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Am J Physiol Endocrinol Metab 291: E147-E151, 2006. First published February 7, 2006; doi:10.1152/ajpendo.00005.2006
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Attenuated stress-induced catecholamine release in mice lacking the vasopressin V1b receptor

Shuji Itoh,1 Sakiko Yamada,1 Toyoki Mori,1 Takashi Miwa,1 Katsura Tottori,1 Yasufumi Uwahodo,1 Yoshitaka Yamamura,1 Meiko Fukuda,2 Koji Yamamoto,2 Akito Tanoue,3 and Gozoh Tsujimoto4

1Research Institute of Pharmacological and Therapeutical Development; 2Department of Toxicology, Tokushima Research Institute, Otsuka Pharmaceutical, Kagasuno, Tokushima; 3Department of Pharmacology, National Research Institute for Child Health and Development, Okura, Tokyo; and 4Department of Genomic Drug Discovery Science, Graduate School of Pharmaceutical Sciences, Kyoto University Faculty of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, Japan

Submitted 6 January 2006 ; accepted in final form 30 January 2006


   ABSTRACT
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 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
Vasopressin V1b receptor is specifically expressed in the pituitary and mediates adrenocorticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the V1b receptor gene (V1bR–/– mice) vs. wild-type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), was increased in wild-type mice, whereas the increases in NE and DA were not observed in V1bR–/– mice. In wild-type mice, E, but not NE or DA, was increased in response to social isolation stress, whereas the increase in E was not observed in V1bR–/– mice. These results suggest that the V1b receptor regulates stress-induced catecholamine release. Because it has been suggested that arginine-vasopressin (AVP) is related to the development of depression, we also evaluated immobility time in the forced swimming test, and we found no significant change in V1bR–/– mice. Taken together, these findings suggest that, in addition to the previously elucidated effect on the hypothalamic-pituitary-adrenal axis, vasopressin activity via V1b receptors regulates stress-induced catecholamine release.

V1b receptor knockout mice; norepinephrine; epinephrine; dopamine; immobility time in the forced swimming test

ARGININE VASOPRESSIN (AVP) has diverse physiological functions, and these physiological effects are mediated through the binding of AVP to specific receptor subtypes of the target cells. AVP receptors are G protein coupled and are divided into at least three types (V1a, V1b, and V2). The V1a (vascular/hepatic) and V1b (anterior pituitary) receptors act via phosphatidylinositol hydrolysis and Ca2+ mobilization (9). The V1a receptor mediates physiological effects such as smooth muscle cell contraction and proliferation, platelet aggregation, and glycogenolysis. The V1b receptor exists in the anterior pituitary, where it stimulates corticotropin release. The V2 receptor is found primarily in the kidney and mediates the antidiuretic effect of AVP via adenylate cyclase/cyclic AMP signals (20) and aquaporin 2 trafficking (15). All of these receptors have been cloned (11, 12, 13) and belong to the family of seven membrane-spanning G protein-coupled receptors.

AVP is synthesized primarily in the magnocellular neurons of the hypothalamic paraventricular nuclei (PVN) and in the supraoptic nuclei that project to the posterior pituitary. In addition, parvocellular neurons of the PVN coexpressing AVP and corticotropin-releasing hormone (CRH) coordinate hypothalamic-pituitary-adrenal (HPA) system activity and project to the external layer of the median eminence, where AVP and CRH are released into the portal blood (1).

Numerous investigations have revealed a potent synergism between AVP and CRH to stimulate pituitary adrenocorticotropin (ACTH) release both in vitro and in vivo (1). Recent studies using mice lacking the type 1 CRH receptor gene (Crhr1–/– mice) provided further indirect evidence that this vasopressinergic system can work as a compensatory mechanism to maintain HPA activity (14, 21). Furthermore, we previously established mice lacking the V1b receptor gene (V1bR–/– mice) and confirmed that circulating concentrations of ACTH and corticosterone were lower in V1bR–/– mice than in wild-type mice in a resting condition, under stimulation with exogenous administered AVP, and in a stressed condition, thus clearly demonstrating that the V1b receptor plays a crucial role in regulating HPA axis activity (19).

The functions of the adrenal gland, e.g., secretion of steroids and catecholamines, are mainly controlled by physiological regulators such as ACTH and acetylcholine. Several other neuromodulators or neuropeptides, including AVP locally secreted by the adrenal medulla, also regulate adrenal activity by autocrine/paracrine mechanisms (4). We previously examined the physiological role of AVP in the adrenal gland in V1bR–/– mice and reported that AVP influenced corticosterone secretion from the adrenal cortex by regulating HPA axis activity (19). In the present study, we investigated the physiological role of AVP in catecholamine secretion in V1bR–/– mice and demonstrated that AVP plays a crucial role in catecholamine secretion via V1b receptors in the adrenal medulla under both acute and chronic stress conditions.


