Behavior In Syrian Hamsters Research Articles

CRISPR-Cas9 editing of the arginine–vasopressin V1a receptor produces paradoxical changes in social behavior in Syrian hamsters

Studies from a variety of species indicate that arginine–vasopressin (AVP) and its V1a receptor (Avpr1a) play a critical role in the regulation of a range of social behaviors by their actions in the social behavior neural network. To further investigate the role of AVPRs in social behavior, we performed CRISPR-Cas9–mediated editing at the Avpr1a gene via pronuclear microinjections in Syrian hamsters (Mesocricetus auratus), a species used extensively in behavioral neuroendocrinology because they produce a rich suite of social behaviors. Using this germ-line gene-editing approach, we generated a stable line of hamsters with a frame-shift mutation in the Avpr1a gene resulting in the null expression of functional Avpr1as. Avpr1a knockout (KO) hamsters exhibited a complete lack of Avpr1a-specific autoradiographic binding throughout the brain, behavioral insensitivity to centrally administered AVP, and no pressor response to a peripherally injected Avpr1a-specific agonist, thus confirming the absence of functional Avpr1as in the brain and periphery. Contradictory to expectations, Avpr1a KO hamsters exhibited substantially higher levels of conspecific social communication (i.e., odor-stimulated flank marking) than their wild-type (WT) littermates. Furthermore, sex differences in aggression were absent, as both male and female KOs exhibited more aggression toward same-sex conspecifics than did their WT littermates. Taken together, these data emphasize the importance of comparative studies employing gene-editing approaches and suggest the startling possibility that Avpr1a-specific modulation of the social behavior neural network may be more inhibitory than permissive.

Sex and social status modify the effects of fluoxetine on socioemotional behaviors in Syrian hamsters and rhesus macaques

Social subordination increases risk for psychiatric disorders, while dominance increases resilience to these disorders. Fluoxetine, a selective serotonin (5HT) reuptake inhibitor whose actions are mediated in part by the 5HT1A receptor (5HT1AR), has sex- and social status-specific effects on socioemotional behavior and aggressive behavior. However, the impact of social status on these sex-specific effects remains unclear. The current study evaluated the impact of acute fluoxetine treatment and social status on dominance-related behaviors in female and male hamsters, and the impact of chronic fluoxetine treatment on socioemotional behavior and 5HT1AR binding potential (5HT1ARBP) in female rhesus macaques. We hypothesized that sex differences in the effects of fluoxetine on aggression in hamsters would be diminished in dominant and enhanced in subordinate males and that aggression in female hamsters would be enhanced in dominants and diminished in subordinates. In female rhesus macaques, we hypothesized that chronic fluoxetine would alter socioemotional behaviors and site-specific 5HT1ARBP in a status-dependent manner. Male (n = 46) and female (n = 56) hamsters were paired with conspecifics for three days to establish social rank. Hamsters received a single dose of 20 mg/kg fluoxetine or vehicle two-hours prior to a test with a non-aggressive intruder. Female rhesus monkeys (n = 14) housed were administered fluoxetine (2.8 mg/kg/day) or vehicle injections chronically for 14-days, separated by a three-week washout period. On Day 15, positron emission tomography neuroimaging for 5HT1ARBP was conducted. Fluoxetine treatment decreased aggression in subordinate female monkeys and subordinate female hamsters but not in dominant females of either species. Fluoxetine decreased aggression in dominant but not in subordinate male hamsters. Fluoxetine also reduced and increased prefrontal 5HT1ARBP in dominant and subordinate females, respectively. Taken together, these results provide cross-species evidence that social status and sex impact how increased 5HT modulates agonistic behavior.

