Flank Marking Behavior Research Articles

Agonistic encounters and brain activation in dominant and subordinate male greater long-tailed hamsters

During an agonistic encounter test, dominant male greater long-tailed hamsters ( Tscheskia triton) initiated attacks sooner and displayed higher levels of aggression and flank marking behavior than their subordinate counterparts. Accordingly, subordinate males exhibited more defensive behavior than dominant ones. Specific patterns of neuronal activation, measured by Fos-immunoreactive staining (Fos-ir), were found in the hamster brain following agonistic interactions. Increased Fos-ir was observed in the bed nucleus of the stria terminalis (BST), ventromedial hypothalamus (VMH), and medial (MeA) and anterior cortical (ACo) nuclei of the amygdala (AMYG) in both dominant and subordinate males. In contrast, dominant males had significantly higher Fos-ir densities in the medial preoptic area (MPOA) than subordinate males, whereas subordinate males expressed higher densities of Fos-ir in the anterior hypothalamus (AH) and central nucleus of the amygdala (CeA). Additionally, Fos-ir levels in the MPOA were significantly correlated with aggression and Fos-ir levels in the AH and CeA were correlated with defensive behavior. Together, our data indicate distinct patterns of neuronal activation associated with agonistic encounters in a behavior-specific manner in male greater long-tailed hamsters.

Testicular hormone exposure during adolescence organizes flank-marking behavior and vasopressin receptor binding in the lateral septum

Adolescence is a period during which many social behaviors emerge. One such behavior, flank marking, is a testosterone-modulated scent marking behavior that communicates dominance status between adult male Syrian hamsters. Testosterone modulates flank-marking behavior by altering neural transmission of vasopressin within a forebrain circuit. This study tested whether testicular hormones secreted during adolescence play purely a transient activational role in the display of flank-marking behavior, or whether adolescent steroid hormone secretions also cause long-term organizational changes in vasopressin binding within brain regions underlying flank-marking behavior. We tested this hypothesis by manipulating whether testicular secretions were present during adolescent development and then tested for flank-marking behavior and vasopressin receptor binding within the flank-marking neural circuit in young adulthood. Specifically, males were gonadectomized immediately before or after adolescence, replaced with testosterone 6 weeks following gonadectomy in young adulthood, and behavior tested 1 week later. Adult testosterone treatment activated flank-marking behavior only in males that were exposed to testicular hormones during adolescence. In addition, males exposed to testicular hormones during adolescence exhibited significantly less vasopressin receptor binding within the lateral septum than males deprived of adolescent hormones, suggesting that hormone-dependent remodeling of synapses normally occurs in the lateral septum during adolescence. These data highlight the importance of gonadal steroid hormone exposure during adolescence for the organization of neural circuits and social behavior.

Puberty: a finishing school for male social behavior.

The classical view of steroid-dependent organization of brain and behavior holds that gonadal steroid hormones, acting during an early critical period of development, cause permanent structural changes in neural circuits that determine behavioral responses to hormones in adulthood. This classical view has been modified to incorporate evidence that organizational effects of steroids can occur outside of the established perinatal critical period and that multiple critical periods may exist during development. Experiments in this laboratory indicate that steroid-dependent organization of neural circuits underlying male social behaviors occurs during puberty. This work shows that adult-typical reproductive and flank marking behaviors cannot be activated by gonadal steroids in male Syrian hamsters prior to puberty, suggesting that developmentally timed processes during puberty render the nervous system responsive to activating effects of gonadal steroids in adulthood. Additional experiments demonstrate that the presence or absence of gonadal hormones during puberty is a major factor in the ability of steroids to activate reproductive and flank marking behavior in adult male hamsters and in androgen receptor expression within the neural circuit underlying these behaviors. Thus, gonadal hormones during puberty appear to exert long-lasting changes in neural circuits that are responsible for the programming of activational responses to steroids later in adulthood. A two-stage model for maturation of male social behaviors is proposed: a perinatal critical period for sexual differentiation of neural circuits, followed by the pubertal period, during which gonadal steroids further organize the circuits to enhance behavioral responsiveness to hormones in adulthood. Whether puberty is a critical period for the proposed second wave of steroid-dependent organization of behavioral circuits remains to be determined.

