Stress models of depression: Forming genetically vulnerable strains

Henn, Fritz A.; Vollmayr, Barbara

doi:10.1016/j.neubiorev.2005.03.019

Cited by 246 publications

(162 citation statements)

References 48 publications

(48 reference statements)

Supporting

Mentioning

150

Contrasting

Unclassified

Order By: Relevance

“…Chronic restraint decreased motivation on the appetitive operant conditioning paradigm, which is consistent with anhedonia and decreased motivation (Barr & Phillips, 1998;Konkle et al, 2003), hallmark features of depression (Frazer & Morilak, 2005;Henn & Vollmayr, 2005). Chronic restraint increases adrenal size, which coincides with adrenal hypertrophy evident in major depression (Nemeroff, Krishnan, Reed, Leder, Beam, & Dunnick, 1992).…”

Section: Discussionmentioning

confidence: 52%

Chronic stress impairs spatial memory and motivation for reward without disrupting motor ability and motivation to explore.

Kleen

Sitomer

Killeen

et al. 2006

Behavioral Neuroscience

149

112

View full text Add to dashboard Cite

This study uses an operant, behavioral model to assess the daily changes in the decay rate of shortterm memory, motivation, and motor ability in rats exposed to chronic restraint. Restraint decreased reward-related motivation by 50% without altering memory decay rate or motor ability. Moreover, chronic restraint impaired hippocampal-dependent spatial memory on the Y maze (4-hr delay) and produced CA3 dendritic retraction without altering hippocampal-independent maze navigation (1-min delay) or locomotion. Thus, mechanisms underlying motivation for food reward differ from those underlying Y maze exploration, and neurobiological substrates of spatial memory, such as the hippocampus, differ from those that underlie short-term memory. Chronic restraint produces functional, neuromorphological, and physiological alterations that parallel symptoms of depression in humans.

show abstract

Section: Discussionmentioning

confidence: 52%

Chronic stress impairs spatial memory and motivation for reward without disrupting motor ability and motivation to explore.

Kleen

Sitomer

Killeen

et al. 2006

Behavioral Neuroscience

149

112

View full text Add to dashboard Cite

show abstract

“…We acknowledge that the modest changes in mRNA levels observed in our study do leave open the question of whether the changes in Bcl-2 family genes mRNA are essential and/ or sufficient for opposing behavioral changes caused by RUS and antidepressants. We understand that the juxtaposition of RUS and antidepressants in this study is based on the underlying assumption that RUS is, at least in part, a valid animal model of depression (Henn and Vollmayr, 2005). Our data suggest that there may be a relationship between stress and ADT through their opposing effects on the apoptotic gene expression.…”

Section: Discussionmentioning

confidence: 86%

Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Kosten

Galloway

Duman

et al. 2007

Neuropsychopharmacol

147

View full text Add to dashboard Cite

Apoptosis has been proposed as a contributing cellular mechanism to the structural alterations that have been observed in stress-related mood disorders. Antidepressants, on the other hand, are hypothesized to exert trophic and/or neuroprotective actions. The present study examined the regulation of the major antiapoptotic (Bcl-2, Bcl-xl) and proapoptotic (Bax) genes by repeated unpredictable stress (an animal model of depression) and antidepressant treatments (ADT). In adult rats, exposure to unpredictable stress reduced Bcl-2 mRNA levels in the central nucleus of the amygdala (CeA), cingulate (Cg), and frontal (Fr) cortices. Bcl-xl mRNA was significantly decreased in hippocampal subfields. In contrast, chronic administration of clinically effective antidepressants from four different classes, ie fluoxetine, reboxetine, tranylcypromine, and electroconvulsive seizures (ECS) upregulated Bcl-2 mRNA expression in the Cg, Fr, and CeA. Reboxetine, tranylcypromine, and ECS selectively increased Bcl-xl, but not Bcl-2 mRNA expression in the hippocampus. Chemical ADT but not ECS, robustly enhanced Bcl-2 expression in the medial amygdaloid nucleus and ventromedial hypothalamus. Fluoxetine did not influence Bcl-xl expression in the hippocampus, but it was the only ADT that decreased Bax expression in this region. In the CeA, again in direct contrast to the stress effects, exposure to all classes of ADTs significantly increased Bcl-2 mRNA. The selective regulation of Bcl-xl and Bax in hippocampal subfields and of Bcl-2 in the Cg cortex, amygdala, and hypothalamus suggests that these cellular adaptations contribute to the long-term neural plastic adaptations to stress and ADTs in cortical, hypothalamic, and limbic brain structures.

show abstract

“…[46][47][48] In this model, the HPA axis is undisturbed under basal conditions, which does not apply to the cases of stress models accomplished from selectively bred or genetically vulnerable strains. 49 Also patients who are recovered from depression but still carry vulnerability to further disease episodes have near normal HPA axis activity though symptom-free. 26 On the other hand, central CRH hypersecretion is not necessarily reflected by the peripheral stress hormone excess, as clinical response to CRHR1 antagonists in depression is not straightforwardly predicted by the peripheral stress hormone assessments.…”

Section: Discussionmentioning

confidence: 99%

Conditional corticotropin-releasing hormone overexpression in the mouse forebrain enhances rapid eye movement sleep

Kimura

Müller-Preuß

et al. 2009

Mol Psychiatry

View full text Add to dashboard Cite

Impaired sleep and enhanced stress hormone secretion are the hallmarks of stress-related disorders, including major depression. The central neuropeptide, corticotropin-releasing hormone (CRH), is a key hormone that regulates humoral and behavioral adaptation to stress. Its prolonged hypersecretion is believed to play a key role in the development and course of depressive symptoms, and is associated with sleep impairment. To investigate the specific effects of central CRH overexpression on sleep, we used conditional mouse mutants that overexpress CRH in the entire central nervous system (CRH-COE-Nes) or only in the forebrain, including limbic structures (CRH-COE-Cam). Compared with wild-type or control mice during baseline, both homozygous CRH-COE-Nes and -Cam mice showed constantly increased rapid eye movement (REM) sleep, whereas slightly suppressed non-REM sleep was detected only in CRH-COE-Nes mice during the light period. In response to 6-h sleep deprivation, elevated levels of REM sleep also became evident in heterozygous CRH-COE-Nes and -Cam mice during recovery, which was reversed by treatment with a CRH receptor type 1 (CRHR1) antagonist in heterozygous and homozygous CRH-COE-Nes mice. The peripheral stress hormone levels were not elevated at baseline, and even after sleep deprivation they were indistinguishable across genotypes. As the stress axis was not altered, sleep changes, in particular enhanced REM sleep, occurring in these models are most likely induced by the forebrain CRH through the activation of CRHR1. CRH hypersecretion in the forebrain seems to drive REM sleep, supporting the notion that enhanced REM sleep may serve as biomarker for clinical conditions associated with enhanced CRH secretion.

show abstract

Stress models of depression: Forming genetically vulnerable strains

Cited by 246 publications

References 48 publications

Chronic stress impairs spatial memory and motivation for reward without disrupting motor ability and motivation to explore.

Chronic stress impairs spatial memory and motivation for reward without disrupting motor ability and motivation to explore.

Repeated Unpredictable Stress and Antidepressants Differentially Regulate Expression of the Bcl-2 Family of Apoptotic Genes in Rat Cortical, Hippocampal, and Limbic Brain Structures

Conditional corticotropin-releasing hormone overexpression in the mouse forebrain enhances rapid eye movement sleep

Contact Info

Product

Resources

About