The guinea pig forced swim test as a new behavioral despair model to characterize potential antidepressants

Wicke, Karsten; Rex, André; Jongen-Rêlo, Ana L.; Groth, Ilona; Groß, Gerhard

doi:10.1007/s00213-007-0874-0

Cited by 14 publications

(16 citation statements)

References 34 publications

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“…In addition, mean body temperature of guinea pigs has been reported to decrease less than 0.5°C following 5-min forced swimming in water maintained at 30 ± 1°C (Wicke et al, 2007). In the present study, water temperature on the first day of training was 30 ± 0.25°C, as in Filliat et al (2002), and was decreased 1°C each subsequent day.…”

Section: Methodsmentioning

confidence: 99%

Galantamine counteracts development of learning impairment in guinea pigs exposed to the organophosphorus poison soman: Clinical significance

et al. 2011

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Galantamine, a drug used to treat Alzheimer’s disease, protects guinea pigs against the acute toxicity and lethality of organophosphorus (OP) compounds, including soman. Here, we tested the hypothesis that a single exposure of guinea pigs to 1xLD50 soman triggers cognitive impairments that can be counteracted by galantamine. Thus, animals were injected intramuscularly with saline (0.5 ml/kg) or galantamine (8 mg/kg) and 30 min later injected subcutaneously with soman (26.3 µg/kg) or saline. Cognitive performance was analyzed in the Morris water maze (MWM) four days or three months after the soman challenge. Fifty percent of the saline-injected animals that were challenged with soman survived with mild-to-moderate signs of acute toxicity that subsided within a few hours. These animals showed no learning impairment and no memory retention deficit, when training in the MWM started four days post-soman challenge. In contrast, animals presented significant learning impairment when testing started three months post-challenge. Though the magnitude of the impairment correlated with the severity of the acute toxicity, animals that presented no or only mild signs of toxicity were also learning impaired. All guinea pigs that were treated with galantamine survived the soman challenge with no signs of acute toxicity and learned the MWM task as control animals, regardless of when testing began. Galantamine also prevented memory extinction in both saline-and soman-challenged animals. In conclusion, learning impairment develops months after a single exposure to 1xLD50 soman, and galantamine prevents both the acute toxicity and the delayed cognitive deficits triggered by this OP poison.

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Section: Methodsmentioning

confidence: 99%

Galantamine counteracts development of learning impairment in guinea pigs exposed to the organophosphorus poison soman: Clinical significance

et al. 2011

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“…Desipramine, a relatively selective NE reuptake inhibitor, exerts antidepressant-like effects on behavior in rodent models (Poncelet et al , 1986; Wallace-Boone et al , 2007; Wicke et al , 2007). It decreases immobility in the forced-swim and tail-suspension tests in rats and mice (Dableh et al , 2005; Duman et al , 2007; Zhang et al , 2002, 2008) and decreases response rate and increases reinforcement rate in rats responding under a differential-reinforcement-of-low-rate (DRL) schedule (Dekeyne et al , 2002; O’Donnell, 1990).…”

Section: Introductionmentioning

confidence: 99%

Postsynaptic α-2 Adrenergic Receptors are Critical for the Antidepressant-Like Effects of Desipramine on Behavior

Zhang

Whisler

Huang

et al. 2008

Neuropsychopharmacol

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The antidepressant desipramine inhibits the reuptake of norepinephrine (NE), leading to activation of both pre-and postsynaptic adrenergic receptors, including a-1, a-2, b-1, and b-2 subtypes. However, it is not clear which adrenergic receptors are involved in mediating its antidepressant effects. Treatment of mice with desipramine (20 mg/kg, i.p.) produced an antidepressant-like effect, as evidenced by decreased immobility in the forced-swim test; this was antagonized by pretreatment with the a-2 adrenergic antagonist idazoxan (0.1-2.5 mg/kg, i.p.). Similarly, idazoxan, administered peripherally (0.5-2.5 mg/kg, i.p.) or centrally (1-10 mg, i.c.v.), antagonized the antidepressant-like effect of desipramine in rats responding under a differential-reinforcement-of-low-rate (DRL) 72-s schedule, ie, decreased response rate and increased reinforcement rate. By contrast, pretreatment with the b-adrenergic antagonists propranolol and CGP-12177 or the a-1 adrenergic antagonist prazosin did not alter the antidepressant-like effect of desipramine on DRL behavior. The lack of involvement of b-adrenergic receptors in mediating the behavioral effects of desipramine was confirmed using knockout lines. In the forced-swim test, the desipramine-induced decrease in immobility was not altered in mice deficient in b-1, b-2, or both b-1 and b-2 adrenergic receptors. In addition, desipramine (3-30 mg/kg) produced an antidepressant-like effect on behavior under a DRL 36-s schedule in mice deficient in both b-1 and b-2 adrenergic receptors. As antagonism of presynaptic a-2 adrenergic receptors facilitates NE release, which potentiates the effects of desipramine, the present results suggest that postsynaptic a-2 adrenergic receptors play an important role in its antidepressant effects.