Prenatal nicotine exposure and behavior.

Prenatal exposure to nicotine has been associated with changes in behavioral indices in offspring. Flank marking, a scent-marking behavior in golden hamsters, appears to be controlled by arginine vasopressin (AVP) neurons in the hypothalamus. The present study examines the effects of prenatal exposure to nicotine on the vasopressinergic system associated with flank marking behavior.

Galanin antagonizes vasopressin-stimulated flank marking in male golden hamsters

Microinjection of vasopressin (VP) into the anterior hypothalamus (AH) of golden hamsters induces a rapid bout of flank marking, a stereotyped scent marking behavior used for olfactory communication. In rats, VP is colocalized with galanin (GAL) in several brain regions. GAL has been shown to antagonize the postsynaptic actions of other cosecreted neurotransmitters including acetylcholine and norepinephrine; however, the ability of GAL to modulate the postsynaptic actions of VP has not been assessed. Here, we report that coadministration of GAL can block VP-induced flank marking in golden hamsters in a dose dependent manner. These findings provide the first evidence in any species that GAL can antagonize the central actions of VP. Using slice binding and receptor autoradiography, we have identified GAL binding sites in the AH and two other regions implicated in flank marking behavior (the lateral septum and central grey). These findings raise the possibility that endogenous GAL may function as an inhibitory modulator of this stereotypic scent marking behavior.

Flank-marking behavior and the neural distribution of vasopressin innervation in golden hamsters with suprachiasmatic lesions.

In golden hamsters, microinjections of arginine-vasopressin (AVP) within the anterior hypothalamus trigger a stereotyped scent-marking behavior, flank marking. Our experiment was carried out to test the contribution of AVP neurons within the suprachiasmatic nucleus (SCN) in the control of this behavior. Our results suggest that the SCN does not contribute to flank-marking behavior. Whereas SCN lesions disrupted circadian rhythms of wheel running, the same lesions did not disrupt flank-marking. The results also suggest that neurons located outside the SCN contribute significantly to the vasopressinergic innervation of the brain and the expression of AVP-dependent behaviors, such as flank-marking behavior. Although AVP-immunoreactive fibers were severely (ca. 95%) depleted from several forebrain areas in SCN-lesioned hamsters, the effect of the lesions was much more limited within the forebrain areas involved in flank-marking behavior as well as within the midbrain and hindbrain.

Flank-marking behavior and the neural distribution of vasopressin innervation in golden hamsters with suprachiasmatic lesions.

Flank-marking behavior and the neural distribution of vasopressin innervation in golden hamsters with suprachiasmatic lesions.

Vasopressin and developmental onset of flank marking behavior in golden hamsters

Golden hamsters start displaying flank marking behavior (a form of scent marking) around postnatal day 20 (P-20). Because the behavior is dependent upon the central activity of arginine vasopressin (AVP), the present study was conducted to correlate this activation with changes in the vasopressinergic system. A first set of experiments was performed to compare flank marking activity between P-18 and P-22. A second set of experiments was performed to compare the density of AVP receptors between the age periods and assess responsiveness to AVP microinjection. Finally, a third set of experiments incorporated immunocytochemistry, radioimmunoassay, in situ hybridization, and Northern blot analysis to determine the location and numbers of AVP immunoreactive neurons and the level of mRNA correlating with the developmental onset of flank marking behavior. Our results show that flank marking develops between P-18 and P-22. Male and female hamsters do not display odor-induced flank marking anytime before P-19. However, all animals show odor-induced flank marking by P-22. The onset of flank marking does not appear to be associated with any change in AVP receptor binding in the anterior hypothalamus. Indeed, flank marking can be triggered in hamsters on P-18 by the microinjection of AVP in the anterior hypothalamus. This would suggest that the postsynaptic mechanisms contributing to the transduction of the AVP signal and the motor control of flank marking are intact prior to the onset of odor-induced flank marking. In contrast, AVP levels in the hypothalamus and pituitary increase by two to threefold between P-18 and P-22, suggesting that changes in AVP synthesis and release from presynaptic sites may contribute to the onset of flank marking. Interestingly, there is no change in AVP mRNA between P-18 and P-22, which raises questions about posttranslational processing during this developmental period. These results suggest that heightened synthesis and release of AVP between P-18 and P-22 may contribute to the developmental onset of flank marking. © 1996 John Wiley & Sons, Inc.

