Psychotropic effects of adrenergic β-blockers on agonistic behavior between resident and intruder mice
The present study was conducted to investigate the effect of adrenergic beta-blockers on agonistic behavior in male mice, using quantitative ethological methods. Agonistic behavior was evoked using a resident-intruder paradigm. The following drugs were administered orally at four dose levels (vehicle, 5, 10 and 20 mg/kg) to either resident or intruder mice: dl-propranolol, practolol, d-propranolol, and l-propranolol. When the resident was treated with either dl-propranolol or l-propranolol, aggressive episodes (offensive sideways posture, attack bite, tail rattle) were suppressed significantly in a dose-dependent manner, whereas practolol and d-propranolol were ineffective. All treatments except the high dose of l-propranolol failed to affect the resident's solitary behavior (locomotion). When the intruder was treated with beta-blockers, agonistic behavior was not altered. Since practolol does not cross the blood-brain barrier, the differential suppression of agonistic behavior is due to the central action of beta-blockers. d-Propranolol does cross the blood-brain barrier but is devoid of beta-receptor blocking property; hence l-propranolol suppression of agonistic behavior implies inactivation of brain adrenergic beta-receptors. The findings seem to indicate that beta-blockers such as dl-propranolol and l-propranolol have a psychotropic action.
Available from: Peter Holzer
- "However, our data obtained with propranolol rule out any implication of ␤-adrenoceptors in the increased nocturnal consumption of water exhibited by Y2−/− and Y4−/− mice. We think this conclusion to be valid because (±)-propranolol injected systemically at doses in the range of 10 mg/kg reaches and blocks both peripheral and central ␤-adrenoceptors of mice without causing sedation  . Although angiotensin II is a potent dipsogenic messenger in the brain  , we do not think that this peptide contributes to the elevated nocturnal water consumption seen in Y2−/− and Y4−/−mice. "
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ABSTRACT: Neuropeptide-Y (NPY) is involved in the regulation of ingestive behaviour and energy homeostasis. Since deletion of the NPY Y2 and Y4 receptor gene increases and decreases food intake, respectively, we examined whether water intake during the light and dark phases is altered in Y2 and Y4 receptor knockout mice. The water consumption of mice staying in their home cages was measured by weighing the water bottles at the beginning and end of the light phase during 4 consecutive days. Control, Y2 and Y4 receptor knockout mice did not differ in their water intake during the light phase. However, during the dark phase Y2 and Y4 receptor knockout mice drank significantly more (46-63%, P<0.05) water than the control mice. The total daily water intake over 24 h was also enhanced. The enhanced water intake during the dark phase was not altered by the beta-adrenoceptor antagonist propranolol or the angiotensin AT1 receptor antagonist telmisartan (each injected intraperitoneally at 10 mg/kg). These data indicate that NPY acting via Y2 and Y4 receptors plays a distinctive role in the regulation of nocturnal water consumption. While beta-adrenoceptors and angiotensin AT1 receptors do not seem to be involved, water intake in Y2 and Y4 receptor knockout mice may be enhanced because presynaptic autoinhibition of NPY release and inhibition of orexin neurons in the central nervous system are prevented.
Behavioural Brain Research 05/2006; 168(2):255-60. DOI:10.1016/j.bbr.2005.11.013 · 3.03 Impact Factor
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ABSTRACT: The psychotropic actions of crude ginseng saponins, pure ginsenoside Rb1 (GS-Rb1) and ginsenoside Rg1 (GS-Rg1) obtained from the root of Panax ginseng, were evaluated from their effects on agonistic behavior in mice. A resident-intruder test situation was used. When the resident mouse was treated with crude ginseng saponins (25, 50 and 100 mg/kg i.p.), aggressive episodes (offensive sideways posture and attack bite) were significantly suppressed in a dose-dependent manner. However, the agonistic behavior was not altered when the intruder was treated with crude ginseng saponins. GS-Rb1 (2.5, 5 ad 10 mg/kg i.p.) also significantly suppressed aggressive episodes when given to the resident, whereas GS-Rg1 (2.5, 5 and 10 mg/kg i.p.) was ineffective. Neither Gs-Rb1 nor GS-Rg1 given to the intruder caused any significant changes in the behavior of the resident. Although the highest dose of crude ginseng saponins suppressed locomotion frequency, it appears that both crude ginseng saponins and GS-Rb1 possess a specific psychotropic action on agonistic behavior.
European Journal of Pharmacology 03/1988; 146(2-3-146):291-297. DOI:10.1016/0014-2999(88)90305-6 · 2.53 Impact Factor
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ABSTRACT: We investigated how repeated agonistic confrontations affect the hypnotic effect of pentobarbital (PB) in male mice, using a resident-intruder paradigm. PB concentrations in the cortex, midbrain and brainstem were determined. Agonistic confrontations were terminated after 10 or 20 attack bites, and were repeated for 5 consecutive days. Immediately after the last encounter, PB (55 mg/kg, IP) was administered to both resident and intruder mice. Compared to the control group, intruders exposed to 20 daily attack bites showed a significant prolongation of the latency to sleep and a shortening of the duration of sleeping time. At the stage of induction, no significant difference in brain PB levels was found between the defeated and control intruders. At the stage of recovery, however, the defeated intruders showed a significantly low level of PB in all brain areas. In contrast, attacking resident mice did not show any significant changes in either the hypnotic effect or regional brain concentration of PB. Because pretreatment with naloxone prior to daily agonistic confrontation antagonized the alteration in PB-induced hypnosis, it seems that endogenous opioid mechanisms may participate in this phenomenon. The present study indicates that susceptibility to a hypnotic drug can be altered by chronic social conflict experience.
Psychopharmacology 12/1988; 97(1):30-34. DOI:10.1007/BF00443408 · 3.88 Impact Factor
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