Behavioural and neurochemical effects induced by chronic mild stress applied to two different rat strains

Bekris, Stathis; Αντωνίου, Κατερίνα; Daskas, S.; Papadopoulou-Daifoti, Z.

doi:10.1016/j.bbr.2005.01.005

Cited by 253 publications

(182 citation statements)

References 73 publications

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“…Specifically, they were less active in the forced swim test, a gold-standard measure of depression in rodents (Cryan, et al, 2005). They also consumed less of a dilute palatable sucrose solution with repeated access to it; a pattern interpreted to reflect anhedonia (Bekris, et al, 2005;Grippo, et al, 2006). We obtained modestly significant results with this measure, but the strength of the effect may have been compromised by the fact that the results rely on the ingestion of a palatable substance in rats with prior access to PF.…”

Section: Discussionmentioning

confidence: 67%

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A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression

Chandler‐Laney

Castañeda

Pritchett

et al. 2007

Pharmacology Biochemistry and Behavior

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A history of dieting is common in individuals suffering from eating disorders for which depression and mood disturbances are also comorbid. We investigated the effect of a history of caloric restriction (HCR) in rats that involved cyclic food restriction and refeeding with varying levels of access to palatable food (PF) on: 1) responses to the SSRI, fluoxetine; 2) monoamine levels in brain regions central to the control of feeding, reward, and mood regulation; and 3) behavioral tests of anxiety and depression. HCR coupled with intermittent but not daily access to PF exaggerated rats' anorectic response to fluoxetine (p<0.05); was associated with a significant 71% and 58% reduction of 5-HT and dopamine, respectively, in the medial prefrontal cortex; and induced behaviors consistent with models of depression. HCR, irrespective of access to PF, abolished the strong association between 5-HT and dopamine turnover in the nucleus accumbens in control rats (r =0.71 vs. -0.06, p<0.01). Access to PF, irrespective of HCR, reduced hypothalamic dopamine. Together, these findings suggest that a history of frequent food restriction-induced weight fluctuation imposes neurochemical changes that negatively impact feeding and mood regulation.

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Section: Discussionmentioning

confidence: 67%

“…Anhedonia is interpreted from reduced intake of a dilute sucrose solution with repeated access to it (Bekris, et al, 2005;Grippo, et al, 2006). Weight-matched (N = 8 Intermittent PF/HCR and N = 8 Intermittent PF/no-HCR) rats were selected prior to any cycling and used for these tests throughout cycling.…”

Section: Depression Testsmentioning

confidence: 99%

A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression

Chandler‐Laney

Castañeda

Pritchett

et al. 2007

Pharmacology Biochemistry and Behavior

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“…Those animals developing exploratory deficits in response to chronic stress consistently display increased floating during forced swimming and decreased preference for sweet tastes (Berger et al, 2004, behaviors widely used to model depression and anhedonia in rats and mice (Detke et al, 1995, Crowley et al, 2004. Indeed, in the chronic mild stress model of depression in both rats and mice, decrements in both exploratory behavior and reward seeking are prominent features (Willner et al, 1992, Argyropoulos and Nutt, 1997, Bielajew et al, 2002, Anisman and Matheson, 2005, Bekris et al, 2005, Gronli et al, 2005. Similar results have also been reported following chronic social stress (Rygula et al, 2005).…”

Section: Chronic Crf Receptor Agonism In the Drn And Behaviormentioning

confidence: 64%

Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

et al. 2007

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Corticotropin releasing factor (CRF) family peptides play key roles in integrating neural responses to stress. Both major CRF receptors have been pharmacologically identified in the dorsal raphe nucleus (DRN), a stress sensitive and internally heterogeneous nucleus supplying many forebrain regions with serotonergic input. Despite the involvement of chronic stress and serotonergic dysfunction in human mood and anxiety disorders, little is known about the effects of chronic CRF receptor activation on the DRN. We infused ovine CRF (1ng/hr), urocortin II (UCNII, 1ng/hr), or vehicle alone into rat DRN over 6 days. During infusion, animals were allowed to freely explore an open field for 15 minutes on each of two days, with the addition of a novel object on the second day. Following behavioral testing, 5-HT 1A , 5-HT 1B , serotonin transporter (SERT), and tryptophan hydroxylase-2 (Tph2) expression were examined through the DRN by in situ hybridization. Ovine CRF infusion resulted in significantly decreased novel object touches, climbs, as well as increased latency to first novel object contact. UCNII had a similar but less dramatic effect, decreasing only climbing behavior. Both ovine CRF and UCNII blunted the decrease in corner time expected on reexposure to the open field. Both peptides also produced regionally specific changes in gene expression: 5-HT 1A expression was increased 30% in the mid-rostral ventromedial DRN, while SERT was decreased by 30% in the mid-caudal shell dorsomedial DRN. There also appeared to be a shift in the relative level of Tph2 expression between the ventromedial and core dorsomedial DRN at the mid-rostral level. Changes in 5-HT 1A , SERT, and relative Tph2 mRNA abundance were correlated with novel object exploration. These findings suggest chronic intra-DRN administration of CRF agonists decreases exploratory behavior, while producing subregionally limited changes in serotonergic gene expression. These studies may be relevant to mechanisms underlying behavioral changes after chronic stress. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptDepression and anxiety disorders are among the leading causes of morbidity, mortality, and disability in the United States (Greenberg et al., 2003). They are often comorbid, and both are highly associated with chronic exposure to stress. Multiple lines of evidence suggest that chronic and inescapable stress produce long lasting effects on brain function and behavior that play a prominent role in the development, maintenance, and recurrence of both depression and a variety of anxiety disorders (Gulley and Nemeroff, 1993, Arborelius et al., 1999, Ressler and Nemeroff, 2000.Altered serotonin neurotransmission appears to be a central mechanism inducing both depressive (Maes and Meltzer, 1995) and anxiety disorders (Ressler and Nemeroff, 2000). The majority of serotonergic fibers to forebrain regions thought to be involved in mood and anxiety regulation arise from the dorsal raphe nucleus (DRN) and median raphe nucleus (MRN) ...

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“…The chronic stress paradigm is considered to have a greater etiological relevance and face validity in mimicking MDD than other animal models, and therefore has become one of the most widely used preclinical paradigms of affective disorders [195]. Chronic mild stress causes significant reductions in absolute and relative sucrose intake in rats, that is associated with a decrease in striatal DA activity, and is reversed after chronic antidepressant administration with imipramine [196]. Decreased DA release to the NAc has been shown to occur after exposure to chronic repeated or an unavoidable stress regimen in rats [189,197,198], suggesting that stress significantly reduces mesolimbic DA transmission in rodent models.…”

Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Behavioural and neurochemical effects induced by chronic mild stress applied to two different rat strains

Cited by 253 publications

References 73 publications

A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression

A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression

Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

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