Vasopressin and developmental onset of flank marking behavior in golden hamsters

Golden hamsters start displaying flank marking behavior (a form of scent marking) around postnatal day 20 (P-20). Because the behavior is dependent upon the central activity of arginine vasopressin (AVP), the present study was conducted to correlate this activation with changes in the vasopressinergic system. A first set of experiments was performed to compare flank marking activity between P-18 and P-22. A second set of experiments was performed to compare the density of AVP receptors between the age periods and assess responsiveness to AVP microinjection. Finally, a third set of experiments incorporated immunocytochemistry, radioimmunoassay, in situ hybridization, and Northern blot analysis to determine the location and numbers of AVP immunoreactive neurons and the level of mRNA correlating with the developmental onset of flank marking behavior. Our results show that flank marking develops between P-18 and P-22. Male and female hamsters do not display odor-induced flank marking anytime before P-19. However, all animals show odor-induced flank marking by P-22. The onset of flank marking does not appear to be associated with any change in AVP receptor binding in the anterior hypothalamus. Indeed, flank marking can be triggered in hamsters on P-18 by the microinjection of AVP in the anterior hypothalamus. This would suggest that the postsynaptic mechanisms contributing to the transduction of the AVP signal and the motor control of flank marking are intact prior to the onset of odor-induced flank marking. In contrast, AVP levels in the hypothalamus and pituitary increase by two to threefold between P-18 and P-22, suggesting that changes in AVP synthesis and release from presynaptic sites may contribute to the onset of flank marking. Interestingly, there is no change in AVP mRNA between P-18 and P-22, which raises questions about posttranslational processing during this developmental period. These results suggest that heightened synthesis and release of AVP between P-18 and P-22 may contribute to the developmental onset of flank marking.

Septo-hypothalamic organization of a stereotyped behavior controlled by vasopressin in golden hamsters

In golden hamsters, microinjections of arginine vasopressin (AVP) within the anterior hypothalamus (AH) and lateral septum (LS) elicit the display of a stereotyped behavior: flank marking. As these areas are reciprocally connected, we tested whether AVP-sensitive sites constitute an organized network. Flank marking was recorded in animals with ibotenic acid lesions within the AH or LS after AVP injections within the LS or AH. While AVP injections in the AH and LS induced high flank-marking scores, certain lesions blocked the behavior. Lesions of the LS failed to affect flank marking induced by injections within the AH. In contrast, unilateral AH lesions blocked flank marking induced either by LS injections or AH injections in the contralateral side. These results suggest that the bilateral integrity of the AH is critical for the activation of flank-marking behavior by AVP. Together, these data suggest that the AH is an important relay of the neural network controlling flank-marking behavior.