   MATERIALS AND METHODS
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 MATERIALS AND METHODS
RESULTS
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Animals. V1bR–/– mice and wild-type mice (C57BL6J x 129SVJ mix) were established as previously reported (10). Animals were bred at Otsuka Pharmaceutical, and male animals were used for the present study. All animals were housed in a room with a controlled environment (12:12-h light-dark cycle with lights on at 0700, temperature at 23 ± 2°C, and humidity at 60 ± 10%) and provided with food (MF, Oriental Yeast) and water ad libitum. The care and handling of the animals were in accordance with the Guidelines for Animal Care and Use at Otsuka Pharmaceutical, October 1, 1994.

Acute forced swimming stress. Male mice were subjected to forced swimming stress as a predominantly physical stressor (16). Between 0730 and 1000 on the day of testing, each mouse was placed in a glass beaker (diameter 9 cm, height 25 cm) filled with tap water (23–24°C) for 0.5 to 10 min. Immediately after stress exposure, the animals were then returned to their home cages, and blood for determination of plasma catecholamines was collected by decapitation.

Chronic isolation stress. The chronic isolation stress mice (V1bR–/– mice, n = 18; wild-type mice, n = 10) were housed individually in cages (16 x 12 x 12 cm) for 6 wk, as described above. The nonstress mice (n = 10 each) were divided into two groups and housed in cages (5 per cage) for 6 wk as described above. The mice in each group were assigned to two groups based on body weight using Statistical Analysis System software (release 8.1).

Measurement of immobility time in forced swimming test. Immobility time measured in the forced swimming test (FST) appears to be suitable for screening antidepressant agents. The test method used was a slight modification of that described by Porsolt et al. (16). One week before the exposure to acute forced swimming stress or the end of chronic isolation stress, the mice were individually forced to swim inside a vertical acrylic cylinder (diameter 9 cm, height 25 cm) containing 9.5-cm-deep water maintained at 23–24°C. The total duration of immobility (immobility time) was recorded by an observer blinded to the genotype of the mice for 10 or 4 min starting at 2 min after the mice were placed in the water. The mice were judged to be immobile when they ceased struggling and remained floating motionless in the water or made only those movements necessary to keep their heads above the surface.

Measurement of plasma catecholamines. After exposure to forced swimming stress for 10 min, the mice were decapitated for blood collection. It took about 1 min elapsing between the end of stress exposure and decapitation. The animals exposed to chronic isolation stress were housed under the same conditions for 1 wk after the FST and then decapitated for blood collection. The animals were decapitated between 0700 and 1030, and blood samples were collected into prechilled tubes containing EDTA-2Na. The collected blood was centrifuged at 1,000 g for 15 min to obtain plasma. The plasma was stored at –80°C until the measurement of catecholamine levels. Plasma norepinephrine (NE), dopamine (DA), and epinephrine (E) were determined by high-performance liquid chromatography with automatic system (HLC725CAII, Toso, Japan) in FALCO Biosystems (Kyoto, Japan).

Statistical analysis. All values were expressed as means ± SE. Interaction between the genotype and the stress groups was assessed by two-way ANOVA. Differences between the V1bR–/– and the wild-type mice or between stressed and nonstressed groups were assessed by two-tailed t-test. In all comparisons, P < 0.05 was used as the criterion for statistical significance.


   RESULTS
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Changes in catecholamine release induced by acute forced swimming stress. Basal plasma E, NE, and DA levels were, respectively, 5.8 ± 0.4, 7.6 ± 0.7, and 0.6 ± 0.1 ng/ml in wild-type mice (n = 8) and 5.8 ± 0.8, 7.7 ± 0.8, and 0.6 ± 0.1 ng/ml in V1bR–/– mice (n = 10), showing no statistically significant differences between the two genotypes. As shown in Fig. 1, when animals were exposed to acute stress by forced swimming, plasma NE level was significantly increased in wild-type mice (7.6 ± 0.7 vs. 9.8 ± 0.6 ng/ml), whereas the increase in NE was not observed in V1bR–/– mice (7.7 ± 0.8 vs. 7.6 ± 0.7 ng/ml), and E and DA did not change significantly due to forced swimming stress in either V1bR–/– mice or wild-type mice.


Figure 1
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  		Fig. 1. Epinephrine, norepinephrine, and dopamine release in response to acute forced swimming stress in wild-type (WT) and V1b-receptor knockout (V1bR–/–) mice. Open and filled bars indicate blood levels of epinephrine, norepinephrine, and dopamine at baseline (nonstressed) and in a stressed condition, respectively. Values are expressed as means ± SE of 8 animals each in nonstress groups and 11 animals each in stressed groups. *P < 0.05 vs. corresponding nonstress group (2-tailed t-test).

