Impact of water temperature and stressor controllability on swim stress-induced changes in body temperature, serum corticosterone, and immobility in rats

Drugan, Robert C.; Eren, Senem; Hazi, Agnes; Silva, Jennifer; Christianson, John P.; Kent, Stephen

doi:10.1016/j.pbb.2005.09.011

Cited by 48 publications

(36 citation statements)

References 18 publications

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“…It is possible that only prolonged imipramine treatment could have a significant effect on serum corticosterone levels, which is in accordance with clinical research, showing an effect just after prolonged treatment [36]. In Sprague-Dawley rats, the animals receiving chronic imipramine treatment had significantly less resting ACTH and corticosterone levels than the saline a significant elevation in stress hormone levels [20,21]. Based on our assumption, that floating or immobility reflects a state of "depressiveness" [14], and depression is accompanied by hyperactive HPA axis [22], one would expect that rats floating more have an increased ACTH/corticosterone response.…”

Section: Discussionsupporting

confidence: 55%

Do stress hormones connect environmental effects with behavior in the forced swim test?

et al. 2011

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Section: Discussionsupporting

confidence: 55%

Do stress hormones connect environmental effects with behavior in the forced swim test?

et al. 2011

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“…Most studies using animal models of depression measure signs of helplessness that are caused by exposure to an unnatural stressor such as forced walking (6, 7) or forced SWIM (16). A more authentic animal model would be based on spontaneous despair behavior; we measured this in our study by using a modified FST without the stressors that could contribute to an escape deficit (16).…”

Section: Discussionmentioning

confidence: 99%

“…A more authentic animal model would be based on spontaneous despair behavior; we measured this in our study by using a modified FST without the stressors that could contribute to an escape deficit (16). We modified the usual FST by filling the tank with warm water, habituating rats to handling, and providing the rats with a flotation aid.…”

Section: Discussionmentioning

confidence: 99%

Light deprivation damages monoamine neurons and produces a depressive behavioral phenotype in rats

González

Aston‐Jones

2008

Proc. Natl. Acad. Sci. U.S.A.

170

132

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Light is an important environmental factor for regulation of mood. There is a high frequency of seasonal affective disorder in high latitudes where light exposure is limited, and bright light therapy is a successful antidepressant treatment. We recently showed that rats kept for 6 weeks in constant darkness (DD) have anatomical and behavioral features similar to depressed patients, including dysregulation of circadian sleep-waking rhythms and impairment of the noradrenergic (NA)-locus coeruleus (LC) system. Here, we analyzed the cell viability of neural systems related to the pathophysiology of depression after DD, including NA-LC, serotoninergic-raphe nuclei and dopaminergicventral tegmental area neurons, and evaluated the depressive behavioral profile of light-deprived rats. We found increased apoptosis in the three aminergic systems analyzed when compared with animals maintained for 6 weeks in 12:12 light-dark conditions. The most apoptosis was observed in NA-LC neurons, associated with a significant decrease in the number of cortical NA boutons. Behaviorally, DD induced a depression-like condition as measured by increased immobility in a forced swim test (FST). DD did not appear to be stressful (no effect on adrenal or body weights) but may have sensitized responses to subsequent stressors (increased fecal number during the FST). We also found that the antidepressant desipramine decreases these neural and behavioral effects of light deprivation. These findings indicate that DD induces neural damage in monoamine brain systems and this damage is associated with a depressive behavioral phenotype. Our results suggest a mechanism whereby prolonged limited light intensity could negatively impact mood.epression is associated with decreased function in the noradrenergic (NA) locus coeruleus (LC), serotoninergic (5-HT) dorsal raphe (DR) and median raphe (MnR), and dopaminergic (DA) ventral tegmental area (VTA) systems (1-4). Behaviorally, depression is characterized by lethargy, feelings of helplessness, and profound alterations of sleep-wake rhythms (5). In at least some cases, depression is associated with decreased light availability (e.g., seasonal affective disorder) and a blunted amplitude and phase delay of circadian rhythms (5). Also, degeneration of NA fibers from LC has been associated with stress-induced depression in rats (6, 7). Recently, we showed that, as compared with animals on a 12:12 light-dark (LD) schedule, rats kept for 6 weeks in constant darkness (DD) exhibit decreased NA-LC fibers and boutons in the frontal cortex, a delayed onset of active/rest periods, and a decreased circadian amplitude of the sleep-waking rhythm (8). These results raise the possibility that the absence of light could contribute to depression, perhaps in part through effects on monoamine systems. Here, we evaluated the integrity of brain NA, 5-HT, and DA neurons, and depressive behavioral profiles, of animals kept in long-term DD to test the hypothesis that decreased function in one or more of these neural systems promotes...

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“…Furthermore, for aged animals, LTD did not correlate with the amount of time in the pool, a measure of the exposure to swim stress. Finally, it might be assumed that animals which fail to acquire a spatial discrimination may exhibit increased stress due to a perceived lack of control of the stressor (Drugan et al 2005). In the current study, animals that failed to learn were removed from consideration.…”

Section: Ltd and Memorymentioning

confidence: 99%

Susceptibility to induction of long-term depression is associated with impaired memory in aged Fischer 344 rats

Foster

Kumar

2007

Neurobiology of Learning and Memory

107

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The current study employed aged and young male Fischer 344 rats to examine the relationship between long-term depression (LTD), age, and memory. Memory performance was measured on two tasks that are sensitive to hippocampal function; inhibitory avoidance and spatial discrimination on the Morris water maze. The slope of the extracellular excitatory postsynaptic field potential was recorded from CA3-CA1 synapses in hippocampal slices. Low frequency stimulation (LFS) induced a modest LTD only in aged animals under standard recording conditions. The decrease in synaptic transmission examined only in aged animals correlated with memory scores on the spatial task and LTD was not observed in aged animals with the highest memory scores. LTD induction was facilitated by increasing the Ca 2+ /Mg 2+ ratio of the recording medium or employing a paired-pulse stimulation paradigm. Age differences disappeared when LFS was delivered under conditions of elevated Ca 2+ /Mg 2+ in the recording medium. Using multiple induction episodes under conditions which facilitate LTD-induction, no age-related difference was observed in the maximum level of LTD. The results indicate that the increased susceptibility to LTD induction is associated with impaired memory and results from a shift in the induction process. The possible relationship between LTD and memory function is discussed.

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Impact of water temperature and stressor controllability on swim stress-induced changes in body temperature, serum corticosterone, and immobility in rats

Cited by 48 publications

References 18 publications

Do stress hormones connect environmental effects with behavior in the forced swim test?

Do stress hormones connect environmental effects with behavior in the forced swim test?

Light deprivation damages monoamine neurons and produces a depressive behavioral phenotype in rats

Susceptibility to induction of long-term depression is associated with impaired memory in aged Fischer 344 rats

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