An iodinated vasopressin (V 1) antagonist blocks flank marking and selectively labels neural binding sites in golden hamsters

An arginine-vasopressin (AVP) derivative, [d(CH 2) 5,Sar 7]AVP (SAVP), has been characterized as an antagonist to vasopressin V 1 receptors. Using AVP-dependent flank-marking behavior as a bioassay, it was possible to verify that iodinated SAVP (I-SAVP) retains biological activity within the central nervous system, as the antagonist blocked the behavior. Furthermore, 125I-SAVP was used to localize specific V 1 binding sites in the brain. The resulting binding was localized to discrete anatomical sites, and highly specific to V 1-like receptors. While we confirmed previous findings using 3H-AVP in golden hamsters, we also identified binding in many areas previously unreported (e.g., arcuate and paraventricular nuclei of the hypothalamus, tenia tecta, posteromedial cortical nucleus of the amygdala, and zona incerta), suggesting that 125I-SAVP provides a greater level of resolution. In addition, specific binding was observed in the lateral septum, anterior hypothalamus, and midbrain central gray, areas that have previously been shown to trigger flank marking in response to AVP microinjection. The presence of AVP binding sites in limbic and mesencephalic areas involved in the regulation of flank marking suggests that this neuropeptide may play an important role as a neurotransmitter at multiple levels in the neural circuits controlling this behavior.

Functionally and Anatomically Distinct Populations of Vasopressinergic Magnocellular Neurons in the Female Golden Hamster

The present study was done to determine whether the vasopressinergic neurons in the hypothalamus controlling flank marking behavior are distinct from the magnocellular neurons comprising the hypothalamo-neurohypophysial system. Animals were either hypophysectomized or injected with a suicide transport lectin, volkensin, into the neurohypophysis. Both procedures resulted in a pronounced loss of vasopressin-immunoreactive perikarya throughout the hypothalamus concomitant with increases in water intake and urine output and decreases in circulating levels of vasopressin. The loss of the hypothalamo-neurohypophysial system was most pronounced in volkensin-treated animals that presented with frank diabetes insipidus and exceedingly low levels of plasma vasopressin. However, the vasopressinergic fibers and magnocellular neurons in and around the anterior hypothalamus implicated in the control of flank marking survived the volkensin treatment. Volkensin-treated animals exhibited levels of flank marking typical of untreated animals. These data suggest the presence of anatomically and functionally distinct populations of vasopressinergic magnocellular neurons in the hypothalamus of the golden hamster.

Vasopressin in the brain of the golden hamster: The distribution of vasopressin binding sites and of immunoreactivity to the vasopressin‐related glycopeptide

Using in vitro light microscopic autoradiography and immunocytochemistry, the distribution of vasopressin binding sites and that of the vasopressin-related glycopeptide are described in the brain of golden hamster (Mesocricetus auratus). Vasopressin binding sites and immunoreactive axons were observed in the suprachiasmatic nucleus, in the anterior hypothalamus/median preoptic area, in the medial preoptic nucleus, in the bed nucleus of the stria terminalis, in the habenular complex, in the thalamic paraventricular nucleus, and in the nucleus of the solitary tract. In addition we observed binding sites in regions where no immunoreactivity could be evidenced: the lateral septal nucleus, the central amygdaloid nucleus, the subiculum, the dentate gyrus, the anterodorsal and anteroventral thalamic nuclei, the superior colliculus, the vestibular nuclei, and in the prepositus hypoglossal nucleus. In the golden hamster, exogenous vasopressin excites single neurones located in the suprachiasmatic nucleus and induces flank-marking behavior when microinjected into the preoptic area. Our results provide a morphological basis for similar effects exerted by endogenous vasopressin. A comparison of the present data with those previously described in the rat reveals marked species differences in the brain distribution of vasopressin and of its binding sites.

Kainic Acid Lesion of Vasopressinergic Neurons in the Hypothalamus Disrupts Flank Marking Behavior in Golden Hamsters

