Impairment of the spatial learning and memory induced by learned helplessness and chronic mild stress

Li, Song; Che, Wang; Wang, Minwei; Murakami, Yukihisa; Matsumoto, Kinzo

doi:10.1016/j.pbb.2006.01.004

Cited by 292 publications

(211 citation statements)

References 52 publications

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“…The present observation finds support from previous report on duration dependent increase in hippocampal neurodegeneration following exposure to HH for 7 days with gradual decreases on prolonged exposure for 21 days [41]. Increase in proinflammatory cytokines and decreased neurotrophic factors level in brain also affect the anxiety-like behaviors in rats [42]. Neurotransmitters like serotonin, nor-epinephrine and stress hormone corticosterone undergoes a duration dependent alteration in brain on exposure to various stressors and play an important role in anxiety and depression like behaviors in rats [43].…”

supporting

confidence: 92%

Exposure to Hypobaric Hypoxia and Reoxygenation Induces Transient Anxiety-Like Behavior in Rat

Baitharu¹,

Jain²,

Deep³

et al. 2013

JBBS

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Chronic exposure to hypobaric hypoxia (HH) causes memory impairment and prolonged state of mental confusion. However, effect of high altitude exposure on mood state and its underlying mechanisms have been poorly studied. Present study was undertaken to investigate the mood state alteration following chronic exposure to HH. Male Sprague Dawley rats were divided into five groups and exposed to hypoxia for 3, 7, 14 and 21 days in an animal decompression chamber at an altitude of 25,000ft. Anxiety-and depression-like behaviors were assessed by using various mazes along with changes in serotonin and glutamate level. Our study revealed a decrease in exploratory, grooming and rearing behavior in open field test following initial exposure to HH for 7 days without affecting the locomotory behavior. Initial exposure to HH-decreased time spent in open arm of elevated plus maze indicating induction of anxiety-like behavior which normalized on prolonged hypoxic exposure for 21 days. Hypoxic exposure for 7 days induced anhedonia and increased despair behavior in rat while there was steady improvement in these behaviors when exposed for 21 days. Decrease in serotonin level was noted in hippocampus along with elevated corticosterone and glutamate level which gradually decreased on prolonged exposure to HH. These findings suggest that initial exposure to HH increases transient anxiety-like behavior in rats followed by gradual improvement in mood state on prolonged exposure. Further, the study also indicates the involvement of serotonergic system in mood state alteration at high altitude following chronic exposure and reoxygenation.

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supporting

confidence: 92%

Exposure to Hypobaric Hypoxia and Reoxygenation Induces Transient Anxiety-Like Behavior in Rat

Baitharu¹,

Jain²,

Deep³

et al. 2013

JBBS

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“…Antidepressant treatment has been shown to block many of the hippocampal sequelae of chronic stress (25)(26)(27)(55)(56)(57), and therefore, we sought to determine if fluoxetine had a similar effect on histone H3 methylation. Chronic treatment with fluoxetine during CRS did produce elevated levels of K9 methylation.…”

Section: Discussionmentioning

confidence: 99%

“…In animal models, chronic stress reduces hippocampal neurogenesis (20) and the complexity of dendritic arbors (21)(22)(23) as well as impairing function in assays of hippocampal dependent spatial memory and LTP (19,24). Many of these changes can be blocked pharmacologically with anti-depressant drugs such as fluoxetine (25)(26)(27)(28).…”