Galanthum nivalis Extract is Neurologically Active and Improves Anxiety and Social Interactions in Mesocricetus auratus

Background: Galanthum nivalis has been used throughout history for its medicinal properties. Although traditionally used as an antidote to poison, G. nivalis has also recently been found to have effects in neurological conditions such as Alzheimer’s Disease and mild cognitive impairment. Recent studies also suggest that it may have neurological activity that may be beneficial for psychiatric and neurological disorders like anxiety. </P><P> Objective: This study aimed to assess the neurological activity of G. nivalis extract using a behavioral test of anxiety-like behavior in Syrian hamsters. Methods: G. nivalis extract was administered daily to hamsters while undergoing a semi-naturalistic version of the open field test to assess anxiety. Hamsters were video recorded during their natural active times beginning an hour before and ending an hour after lights-on and lights-off. Free roaming behaviors were scored in a 2 x 4 m open pen with enrichment objects for hamsters to interact with. After 10 days, hamsters were subjected to a social interaction test with a novel conspecific. Results: Hamsters receiving G. nivalis extract showed increased time that was spent free-roaming and a greater proportion of that time was spent moving. They also spent more time interacting with enrichment objects in the open pen. The social interaction test showed that hamsters receiving G. nivalis extract spent more time playing with a novel conspecific. Conclusion: G. nivalis extract is a neurologically active natural product with behaviorally relevant effects. It improved anxiety-like behavior in hamsters, as evidenced by increased time free roaming, moving, and interacting with objects, while improving social interactions.

A modified anxious behavior test for hamsters

BackgroundLatency to feed in a novel environment assesses anxious behavior in rodents, but it is unclear whether it distinguishes anxiety from consumption or appetite. New methodThe anxiety-related feeding/exploration conflict (AFEC) test was used here to assess anxious behavior in Syrian hamsters for which increased cheek-pouching of food, but not overconsumption of it, reflects appetitive drive, and orexigenic stimuli do not increase consumption. The setup of the test prevented cheek-pouching. Comparison with existing methodsLatency to approach test food provided an additional control for non-emotional effects of treatments. Feed and approach latencies in the test cage were normalized to those in the home cage to factor out non-emotional effects. ResultsFeed latency and the feed latency ratio (test cage/home cage) were reduced by acute treatment with benzodiazepine, diazepam, or beta-adrenergic receptor antagonist, propranolol, or chronic treatment with norepinephrine reuptake inhibitor, desipramine. Reductions of feed latency and the feed latency ratio were not associated with hyperphagia, and these behaviors were unaltered by acute treatment with opioid receptor antagonist, naltrexone. Latency to approach food in the test cage, with and without normalization, was unaltered by these treatments. Finally, overnight fasting elevated feed latency without hyperphagia, and this effect was attenuated by chronic desipramine treatment. ConclusionsThese results suggest that the AFEC test assesses anxious, but not appetitive or consummatory, behavior, and that its sensitivity increases with food deprivation of hamsters.

Copulatory and Agonistic Behavior in Syrian Hamsters Following Social Defeat

Syrian hamsters are highly aggressive animals that reliably defend their home territory. After social defeat, however, hamsters no longer defend their home cage but instead display submissive and defensive behavior toward an intruder, a response that we have termed conditioned defeat. Plasma testosterone is significantly reduced in Syrian hamsters following repeated defeat suggesting that social defeat might also impair copulatory behavior. The present study aimed to determine whether copulatory behavior in male Syrian hamsters is suppressed following repeated social defeats and additionally whether exposure to a hormone-primed stimulus female after social defeat reduces the behavioral response to defeat. Hamsters were paired with an aggressive opponent for one or nine defeats using a resident-intruder model, while controls were placed into the empty cage of a resident aggressor. On the day after the last treatment, half of the hamsters were paired with a receptive female for 10 min. There were no significant differences in the copulatory behavior of defeated versus non-defeated hamsters, and the opportunity to copulate had no effect on subsequent conditioned defeat testing, as defeated animals displayed significantly more submissive behavior than did non-defeated animals. The current data suggest that conditioned defeat is not necessarily a maladaptive response to social stress, at least in terms of reproductive behavior, but may instead represent a viable behavioral strategy adopted by losing animals following social defeat. Further, these data indicate that conditioned defeat is relatively persistent and stable, as the opportunity to copulate does not reduce the subsequent display of submissive behavior.

