Curcumin reverses the effects of chronic stress on behavior, the HPA axis, BDNF expression and phosphorylation of CREB

Xu, Ying; Ku, Bao-Shan; Tie, Lu; Yao, Heng‐Chen; Jiang, Wen; Ma, Xiaojing; Li, Xuejun

doi:10.1016/j.brainres.2006.09.009

Cited by 272 publications

(146 citation statements)

References 40 publications

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“…In this experiment, in contrast to the experimental design used in the study by Vecsey et al (2009), animals were sleep deprived for 72 h by multiple platform method and then trained in the fearconditioning task. This extensive sleep-deprivation procedure along with fear conditioning may elevate stress, which has been shown to affect phosphorylation of CREB to a greater extent than gentle handling alone (Xu et al 2006).…”

Section: Camp-pka-pde4mentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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Section: Camp-pka-pde4mentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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“…More specifically, curcumin is a potent antioxidant that can lower markers of oxidative stress (Naik et al, 2011, Rai et al, 2010, modulate immuno-inflammation by acting as a COX-2 inhibitor (Lee et al, 2011, Plummer et al, 1999 and lower pro-inflammatory cytokines (Basnet andSkalko-Basnet, 2011, Belcaro et al, 2010), provide significant neuroprotection , Xu et al, 2007, modulate HPA activity , Li et al, 2009) and influence monoamine transmission through its effect on serotonergic and dopaminergic activity (Bhutani et al, 2009, Kulkarni et al, 2008, Xia et al, 2007. In animal studies, antidepressant effects of curcumin have been attributed to its serotonergic, dopaminergic, neuroprotective and HPA-modulating effects , Kulkarni et al, 2008, Xu et al, 2006. Two clinical trials have also now been completed investigating the antidepressant effects of curcumin in people with major depression.…”

Section: Introductionmentioning

confidence: 99%

Curcumin for the treatment of major depression: A randomised, double-blind, placebo controlled study

Lopresti

Maes

Maker

et al. 2014

Journal of Affective Disorders

172

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“…TREK-1 K + channels are widely distributed throughout the brain where deletion of TREK-1 in knockout mice produces a depression-resistant phenotype, suggesting that TREK-1 antagonists might display antidepressant actions [30,31]. Accordingly, antidepressant effects of curcumin have been reported in rats [32,33].…”

Section: Discussionmentioning

confidence: 99%

Curcumin inhibits bTREK-1 K+ channels and stimulates cortisol secretion from adrenocortical cells

Enyeart

Liu

Enyeart

2008

Biochemical and Biophysical Research Communications

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Bovine adrenal zona fasciculata (AZF) cells express bTREK-1 K + channels that set the resting membrane potential. Inhibition of these channels by adrenocorticotropic hormone (ACTH) is coupled to membrane depolarization and cortisol secretion. Curcumin, a phytochemical with medicinal properties extracted from the spice turmeric, was found to modulate both bTREK-1 K + currents and cortisol secretion from AZF cells. In whole-cell patch clamp experiments, curcumin inhibited bTREK-1 with an IC 50 of 0.93μM by a mechanism that was voltage-independent. bTREK-1 inhibition by curcumin occurred through interaction with an external binding site and was independent of ATP hydrolysis. Curcumin produced a concentration-dependent increase in cortisol secretion that persisted for up to 24 h. At a maximally effective concentration of 50 μM, curcumin increased secretion as much as10-fold. These results demonstrate that curcumin potently inhibits bTREK-1 K + channels and stimulates cortisol secretion from bovine AZF cells. The inhibition of bTREK-1 by curcumin may be linked to cortisol secretion through membrane depolarization. Since TREK-1 is widely expressed in a variety of cells, it is likely that some of the biological actions of curcumin, including its therapeutic effects, may be mediated through inhibition of these K + channels.

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Curcumin reverses the effects of chronic stress on behavior, the HPA axis, BDNF expression and phosphorylation of CREB

Cited by 272 publications

References 40 publications

The impact of sleep loss on hippocampal function

The impact of sleep loss on hippocampal function

Curcumin for the treatment of major depression: A randomised, double-blind, placebo controlled study

Curcumin inhibits bTREK-1 K+ channels and stimulates cortisol secretion from adrenocortical cells

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