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“…The animals swam up to 10 min or until they presented signs of fatigue or danger of drowning. It is important to remember that guinea pigs only breathe through their noses, minimizing the risk of water aspiration [16,17] . It is important to emphasize that in this protocol of stress induction, there are both psychological and physical stressors, and it is not possible to separate the role of each component in the functional and inflammatory responses.…”

Section: Forced Swim Stressmentioning

confidence: 99%

“…There are several animal models of stress induction [12][13][14][15][16][17] . The forced swim stress is a type of unavoidable stress that induces an effort to survive with an escape deficit [16,17] .…”

Section: Introductionmentioning

confidence: 99%

“…The forced swim stress is a type of unavoidable stress that induces an effort to survive with an escape deficit [16,17] . Furthermore, this method has been used as an animal model of behavioral despair/depression associated with the modulation of inflammatory cells and cytokines [16][17][18][19] . It is important to emphasize that this stress animal model includes both psychological and physical stressors, which in turn influence allergic responses induced by repeated ovalbumin exposures.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Repeated Stress on Distal Airway Inflammation, Remodeling and Mechanics in an Animal Model of Chronic Airway Inflammation

Leick

Reis

Honorio-Neves

et al. 2011

Neuroimmunomodulation

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Background/Aims: Epidemiological studies suggest that stress has an impact on asthmatic exacerbations. We evaluated if repeated stress, induced by forced swimming, modulates lung mechanics, distal airway inflammation and extracellular matrix remodeling in guinea pigs with chronic allergic inflammation. Methods: Guinea pigs were submitted to 7 ovalbumin or saline aerosols (1–5 mg/ml during 4 weeks; OVA and SAL groups). Twenty-four hours after the 4th inhalation, guinea pigs were submitted to the stress protocol 5 times a week during 2 weeks (SAL-S and OVA-S groups). Seventy-two hours after the 7th inhalation, guinea pigs were anesthetized and mechanically ventilated. Resistance and elastance of the respiratory system were obtained at baseline and after ovalbumin challenge. Lungs were removed, and inflammatory and extracellular matrix remodeling of distal airways was assessed by morphometry. Adrenals were removed and weighed. Results: The relative adrenal weight was greater in stressed guinea pigs compared to non-stressed animals (p < 0.001). Repeated stress increased the percent elastance of the respiratory system after antigen challenge and eosinophils and lymphocytes in the OVA-S compared to the OVA group (p < 0.001, p = 0.003 and p < 0.001). Neither collagen nor elastic fiber contents were modified by stress in sensitized animals. Conclusions: In this animal model, repeated stress amplified bronchoconstriction and inflammatory response in distal airways without interfering with extracellular matrix remodeling.

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The guinea pig forced swim test as a new behavioral despair model to characterize potential antidepressants

Cited by 14 publications

References 34 publications

Galantamine counteracts development of learning impairment in guinea pigs exposed to the organophosphorus poison soman: Clinical significance

Galantamine counteracts development of learning impairment in guinea pigs exposed to the organophosphorus poison soman: Clinical significance

Postsynaptic α-2 Adrenergic Receptors are Critical for the Antidepressant-Like Effects of Desipramine on Behavior

Effects of Repeated Stress on Distal Airway Inflammation, Remodeling and Mechanics in an Animal Model of Chronic Airway Inflammation

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