Facilitation of Male Sexual Behavior in Syrian Hamsters by the Combined Action of Dihydrotestosterone and Testosterone

BackgroundTestosterone (T) controls male Syrian hamster sexual behavior, however, neither of T's primary metabolites, dihydrotestosterone (DHT) and estradiol (E2), even in highly supraphysiological doses, fully restores sexual behavior in castrated hamsters. DHT and T apparently interact with androgen receptors differentially to control male sexual behavior (MSB), but whether these two hormones act synergistically or antagonistically to control MSB has received scant experimental attention and is addressed in the present study.Methodology/Principal FindingsSexually experienced male Syrian hamsters were gonadectomized and monitored 5 weeks later to confirm elimination of the ejaculatory reflex (week 0), at which time they received subcutaneous DHT-filled or empty capsules that remained in situ for the duration of the experiment. Daily injections of a physiological dose of 25 µg T or vehicle commenced two weeks after capsule implantation. MSB was tested 2, 4 and 5 weeks after T treatment began. DHT capsules were no more effective than control treatment for long-term restoration of ejaculation. Combined DHT + T treatment, however, restored the ejaculatory reflex more effectively than T alone, as evidenced by more rapid recovery of ejaculatory behavior, shorter ejaculation latencies, and a greater number of ejaculations in 30 minute tests.Conclusions/SignificanceDHT and T administered together restored sexual behavior to pre-castration levels more rapidly than did T alone, whereas DHT and vehicle were largely ineffective. The additive actions of DHT and T on MSB are discussed in relation to different effects of these androgens on androgen receptors in the male hamster brain mating circuit.

Infrequent low dose testosterone treatment maintains male sexual behavior in Syrian hamsters

Testosterone (T) secreted in short pulses several times each day is essential for the maintenance of male sex behavior (MSB) in mammals. Blood T concentrations are relatively low during inter-pulse intervals. Assessment of androgenic influences on MSB of rodents has, with very few exceptions, involved either injections of pure or esterified hormones dissolved in oil or implantation of constant release capsules that generate supraphysiological and/or constantly elevated T concentrations. The minimum daily concentration of T necessary to maintain and restore MSB when T is delivered as a discrete short pulse remains unspecified; nor is it known whether infrequent T pulses in the physiological range sustain MSB. To address these questions, we varied T injection concentrations and frequencies in castrated, sexually-experienced Syrian hamsters. All males injected daily with an aqueous vehicle failed to display the ejaculatory reflex 5 weeks after castration. Once daily 15 μg subcutaneous T injections both maintained and restored MSB, whereas once daily 5 μg T injections resulted in fewer males ejaculating and longer ejaculation latencies. Substantially higher T doses were required to restore MSB in previous studies when T was administered in an oil vehicle. 50 μg T maintained MSB in most hamsters injected once every 4 or 7 days, despite long intervals between injections during which circulating T was undetectable or well below physiological concentrations. Some T regimens that maintained MSB were associated with subnormal seminal vesicle and ventral prostate weights. The demonstration that relatively brief, infrequent elevations of T are sufficient to support MSB provides a useful model to assess the neuroendocrine basis of MSB and raises the possibility that infrequent low dose androgen replacement protocols may restore sex behavior to hypogonadal men without inducing some of the negative side-effects associated with more frequent, higher dose treatments.

Corticotropin-releasing factor receptors in the dorsal raphe nucleus modulate social behavior in Syrian hamsters

