexual exhaustion is suggested to be either a case of negative alliesthesia or of stimulus habituation and the Coolidge effect is, in consequence, an example of dishabituation. Studies in women and men support this proposal. It is emphasized that sexual behavior is best understood as being entirely mechanistic albeit not deterministic.