 
Changes in catecholamine release induced by chronic social isolation stress. Basal plasma E, NE, and DA levels were, respectively, 4.4 ± 0.6, 5.9 ± 0.4, and 0.4 ± 0.0 ng/ml in wild-type mice (n = 10) and 5.6 ± 0.4, 6.2 ± 0.7, and 0.4 ± 0.1 ng/ml in V1bR–/– mice (n = 8), once again showing no statistically significant differences between the two genotypes. As shown in Fig. 2, when the animals were exposed to chronic social isolation stress for 6 wk, wild-type mice showed a statistically significant increase in plasma E (P < 0.01), with nonsignificant increases also seen in plasma NE (P = 0.15) and DA (P =0.05). In contrast to wild-type mice, V1bR–/– mice showed no increase in E (5.6 ± 0.4 vs. 5.2 ± 0.7 ng/ml) due to social isolation stress, nor were any statistically significant changes seen in NE or DA.


Figure 2
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  		Fig. 2. Epinephrine, norepinephrine, and dopamine release in response to chronic isolation stress in WT and V1bR–/– mice. Open and filled bars indicate blood levels of epinephrine, norepinephrine, and dopamine at baseline (nonstressed) and in a stressed condition, respectively. Values are expressed as means ± SE of 10 WT and 8 V1bR–/– mice in nonstress groups and 10 WT and 18 V1bR–/– mice in stressed groups. **P < 0.01 vs. corresponding nonstress group (2-tailed t-test).

 
Immobility time in FST. Immobility time in the FST is commonly used as an index of efficacy of antidepressant drugs in animals, and this is known as the Porsolt method (16). First, we compared the FST immobility time of V1bR–/– mice and wild-type mice using the animals subjected to the acute forced swimming stress. Immobility time during the period of 0–10 min was measured by an observer blinded to the genotype of the mice. Immobility time was 367 ± 17 s for V1bR–/– mice and 378 ± 19 s for wild-type mice, showing no statistically significant difference between the two genotypes.

Next, we evaluated the FST immobility time of V1bR–/– and wild-type mice using the animals exposed or not exposed to chronic social isolation stress. In this trial, immobility time was measured by an observer blinded to the genotype of the mice for 4 min, starting at 2 min after the mice were placed in the water. As shown in Fig. 3, once again there were no statistical differences between V1bR–/– and wild-type mice either with or without social isolation stress.


Figure 3
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  		Fig. 3. Immobility time in Porsolt's forced swimming test (16) in WT and V1bR–/– mice with or without chronic isolation stress. Chronic isolation stress mice were housed individually in cages (16 x 12 x 12 cm) for 6 wk. Nonstressed mice were housed 5 animals per cage for 6 wk. Forced swimming test was performed, and immobility time was measured by an observer blinded to the genotype of the mice for 4 min, starting at 2 min after the mice were placed in the water. Values are expressed as means ± SE of 10 WT and 10 V1bR–/– mice in nonstress groups and 10 WT and 18 V1bR–/– mice in stressed groups. NS, not significant, basal vs. stressed groups.

 

   DISCUSSION
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
In a previous study, using the V1bR–/– mice, we demonstrated that AVP plays a critical role in regulating HPA axis activity via the V1b receptor under a forced swimming stress condition (19). Under various physiological conditions such as stress, the neuromediator acetylcholine is released from the splanchnic nerve and stimulates catecholamine release. In addition to the direct stimulation of catecholamine secretion, AVP secretion is also increased in the adrenal medulla as a result of the nerve stimulation, and AVP might be able to activate catecholamine release. Both V1a and V1b receptor subtypes are expressed in the adrenal medulla, and the V1b receptor has been suggested to be involved in catecholamine secretion (4). Therefore, we analyzed plasma catecholamine levels, using V1bR–/– mice to investigate the functional role of the V1b receptor in the adrenal medulla under stress conditions.

In response to chronic isolation stress, plasma E level was significantly increased, and NE and DA also showed a tendency to increase in wild-type mice, whereas no subclass of catecholamines was increased due to stress stimulation in V1bR–/– mice. These results in wild-type mice were in good agreement with the findings of our previous study in which plasma E, NE, and DA levels were increased when the animals were exposed to isolation stress for 1–6 days (2). However, no such increases in catecholamines were observed in V1bR–/– mice. Thus chronic isolation stress is capable of increasing plasma catecholamine levels in wild-type mice, but not in V1bR–/– mice. When animals were exposed to acute forced swimming stress, increased plasma E level was observed in wild-type mice but not in V1bR–/– mice, although no differences in basal plasma E, NE, and DA levels were seen between wild-type and V1bR–/– mice. These results suggest that the AVP/V1b pathway could play a crucial role in catecholamine release under stress conditions, but not in a resting condition.