In Syrian hamsters (Mesocricetus auratus), social defeat produces a prolonged change in subsequent agonistic behavior termed conditioned defeat. This stress-induced change in behavior is marked by increased submissive and defensive behavior toward a novel, nonaggressive opponent and a complete loss of normal territorial aggression. Corticotropin-releasing factor (CRF) has been shown to affect serotonergic neurons in the dorsal raphe nucleus (DRN) and to modulate learned helplessness via a CRF type-2 receptor (CRF-R2) mechanism. In this study, we tested the hypothesis that a nonselective CRF receptor antagonist (experiment 1: 250 or 500 ng D: -Phe CRF in 200 nl saline), or a selective CRF-R2 antagonist (experiment 2: 500 ng anti-Svg-30 in 200 nl saline), injected into the DRN would reduce the acquisition of conditioned defeat in male hamsters. We also tested similar hypotheses for the expression of conditioned defeat (experiments 3 and 4). Infusion of D: -Phe CRF into the DRN significantly reduced both the acquisition and expression of conditioned defeat compared to vehicle controls, whereas infusion of anti-Svg-30 into the DRN reduced expression but not acquisition. In particular, CRF antagonism in the DRN decreased fleeing from novel opponents but did not reinstate normal territorial aggression after social defeat. Our results suggest that the increased flight associated with conditioned defeat is modulated by CRF-R2 activation within the DRN. Overall, social defeat is an ethologically relevant stressor that appears to activate at least some of the same neural substrates that have been implicated in the control of learned helplessness.

Short duration testosterone infusions maintain male sex behavior in Syrian hamsters

In most mammalian species, reduced androgen availability is associated with marked reductions in male sexuality; conversely, androgen replacement in castrated males restores sex behavior within a few weeks. Testosterone (T) pulse duration, amplitude, frequency, and inter-pulse interval may be as important as total amount of hormone in determining target tissue responsiveness. We remain ignorant of the number and duration of daily T pulses necessary and sufficient to sustain male mating behavior. An in-dwelling infusion system was employed to vary T-pulse frequencies and durations. Daily 4 h infusions of aqueous T (100 μg/0.064 ml) and twice daily 4 h pulses of T (each 50 μg/0.064 ml) were sufficient to maintain ejaculatory behavior of sexually experienced castrated hamsters for 11 weeks post-castration; castrated hamsters infused with vehicle ceased to display the ejaculatory pattern 3 weeks after gonadectomy. Circulating T concentrations of hormone-infused hamsters declined markedly 7 h after the termination of each infusion. These results establish that male sex behavior can be sustained with infusions of relatively low T concentrations for 4 h/day and suggests that the basal concentrations of T sustained by the gonad during inter-pulse intervals may not be necessary for maintenance of sex behavior. 4 h T infusions were sufficient to maintain penile and seminal vesicles weights, but not ventral prostate weights or flank gland dimensions; the threshold for maintaining male sex behavior is lower than that for some androgen-dependent peripheral structures. Development of effective androgen replacement regimens that sustain sex behavior in castrated animals may be useful in the design of androgen replacement therapy for hypogonadal men.

The magnocellular medial preoptic nucleus I. sources of afferent input

The magnocellular medial preoptic nucleus plays a crucial role in the regulation of male sexual behavior in Syrian hamsters. Histological and behavioral studies suggest that the magnocellular medial preoptic nucleus regulates male mating behavior by integrating chemosensory and hormonal signals. The present study is the first to systematically identify the afferent connections of the magnocellular medial preoptic nucleus by tracing the uptake of cholera toxin B from deposits in the magnocellular medial preoptic nucleus of adult male Syrian hamsters. Our findings indicate that the magnocellular medial preoptic nucleus receives 1) chemosensory input from areas in the main and accessory olfactory pathways including the posterior medial bed nucleus of the stria terminalis, anterior medial, anterior cortical and posterior cortical nuclei of the amygdala; 2) input from steroid responsive structures such as the posterior medial nucleus of the amygdala, bed nucleus of the stria terminalis, lateral septum, anteroventral periventricular nucleus, medial preoptic nucleus, ventromedial nucleus of the hypothalamus and arcuate nucleus; 3) input from structures in the brainstem such as the subparafascicular thalamic nucleus, peripeduncular nucleus and the premamillary nucleus in the hypothalamus that carry sensory information from the genitalia. The major afferent input to the magnocellular medial preoptic nucleus was confirmed by injecting anterograde tracer biotinylated dextran amine into the anterior medical nucleus of the amygdala, the posterodorsal part of the medial nucleus of the amygdala, the posteromedial part of the bed nucleus of the stria terminalis and the posterointermediate part of the bed nucleus of the stria terminalis. Our results support the hypothesis that the magnocellular medial preoptic nucleus is part of the chemosensory pathway that receives chemosensory and hormonal input to regulate mating behavior and suggest that the magnocellular medial preoptic nucleus may utilize information from the genitalia to regulate male mating behavior.