Abstract It is well established that flank marking behavior in the Golden hamster is controlled by vasopressin-sensitive neurons localized to the anterior hypothalamus; however, the source(s) of vasopressinergic innervation to this area is unknown. Previous analysis by immunocytochemistry showed distinct populations of vasopressinergic magnocellular neurons localized to the supraoptic nucleus, paraventricular nucleus and the nucleus circularis that did not project to the neurohypophysis. In the present study, these same hypothalamic nuclei were lesioned by microinjection of kainic acid to determine which, if any, of these populations of vasopressin neurons are involved in the control of flank marking. Unilateral lesions in the areas of the nucleus circularis and supraoptic nucleus at the rostro-caudal plane of the anterior hypothalamus abolished odor-induced flank marking behavior. Lesions in the paraventricular nucleus at the level of the anterior hypothalamus did not consistently inhibit flank marking, while lesions of magnocellular neurons rostral or caudal to the anterior hypothalamus were ineffective. The microinjection of vasopressin into the anterior hypothalamus following lesion of the paraventricular and supraoptic nuclei stimulated flank marking, evidence that treatment with kainic acid did not damage the efferent component of this behavior. However, animals with lesions in the nucleus circularis did not respond to the microinjection of vasopressin; hence, it is uncertain whether lesions in this area disrupt vasopressinergic innervation to the anterior hypothalamus or simply destroy the motor neurons controlling flank marking. In summary, the data clearly demonstrate that vasopressin neurons localized primarily to the medial aspect of the supraoptic nucleus are necessary for sensory integration of odor-induced flank marking, and as such, may be one possible source of neurotransmitter controlling this behavior.

Computer‐Aided Mapping of Vasopressin Neurons in the Hypothalamus of the Male Golden Hamster: Evidence of Magnocellular Neurons that do not Project to the Neurohypophysis

Abstract Vasopressin-sensitive neurons in the region of the anterior hypothalamus are necessary for the mediation of flank marking behavior in the Golden hamster. The precise nature of the vasopressinergic innervation to the anterior hypothalamus is unknown. In this study we seek to examine the potential sources of this innervation by mapping and counting the vasopressin-immunoreactive neurons that contribute to the hypothalamo-neurohypophysial system, and those that do not. Vasopressin-immunoreactive neurons in the hypothalamus were visualized by immunocytochemistry. Sections were mapped with a computer-aided microscope system, and labeled neurons counted. Two-dimensional maps were stacked into a three-dimensional wireframe model which could be manipulated for further examination. The average number of vasopressin neurons was 3,135, with over 60% of all perikarya localized to the lateral supraoptic nucleus. In a double-labeling study, neurons contributing to the hypothalamo-neurohypophysial system were retrogradely labeled by the injection of horseradish peroxidase into the neurohypophysis. The enzyme reaction product was visualized by treatment with tetramethylbenzidine followed by nickel-conjugated diaminobenzidine. Sections were subsequently stained for vasopressin by immunocytochemistry. Single- and double-stained neurons from serial sections were mapped and counted. Wireframe and contoured three-dimensional representations were generated. The average number of neurons projecting to the neurohypophysis was 5,619. However, an average of 981 neurons was immunoreactive to vasopressin but devoid of horseradish peroxidase. The greatest number of these non-projecting perikarya were found in and around the anterior hypothalamus, localized primarily in the lateral and medial aspect of the supraoptic nuclei, the ventral area of the paraventricular nucleus, and the nucleus circularis. By comparing the number of non-projecting neurons found by double-staining to the total cell count of the entire vasopressin system, it was estimated that approximately 30% of all vasopressin neurons in and around the anterior hypothalamus did not project to the neurohypophysis. Based on the distribution and localization of the non-projecting perikarya, it is speculated that these neurons may provide neurotransmitter for vasopressin-dependent flank marking in the male Golden hamster.

Evidence for a functional and anatomical relationship between the lateral septum and the hypothalamus in the control of flank marking behavior in golden hamsters