Because V1b receptors are reported to be mainly present on chromaffin cells in the adrenal medulla (4, 6, 8), it is likely that the AVP/V1b receptor is directly involved in catecholamine release from the adrenal medulla and sympathetic nerves. In addition to the direct action of AVP in the adrenal medulla, other factors such as corticosterone stimulate catecholamine release. For example, CRH knockout mice exhibited impaired basal and restraint stress-induced E release (10). In the CRH-deficient mice, the gene expression or enzyme activity of phenylethanolamine N-methyltransferase (PNMT), the synthesis enzyme of E, was decreased. This decrease in PNMT was induced by a decrease in corticosterone, and it resulted in a decreased E level. This is supported by the findings that CRH receptor-deficient mice have impaired corticosterone secretion during stress (18) and that hypophysectomy-induced depletion of corticosterone causes blunted adrenal PNMT gene expression and activity (22). Thus reduced corticosterone level could alter plasma catecholamine levels. Jeong et al. (10) reported increased blood levels of NE in CRH knockout mice, and they also discussed the possibility that decreased corticosterone may contribute to higher NE levels because glucocorticoids are thought to have an inhibitory action on NE release from the sympathetic nerve terminals. V1bR–/– mice showed a reduced response in plasma ACTH level to acute forced swimming stress (19), suggesting that decreased corticosterone levels could cause lower catecholamine release in V1b-deficient mice. However, the increases in plasma corticosterone levels in response to forced swimming stress were comparable between wild-type mice and V1bR–/– mice, suggesting that corticosterone release from the adrenal cortex was not impaired. In response to chronic isolation stress, blood corticosterone level was 17.0 ± 1.5 ng/ml in wild-type mice and 16.1 ± 1.2 ng/ml in V1bR–/– mice (our unpublished data). Therefore, the reduced catecholamine release from the adrenal gland in V1bR–/– mice could be due to an impaired AVP/V1b system in the adrenal medulla rather than to reduced corticosterone level via the HPA axis. Therefore, the precise mechanism of involvement of the V1b receptor in catecholamine release cannot be elucidated, and another explanation might be that different types of stress affect catecholamine release in different ways.

In addition to decreased catecholamine release and HPA activity in response to stress, V1bR–/– mice displayed reduced aggression and impaired social recognition (23), suggesting that the AVP/V1b pathway plays a functional role in modulating emotional processes in the central nervous system. In fact, the V1b-receptor antagonist SSR-149415 produced anxiolytic- (17) and antidepressant-like effects (7). In addition, AVP levels in the plasma and cerebrospinal fluid were decreased in depressed patients, indicating that AVP is related to the development of depression (5). We therefore assessed the AVP/V1b pathway using V1b-deficient mice to examine whether it is involved in the development of depression. In the present study, we compared the FST immobility time of V1bR–/– and wild-type mice according to the Porsolt method (16). The method is used for evaluating anti-depressant drugs such as serotonine-selective reuptake inhibitors or serotonine-noradrenaline reuptake inhibitors. Our results indicated that the basal FST immobility time of V1bR–/– mice did not differ from that of wild-type mice, which is consistent with the results of previous reports where V1bR–/– mice were used (3, 23). Furthermore, in the present study we demonstrated that the FST immobility time of V1bR–/– mice did not differ from that of wild-type mice, even after exposure to chronic isolation stress. These results suggest that the AVP/V1b receptor is not involved in the development of depression. This finding, however, is inconsistent with the results of a study where the selective V1b-receptor antagonist SSR-149415 was used, which did affect FST immobility time in rats (7). One possible explanation for this discrepancy is the existence of some unknown compensatory process. Because V1bR–/– mice lack the receptor throughout development, numerous neurochemical changes may occur during development to compensate for the missing receptor (3). Another possible explanation for the discrepancy is that SSR-149415 may have some nonspecific action other than V1b-receptor antagonism and/or that the sensitivity of FST immobility time varies among animal species or strains.

In conclusion, we demonstrated that the catecholamine release induced by acute and chronic stress is attenuated in mice lacking the vasopressin V1b receptor.


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This work was supported by a research grant from The Japan Health Sciences and in part by research grants from the Scientific Fund of the Ministry of Education, Science and Culture of Japan, and the Ministry of Human Health and Welfare, and by the 21st Century Center of Excellence Program "Knowledge Information Infrastructure for Genome Science".


   FOOTNOTES
 

Address for reprint requests and other correspondence: T. Mori, Research Institute of Pharmacological and Therapeutical Development, Otsuka Pharmaceutical, Ltd., 463–10, Kagasuno, Kawauchi-cho, Tokushima 771–0192, Japan (e-mail: to_mori{at}research.otsuka.co.jp)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


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