Corticotropin-releasing factor receptor subtypes mediating nutritional suppression of estrous behavior in Syrian hamsters

Caloric deprivation inhibits reproduction, including copulatory behaviors, in female mammals. Decreases in metabolic fuel availability are detected in the hindbrain, and this information is relayed to the forebrain circuits controlling estrous behavior by neuropeptide Y (NPY) projections. In the forebrain, the nutritional inhibition of estrous behavior appears to be mediated by corticotropin-releasing factor (CRF) or urocortin-signaling systems. Intracerebroventricular (ICV) infusion of the CRF antagonist, astressin, prevents the suppression of lordosis by food deprivation and by NPY treatment in Syrian hamsters. These experiments sought to determine which CRF receptor type(s) is involved. ICV infusion of the CRF receptor subtype CRFR2-selective agonists urocortin 2 and 3 (UCN2, UCN3) inhibited sexual receptivity in hormone-primed, ovariectomized hamsters. Furthermore, the CRFR2-selective antagonist, astressin 2B, prevented the inhibition of estrous behavior by UCN2 and by NPY, consistent with a role for CRFR2. On the other hand, astressin 2B did not prevent the inhibition of behavior induced by 48-h food deprivation or ICV administration of CRF, a mixed CRFR1 and CRFR2 agonist, suggesting that activation of CRFR1 signaling is sufficient to inhibit sexual receptivity in hamsters. Although administration of CRFR1-selective antagonists (NBI-27914 and CP-154,526) failed to reverse the inhibition of receptivity by CRF treatment, we could not confirm their biological effectiveness in hamsters. The most parsimonious interpretation of these findings is that, although NPY inhibits estrous behavior via downstream CRFR2 signaling, food deprivation may exert its inhibition via both CRFR1 and CRFR2 and that redundant neuropeptide systems may be involved.

Metabolic fuels, neuropeptide Y, and estrous behavior in Syrian hamsters

Of the various environmental factors influencing reproduction, food availability plays a particularly significant role, and an insufficient supply of oxidizable metabolic fuels inhibits reproduction in female mammals. When ovariectomized, steroid-primed hamsters are food deprived for 48 h, estrous behavior is suppressed. However, the specific neuroendocrine alterations that mediate the suppression of estrous behavior are unknown. Several conditions that inhibit female sexual behavior are thought to be associated with altered neuropeptide Y (NPY) activity in the brain. Intracerebroventricular (ICV) infusion of NPY inhibits estrous behavior in ovariectomized steroid-primed rats and hamsters. Furthermore, food-deprived rats have an increase in NPY mRNA in the arcuate nucleus (ARC) of the hypothalamus. Unlike rats, studies in Syrian hamsters have failed to detect any alterations in ARC NPY mRNA following food deprivation. Here we show that ARC NPY immunoreactivity and mRNA is increased in food-deprived hamsters but not in hamsters given other metabolic challenges that inhibit estrous behavior. These findings support the hypothesis that NPY contribute to, but not be critical for, the nutritional inhibition of sexual receptivity.

Forebrain sites of NPY action on estrous behavior in Syrian hamsters

Food deprivation and similar metabolic challenges inhibit estrous behavior in female Syrian hamsters. The relevant metabolic cues appear to be detected in the hindbrain, and this information is then relayed synaptically to the forebrain circuits controlling estrous behavior. Neuropeptide Y (NPY) may be one of the neuropeptides/neurotransmitters serving this function. Infusion of NPY or the Y2/Y5 agonist, peptide YY3-36 (PYY3-36), into the lateral ventricles rapidly inhibits estrous behavior in ovariectomized, steroid-primed hamsters. This experiment sought to determine the neural loci where NPY acts to inhibit estrous behavior. Steroid-primed animals received infusions of artificial cerebrospinal fluid (aCSF) vehicle, 0.024 nmol PYY3-36 and 0.24 nmol PYY3-36 in separate tests 30 min prior to testing for sexual receptivity. Infusion of 0.24 nmol, but not 0.024 nmol, of PYY3-36 reduced lordosis duration when infused into the paraventricular nucleus of the hypothalamus (PVN), the caudal part of the medial preoptic area (MPO), the anterior hypothalamus (AH) or the lateral ventricles. Placements in the ventromedial hypothalamus (VMH), the arcuate nucleus (ARC) and the fourth ventricle were generally without effect. These data suggest that increased endogenous release of NPY into the caudal MPO–AH–PVN continuum during food deprivation could contribute to the observed inhibition of sexual receptivity. The possible contributions of other neuropeptides and neural estrogen receptors to this action of NPY are discussed.