Golden hamsters with established dominant/subordinate relationships communicate their social status by rubbing pheromone-producing flank glands against objects in the environment. This behavior, called flank marking, is controlled by vasopressin-sensitive neurons localized to the anterior hypothalamus. Vasopressinergic magnocellular neurons in the nucleus circularis and medial aspect of the supraoptic nucleus are thought to be a source of neurotransmitter for the initiation of flank marking. The present study was undertaken to examine the extrahypothalamic control of flank marking. The anatomical and functional connections between the lateral septum and the vasopressin-containing nuclear groups in and around the anterior hypothalamus were examined by: (1) tracing afferent and efferent connections following microinjection of horseradish peroxidase and Phaseolus vulgaris-leucoagglutinin into the lateral septum, and (2) recording odor-induced flank marking prior to and following ibotenate lesions in the septum. The greatest number of perikarya retrogradely labeled with horseradish peroxidase were found lateral to the anterior hypothalamus and ventral to the fornix in the area of the lateral hypothalamus. The vasopressin-containing nuclear groups, e.g., paraventricular, supraoptic, suprachiasmatic nuclei, and the nucleus circularis, were devoid of labeled perikarya. Nerve terminals anterogradely labeled with Phaseolus vulgaris-leucoagglutinin were primarily localized to the anterior hypothalamus, in and around the nucleus circularis, and the medial aspect of the supraoptic nucleus. The lateral aspect of the supraoptic nucleus was devoid of nerve terminals as were the paraventricular and suprachiasmatic nuclei. The anatomical connections between the lateral septum and the hypothalamus appear to be necessary for the control of flank marking, since the microinjection of ibotenate into this limbic site significantly reduced odor-induced flank marking as compared to control microinjections of 0.9% NaCl.

Vasopressin immunoreactivity in the anterior hypothalamus is altered during the establishment of dominant/subordinate relationships between hamsters

When paired for 15-min periods for 5–8 consecutive days, castrated, testosterone-treated hamsters consistently assumed the dominant status, based on a higher aggression index ( 18 ± 3) and frequency of flank marking ( 15 ±3) as compared to their castrated, untreated subordinate partners ( −1.3 ± 1 and 2.4 ± 1, respectively). In addition to these hamsters with established dominant/subordinate relationships, control hamsters with no social interactions were killed, and in all animals the vasopressin level in the anterior hypothalamus-medial preoptic area was assessed by counting vasopressin immuno-reactive perikarya following immunocytochemistry, or by radioimmunoassay of vasopressin from tissue punches. In the socialized pairs the subordinate hamsters had a significantly ( P < 0.01) lower number of vasopressin staining perikarya in the anterior hypothalamus, specifically the area of the nucleus circularis, than their dominant partners ( n = 6 pairs). There was also a significantly ( P < 0.001) lower level of vasopressin immunoreactivity in punches taken from the area of the nucleus circularis in subordinate hamsters as compared to their dominant partners ( n = 14 pairs). However, there were no significant differences in the number of perikarya or the concentration of immunoreactive vasopressin between subordinate and dominant hamsters in the supraoptic nucleus, paraventricular nucleus, suprachiasmatic nucleus or bed nucleus of the stria terminalis. The number of perikarya ( n = 5 pairs) and concentration of vasopressin ( n = 8 pairs) for all vasopressin immunoreactive sites, including the nucleus circularis, were similar for testosterone-treated and untreated hamsters that remained isolated and not subjected to daily aggressive encounters. The values in both groups of unsocialized hamsters were also similar to those seen in the testosterone-treated dominant hamsters. In summary, the only difference in the vasopressin level between dominant and subordinate hamsters was observed in the area of the nucleus circularis. Furthermore, the only group of hamsters that differed in both the number of vasopressin immunoreactive perikarya and concentration of vasopressin were castrated controls, i.e. subordinates, that were tested daily with highly aggressive testosterone-treated dominant hamsters. These data provide evidence showing (1) that the diminution in vasopressin immunoreactivity in subordinate hamsters occurs in response to repeated social encounters with aggressive dominant hamsters, (2) that a behavioral manipulation may contribute to changes in the neuroanatomy and/or chemistry of the central nervous system, and (3) that the vasopressinergic neurons of nucleus circularis may be involved in the control of vasopressin-dependent flank marking. The lower level of flank marking behavior in subordinate hamsters may reflect, in part, the level of vasopressin synthesis and release from this population of neurons.