mentioning

confidence: 99%

Regulation of hippocampal H3 histone methylation by acute and chronic stress

Hunter

McCarthy²,

Milne³

et al. 2009

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

261

190

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The hippocampal formation is a brain region noted for its plasticity in response to stressful events and adrenal steroid hormones. Recent work has shown that chromatin remodeling in various brain regions, including the hippocampus, is associated with the effects of stress in a variety of models. We chose to examine the effects of stress, stress duration, corticosterone administration, and fluoxetine treatment on the levels of hippocampal histone H3 methylation at lysines 4, 9, and 27, marks associated, respectively, with active transcription, heterochromatin formation, and transcriptional repression. We found that acute stress increased the levels of H3K9 tri-methylation (H3K9me3) in the dentate gyrus (DG) and CA1, while it reduced levels of H3K9 mono-methylation (H3K9me1) and H3K27 tri-methylation (H3K27me3) in the same regions, and had no effect on levels of H3K4 tri-methylation (H3K4me3). Seven days of restraint stress reduced levels of H3K4me3 in the CA1 and H3K27me3 in the DG and CA1, while increasing basal levels of H3K9me3. Chronic restraint stress (CRS) for 21 days mildly increased levels of H3K4me3 and reduced H3K9me3 levels in the DG. Treatment with fluoxetine during CRS reversed the decrease in DG H3K9me3, but had no effect on the other marks. These results show a complex, surprisingly rapid, and regionally specific pattern of chromatin remodeling within hippocampus produced by stress and anti-depressant treatment that may open an avenue of understanding the interplay of stress and hippocampal gene expression, and reveal the outlines of a potential chromatin stress response that may be diminished or degraded by chronic stress.brain ͉ chromatin ͉ corticosteroids ͉ fluoxetine

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“…However, several studies both in vivo and in vitro implicate the transcription factor cyclic AMP response element-binding protein (CREB) in contributing to the regulation of BDNF expression (Barco et al, 2005;Conti et al, 2002). In addition, specific stressors in adult life have been reported to regulate hippocampal CREB expression (Alfonso et al, 2006;Song et al, 2006) and a decline in CREB expression has been observed in depressed patients (Blendy, 2006;Lai et al, 2003;Yamada et al, 2003). Besides its role in the regulation of BDNF, CREB has been shown to influence both structural and synaptic plasticity in the hippocampus (Josselyn and Nguyen, 2005;Nakagawa et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Stressor-Specific Regulation of Distinct Brain-Derived Neurotrophic Factor Transcripts and Cyclic AMP Response Element-Binding Protein Expression in the Postnatal and Adult Rat Hippocampus

Nair

Vadodaria

Banerjee

et al. 2006

Neuropsychopharmacol

171

120

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Stress regulation of brain-derived neurotrophic factor (BDNF) is implicated in the hippocampal damage observed in depression. BDNF has a complex gene structure with four 5 0 untranslated exons (I-IV) with unique promoters, and a common 3 0 coding exon (V). To better understand the stress regulation of BDNF, we addressed whether distinct stressors differentially regulate exon-specific BDNF transcripts in the postnatal and adult hippocampus. The early life stress of maternal separation (MS) resulted in a time point-dependent differential upregulation of BDNF transcripts restricted to early postnatal life (P14-BDNF II, P21-BDNF IV, V). In adulthood, distinct stressors regulated BDNF transcripts in a signature manner. Immobilization stress, administered once, decreased all BDNF splice variants but had differing effects on BDNF I/II (increase) and III/IV (decrease) when administered chronically. Although immobilization stress reduced BDNF (V) mRNA, chronic unpredictable stress did not influence total BDNF despite altering specific BDNF transcripts. Furthermore, a prior history of MS altered the signature pattern in which adult-onset stress regulated specific BDNF transcripts. We also examined the expression of cyclic AMP response element-binding protein (CREB), an upstream transcriptional activator of BDNF, and observed a CREB induction in the postnatal hippocampus following MS. As a possible consequence of enhanced CREB and BDNF expression following MS, we examined hippocampal progenitor proliferation and observed a significant increase restricted to early life. These results suggest that alterations in CREB/BDNF may contribute to the generation of individual differences in stress neurocircuitry, providing a substrate for altered vulnerability to depressive disorders.

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Impairment of the spatial learning and memory induced by learned helplessness and chronic mild stress

Cited by 292 publications

References 52 publications

Exposure to Hypobaric Hypoxia and Reoxygenation Induces Transient Anxiety-Like Behavior in Rat

Exposure to Hypobaric Hypoxia and Reoxygenation Induces Transient Anxiety-Like Behavior in Rat

Regulation of hippocampal H3 histone methylation by acute and chronic stress

Stressor-Specific Regulation of Distinct Brain-Derived Neurotrophic Factor Transcripts and Cyclic AMP Response Element-Binding Protein Expression in the Postnatal and Adult Rat Hippocampus

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