Endomorphin1-like immunoreactivity in the limbic system of Syrian hamsters ( Mesocricetus auratus)

Recently, endomorphin-1 (Tyr-Pro-Trp-Phe-NH 2; EM1), an endogenous peptide that has high affinity and selectivity for the μ-opiate receptor, has been shown to modulate emotional behavior in mice and social behavior in Syrian hamsters. Endomorphin-1 (EM1) is present throughout the central nervous system in rats, mice, and guinea pigs; however, the distribution of EM1 in hamsters has not been described. The purpose of the present study was to investigate the distribution of EM1-like immunoreactivity (EM1L-IR) in the limbic system of Syrian hamsters using immunocytochemistry. Perikarya containing EM1L-IR were present in the anterior area, dorsomedial, ventromedial, periventricular, posterior, and arcuate nuclei of the hypothalamus. Fibers expressing EM1L-IR were present in the nucleus accumbens, caudate putamen, septum, bed nucleus of the stria terminalis, amygdaloid complex, and hypothalamus. The distribution of EM1 suggests a potential endogenous role for this peptide in major processes modulated by opiates, including affective states and social behavior.

Suppression and recovery of estrous behavior in Syrian hamsters after changes in metabolic fuel availability.

A reduction in the availability of oxidizable metabolic fuels inhibits reproduction. Forty-eight hours of metabolic fuel deprivation inhibits estrous behavior in ovariectomized, steroid-treated Syrian hamsters, but little is known about the time course of this inhibition. Likewise, refeeding reverses deprivation-induced suppression, but the rate of recovery has not been examined. In two experiments we determined 1) the rate at which estrous behavior declines in hamsters treated with metabolic inhibitors and 2) how rapidly sexual receptivity is restored when hamsters are refed after a 48-h fast. We also measured circulating levels of leptin and insulin in an attempt to determine their relationship to the inhibition and restoration of estrous behavior. More than 24 h of metabolic inhibitor administration were required to inhibit lordosis, whereas only 6 h of refeeding were sufficient to restore the display of sexual receptivity to normal levels. Neither plasma insulin nor leptin levels paralleled the changes in estrous behavior. We concluded that 1) suppression of estrous behavior occurs more slowly than recovery after a fast and 2) changes in circulating leptin and insulin probably do not have a critical role in these behavioral changes.

Effects of naltrexone and CCK on estrous behavior and food intake in Syrian hamsters

Food deprivation inhibits estrous behavior in several species of rodents, but little is known about the neurotransmitter systems mediating this phenomenon. We determined whether partial blockade of opioid receptors by continuous infusion of naltrexone and/or acute peripheral injection of cholecystokinin (CCK) administration would overcome the suppressive effects of food deprivation on estrous behavior in Syrian hamsters. Contrary to expectation, naltrexone produced a slight suppression of estrous behavior, and systemic CCK administration had no effect. This dose of naltrexone was sufficient to reduce in vivo binding of [ 3H]naloxone in the brain, and both compounds affected other parameters such as food intake and body weight gain. Thus, the doses of CCK and naltrexone that were used were physiologically effective. These findings suggest that neither peripheral CCK nor opioid systems are likely to play a major role in the suppression of hamster estrous behavior by food deprivation.

