Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Nikulina, Ella M.; Miczek, Klaus A.; Hammer, Ronald P.

doi:10.1038/sj.npp.1300658

Cited by 51 publications

(40 citation statements)

References 46 publications

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“…For instance, it has been demonstrated that repeated defeated stress or restraint stress increase amphetamine-induced locomotor activity in adult rats (Covington and Miczek 2001;de Jong et al 2005;Nikulina et al 2005;Pacchioni et al 2002). Moreover, an acute cocaine challenge induced a significant increase in locomotor activity in adolescent rats that were previously subjected to restraint stress as compared to the control group (Lepsch et al 2005).…”

Section: Discussionmentioning

confidence: 96%

Stress-induced cross-sensitization to amphetamine is related to changes in the dopaminergic system

et al. 2011

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Repeated stress engenders behavioral sensitization. The mesolimbic dopamine system is critically involved in drug-induced behavioral sensitization. In the present study we examined the differences between adolescent and adult rats in stress-induced behavioral sensitization to amphetamine and changes in dopamine (DA) and its metabolite levels in the mesolimbic system. Adolescent or adult rats were restrained for 2 h, once a day, for 7 days. Three days after the last exposure to stress, the animals were challenged with saline or amphetamine (1.0 mg/kg i.p.) and amphetamine-induced locomotion was recorded for 40 min. Immediately after the behavioral tests, rats were decapitated and the nucleus accumbens (NAcc), ventral tegmental area (VTA) and amygdala (AM) were removed to measure tissue levels of DA and its metabolites by HPLC. Exposure to repeated restraint stress promoted behavioral sensitization to amphetamine in both adult and adolescent rats. In adult rats, amphetamine administration increased DA levels in both the stress and control groups in the NAcc and VTA. In adolescent rats, amphetamine increased DA levels in the NAcc in rats exposed to stress. Furthermore, in the AM of adolescent rats in the control group, amphetamine increased the DA levels; however, amphetamine reduced this neurotransmitter in the rats that were exposed to stress. No alteration was observed in the dopamine metabolite levels. Therefore, stress promoted behavioral sensitization to amphetamine and this may be related to changes in DA levels in the mesolimbic system. These changes appear to be dependent on ontogeny.

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Section: Discussionmentioning

confidence: 96%

Stress-induced cross-sensitization to amphetamine is related to changes in the dopaminergic system

et al. 2011

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“…Shaking-crowding consisted of placing 6 rats in a plastic box for 1 hour atop a lab shaker set to generate 220 back-and-forth movements (approximately 2 inch lateral deflection) per min. The resident-intruder social defeat was carried out as described previously (Nikulina et al, 2005; Ruis et al, 1999). Prior to social defeat, the female was removed and the “intruder” Sprague-Dawley rat was introduced into the resident cage.…”

Section: Methodsmentioning

confidence: 99%

Beneficial effects of desipramine on cognitive function of chronically stressed rats are mediated by α1-adrenergic receptors in medial prefrontal cortex

Bondi

Jett

Morilak

2010

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Chronic stress is a risk factor for many psychopathological conditions, including depression and anxiety disorders. Cognitive impairments associated with prefrontal cortical dysfunction are a major component of such illnesses. Using an attentional set shifting test (AST), we have previously shown that elevating noradrenergic activity in rat medial prefrontal cortex (mPFC) can facilitate cognitive set-shifting, and that chronic unpredictable stress (CUS) caused set-shifting deficits. It is not known, however, if noradrenergic modulatory function is compromised by chronic stress, perhaps contributing to the stress-induced cognitive deficit. Thus, the first study investigated whether acutely elevating noradrenergic activity in mPFC still enhances cognitive function after chronic stress. As previously demonstrated, CUS impaired cognitive set-shifting on the AST. This deficit was abolished by acute systemic administration of the α2-adrenergic autoreceptor antagonist, atipamezole. Microdialysis revealed no differences in extracellular norepinephrine (NE) levels in mPFC of CUS-exposed and unstressed control rats at baseline or during behavioral testing, and comparable increases after atipamezole. In the second experiment, rats were treated chronically with the selective NE reuptake blocker, desipramine, during the CUS treatment through behavioral testing. Again, CUS impaired cognitive set-shifting in vehicle-treated rats, and chronic desipramine treatment prevented such deficits. Acute blockade of post-synaptic α1-adrenergic receptors in mPFC prior to testing blocked the beneficial effect of desipramine on cognitive set-shifting. These results suggest that desipramine restores cognitive set-shifting capability that has been compromised by chronic stress by activating α1-adrenergic receptors in the mPFC. Thus, noradrenergic modulatory capability in mPFC remains intact after CUS, and this represents one possible substrate by which antidepressants may exert their beneficial effects in the treatment of depression.

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“…The shaking-crowding procedure was carried out by placing six rats in a cardboard box atop a lab shaker set to produce 220 back-and-forth movements (approximately 2-inch sideways deflection) per min. The resident-intruder social defeat was performed as described previously (Nikulina et al, 2005;Ruis et al, 1999). The 'intruder' Sprague-Dawley test rat was transported to the Long-Evans residents' housing room.…”

Section: Chronic Unpredictable Stress Proceduresmentioning

confidence: 99%

Chronic Unpredictable Stress Induces a Cognitive Deficit and Anxiety-Like Behavior in Rats that is Prevented by Chronic Antidepressant Drug Treatment

Bondi

Rodríguez

Gould

et al. 2007

Neuropsychopharmacol

353

263

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Chronic stress is a risk factor for the development of many psychopathological conditions in humans, including major depression and anxiety disorders. There is a high degree of comorbidity of depression and anxiety. Moreover, cognitive impairments associated with frontal lobe dysfunction, including deficits in cognitive set-shifting and behavioral flexibility, are increasingly recognized as major components of depression, anxiety disorders, and other stress-related psychiatric illnesses. To begin to understand the neurobiological mechanisms underlying the cognitive and emotional consequences of chronic stress, it is necessary to employ an animal model that exhibits similar effects. In the present study, a rat model of chronic unpredictable stress (CUS) consistently induced a cognitive impairment in extradimensional set shifting capability in an attentional set shifting test, suggesting an alteration in function of the medial prefrontal cortex. CUS also increased anxiety-like behavior on the elevated plus-maze. Further, chronic treatment both with the selective norepinephrine reuptake blocker, desipramine (7.5 mg/kg/day), and the selective serotonin reuptake blocker, escitalopram (10 mg/kg/ day), beginning 1 week before CUS treatment and continuing through the behavioral testing period, prevented the CUS-induced deficit in extradimensional set-shifting. Chronic desipramine treatment also prevented the CUS-induced increase in anxiety-like behavioral reactivity on the plus-maze, but escitalopram was less effective on this measure. Thus, CUS induced both cognitive and emotional disturbances that are similar to components of major depression and anxiety disorders. These effects were prevented by chronic treatment with antidepressant drugs, consistent also with clinical evidence that relapse of depressive episodes can be prevented by antidepressant drug treatment.

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Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Cited by 51 publications

References 46 publications

Stress-induced cross-sensitization to amphetamine is related to changes in the dopaminergic system

Stress-induced cross-sensitization to amphetamine is related to changes in the dopaminergic system

Beneficial effects of desipramine on cognitive function of chronically stressed rats are mediated by α1-adrenergic receptors in medial prefrontal cortex

Chronic Unpredictable Stress Induces a Cognitive Deficit and Anxiety-Like Behavior in Rats that is Prevented by Chronic Antidepressant Drug Treatment

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