Inhibition of vasopressin-stimulated flank marking behavior by V 1-receptor antagonists

Flank marking, a form of olfactory communication displayed by hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. In the present study two vasopressin type-1 (V 1) receptor antagonists, d(CH 2) 5Tyr(Me)AVP and dPTyr(Me)AVP were tested for their ability to block flank marking stimulated by the microinjection of arginine vasopressin (AVP) into the anterior hypothalamus. Dose-response curves were established for AVP and flank marking in the presence or absence of different concentrations of each antagonist. DPTyr(Me)AVP was microinjected into the anterior hypothalamus 1 h before microinjection of AVP while d(CH 2) 5Tyr(Me)AVP and AVP were prepared together and delivered as a single microinjection. This procedure was necessary because dPTyr(Me)AVP, but not d(CH 2) 5Tyr(Me)AVP, had agonist activity when initially injected into the anterior hypothalamus in concentrations ranging from 0.90–900 μM. The ED 50 values (μM) for dPTyr(Me)AVP and AVP were 17.9 and 0.90, respectively. The initial agonist activity of dPTyr(Me)AVP was always followed by blocker activity. Both V 1-receptor antagonists caused a dose-dependent decrease in AVP-stimulated flank marking. Maximal inhibition of AVP-stimulated flank marking was produced with approximately 1.0 mM of either antagonist. Both antagonists blocked AVP-stimulated flank marking behavior for over 12 h following their microinjection.

A V1-like receptor mediates vasopressin-induced flank marking behavior in hamster hypothalamus

A vasopressin-sensitive mechanism within the medial preoptic area-anterior hypothalamus (MPOA-AH) appears to be essential for expression of a complex behavior involved in olfactory communication in Golden hamsters called flank marking. The present study investigated whether the induction of flank marking by arginine-vasopressin (AVP) within the MPOA-AH is mediated by a receptor that is more similar to the vasopressor (V1) or the antidiurectic (V2) AVP receptor. Adult male hamsters were anesthetized and implanted with a 26 gauge guide cannula stereotaxically aimed at the MPOA-AH and then microinjected with analogs of vasopressin, oxytocin, and selective V1 and V2 antagonists. Hamsters were tested for flank-marking behavior during a 5 or 10 min observation period following the injection of peptide in a vehicle of 100 nl of saline. None of the 15 analogs of AVP and oxytocin produced more flank marking than the 50.8 +/- 16.2 and 76.8 +/- 4.4 (mean +/- SEM; n = 4) flank marks observed following injection of AVP at the 1 or 10 ng dose, respectively. The number of flank marks produced by each analog was found to be highly related to the pressor activity of that analog at both the 1 ng (rho = +0.74, p less than 0.01) and 10 ng (rho = +0.82, p less than 0.01) doses. In contrast, no statistically reliable relationship between flank marking and the antidiuretic activity of these analogs was found at either dose (1 ng: rho = +0.07, p greater than 0.05; 10 ng: rho = +0.10, p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

A vasopressin antagonist can reverse dominant/subordinate behavior in hamsters

Golden hamsters communicate dominance status by flank marking, a behavior that is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus-medial preoptic area (AH-MPOA). The purpose of the present study was to investigate whether arginine vasopressin (AVP) and an antagonist of AVP could alter or reverse dominant/subordinate relationships in pairs of hamsters. Microinjection of AVP into the AH-MPOA of subordinate hamsters dramatically increased their flank marking despite the presence of their dominant partners. Conversely, microinjection of the AVP antagonist into the AH-MPOA of dominant hamsters blocked flank marking in the presence of their subordinate partners. Surprisingly, the untreated subordinate hamsters significantly increased their own flank marking when tested with their dominant partners treated with the AVP antagonist, thereby reversing the pattern of flank marking normally seen in dominant/subordinate relationships. However, the effect of AVP and the AVP antagonist were limited to the day of treatment. When flank marking behavior was reversed in a pair of hamsters by treatments for three consecutive days, the pair immediately displayed the original dominant/subordinate behavior when treatment was stopped.