Conversion of Testosterone to Estradiol May Not Be Necessary for the Expression of Mating Behavior in Male Syrian Hamsters (Mesocricetus auratus)

Male sexual behavior is mediated in part by androgens, but in several species, mating is also influenced by estradiol formed locally in the brain by the aromatization of testosterone. The role of testosterone aromatization in the copulatory behavior of male Syrian hamsters is unclear because prior studies are equivocal. Therefore, the present study tested whether blocking the conversion of testosterone to estradiol would inhibit male hamster sexual behavior. Chronic systemic administration of the nonsteroidal aromatase inhibitor Fadrozole (2.0 mg/kg/day) for 5 or 8 weeks did not significantly increase mount latency or reduce mount frequency, intromission frequency, ejaculation frequency, or anogenital investigation relative to levels shown by surgical controls. However, Fadrozole effectively inhibited aromatase activity, as evidenced by the suppression of estrogen-dependent progesterone receptor immunoreactivity in the male hamster brain. The JZB39 anti-progesterone receptor antibody labeled significantly more neurons in brains of sham-treated hamsters than in brains of Fadrozole-treated hamsters. These data suggest that aromatization of testosterone to estradiol is not necessary for normal mating behavior in Syrian hamsters.

Role of vasopressin and oxytocin in the control of social behavior in Syrian hamsters(Mesocricetus auratus

Vasopressin (VP) and oxytocin (OT) play an important role in regulating social behavior in a variety of species as a result of their actions in the central nervous system. The following paper reviews the actions of VP and OT in controlling a range of social behaviors involved in communication, aggression and reproduction in the Syrian hamster. These data suggest that social and hormonal stimuli alter the expression of specific social behaviors by altering the release of, or the response to, VP and OT within key elements of the neural circuits controlling these behaviors.

AP lesions block suppression of estrous behavior, but not estrous cyclicity, in food-deprived Syrian hamsters.

Food deprivation inhibits ovulatory cycles and estrous behavior in Syrian hamsters. Lesions of the area postrema (AP) prevented the suppression of estrous behavior in food-deprived hamsters, but they did not prevent the suppression of estrous cyclicity or the increase in running-wheel activity caused by food deprivation. Food deprivation or treatment with pharmacological inhibitors of glycolysis and fatty acid oxidation decreased estrogen-receptor immunoreactivity (ERIR) in the ventromedial hypothalamus (VMH), increased ERIR in the arcuate nucleus (Arc) and the posterior parvicellular paraventricular nucleus (PaPo), but had no effect on ERIR in the posterodorsal medial amygdala or the anterior parvicellular paraventricular nucleus. Lesions of the AP prevented the food deprivation-induced decrease in VMH ERIR and the increase in Arc ERIR, but they did not prevent the increase in ERIR in the PaPo. Thus, whatever physiological cues are produced by food deprivation, an intact AP is required for their transmission to the neural circuits controlling estrous behavior, VMH ERIR, and Arc ERIR. The AP is not essential for transmission of this information to the neural circuits controlling estrous cyclicity, running-wheel activity, or PaPo ERIR.

Sex Differences in Function of a Pheromonally Stimulated Pathway: Role of Steroids and the Main Olfactory System

Exposure to the pheromones contained in female hamster vaginal secretions (FHVS) produces stereotypic, sex-specific behaviors in Syrian hamsters. Using Fos as a marker of neuronal stimulation we have found that (1) FHVS stimulates neurons in the posterior subdivision of the medial nucleus of the amygdala (MeP), the posterior medial subdivision of the bed nucleus of the stria terminalis (BNSTpm), and the magnocellular subdivision of the medial preoptic nucleus (MPN mag); (2) this stimulation is mediated by the main olfactory system; (3) stimulation of the MPN mag is regulated by testosterone in males; (4) stimulation of the BNSTpm and MeP is regulated by testosterone in females; and (5) FHVS does not induce Fos production in the MPN mag in females regardless of the hormonal state. These results support the hypothesis that the main olfactory system plays an important role in the regulation of pheromonally driven behaviors, identifies functional sex differences in pathways that regulate these behaviors, and emphasizes the different roles of the BNSTpm, MeP, and MPN mag in the regulation of male copulatory behavior.