Systematic correlation between spine plasticity and the anxiety/depression-like phenotype induced by corticosterone in mice

Wang, Guohua; Cheng, Yufang; Gong, Mei-Fang; Liang, Bishan; Zhang, Mingzi; Chen, Yu‐Pin; Zhang, Cong; Yuan, Xin

doi:10.1097/wnr.0b013e32836384db

Cited by 38 publications

(33 citation statements)

References 16 publications

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“…Interestingly, corticosterone can cause synaptic degeneration and exert toxic effects on hippocampal neurons, and finally induces depression [14]. It is also well-known that corticosterone exposure induces a decrease in dendritic spine density in hippocampus, which might be one of the pathophysiological mechanisms underlying depression progression [15]. These studies have confirmed that corticosterone is closely related to depression.…”

Section: Introductionmentioning

confidence: 69%

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H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Gao

Zou

et al. 2015

ABBS

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Corticosterone, one of the glucocorticoids, is toxic to neurons and plays an important role in depressive-like behavior and depression. We previously showed that hydrogen sulfide (H 2 S), a novel physiological mediator, plays an inhibitory role in depression. However, the mechanism underlying H 2 S-triggered antidepressant-like role is not clearly known. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, plays a neuroprotective role that is mediated by its high-affinity tropomysin-related kinase B (TrkB) receptor. In this study, to investigate the underlying mechanism of H 2 S-induced antidepressant-like role, we explored whether H 2 S could protect neurons against corticosterone-mediated cyctotoxicity and whether this protective role of H 2 S was involved in the regulation of BDNF-TrkB pathway. Our data demonstrated that sodium hydrosulfide (NaHS), the donor of H 2 S, could prevent corticosterone-induced cytotoxicity, apoptosis, accumulation of intracellular reactive oxygen species (ROS) and loss of mitochondrial membrane potential (MMP) in PC12 cells. NaHS not only induced the up-regulation of BDNF but also prevented the down-regulation of BDNF by corticosterone. It was also found that blocking BDNF-TrkB pathway by K252a, an inhibitor of TrkB, abolished the protection of H 2 S against corticosterone-induced cytotoxicity, apoptosis, accumulation of ROS, and loss of MMP. These results suggest that H 2 S protects against the neurotoxicity of corticosterone by modulation of the BDNF-TrkB pathway.

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Section: Introductionmentioning

confidence: 69%

“…Taken together, our data demonstrated the protective role of H 2 S against the neurotoxicity of corticosterone. It was reported that the neurotoxicity of corticosterone plays an important role in the development of depression [14,15]. In addition, our recent studies have shown that H 2 S has antidepressant-like effect [25,26].…”

Section: Discussionmentioning

confidence: 93%

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Gao

Zou

et al. 2015

ABBS

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“…Decreased spine densities in CA1 neurons has been associated with depression-like behaviors in a light-induced depression model, in the absence of spine changes in CA3 or dendritic changes in CA3 or CA1 [4]. Chronic corticosterone administration, which results in a depressive phenotype, reduces spine density in CA1 and both the spine and behavioral deficits recover with chronic fluoxetine administration [35, 116]. These changes occurred mainly in thin and stubby spines [116].…”

Section: Chronic Stress Alters the Number And Function Of Spine Synapsesmentioning

confidence: 99%

“…Chronic corticosterone administration, which results in a depressive phenotype, reduces spine density in CA1 and both the spine and behavioral deficits recover with chronic fluoxetine administration [35, 116]. These changes occurred mainly in thin and stubby spines [116]. Given the differential incidence of depression in women it is notable that spine morphologic changes in response to CRS are opposite in male and female rats [103].…”

Section: Chronic Stress Alters the Number And Function Of Spine Synapsesmentioning

confidence: 99%

Spine synapse remodeling in the pathophysiology and treatment of depression

Duman

2015

Neuroscience Letters

226

184

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Clinical brain imaging and postmortem studies provide evidence of structural and functional abnormalities of key limbic and cortical structures in depressed patients, suggesting that spine synapse connectivity is altered in depression. Characterization of the cellular determinants underlying these changes in patients are limited, but studies in rodent models demonstrate alterations of dendrite complexity and spine density and function that could contribute to the morphological and functional alterations observed in humans. Rodent studies demonstrate region specific effects in chronic stress models of depression, including reductions in dendrite complexity and spine density in the hippocampus and prefrontal cortex (PFC) but increases in the basolateral amygdala and nucleus accumbens. Alterations of spine synapse connectivity in these regions are thought to contribute to the behavioral symptoms of depression, including disruption of cognition, mood, emotion, motivation, and reward. Studies of the mechanisms underlying these effects demonstrate a role for altered brain derived neurotrophic factor (BDNF) signaling that regulates synaptic protein synthesis. In contrast, there is evidence that chronic antidepressant treatment can block or reverse the spine synapse alterations caused by stress. Notably, the new fast acting antidepressant ketamine, which produces rapid therapeutic actions in treatment resistant MDD patients, rapidly increases spine synapse number in the PFC of rodents and reverses the effects of chronic stress. The rapid synaptic and behavioral actions of ketamine occur via increased BDNF regulation of synaptic protein synthesis. Together these studies provide evidence for a neurotophic and synaptogenic hypothesis of depression and treatment response and indicate that spine synapse connectivity in key cortical and limbic brain regions is critical for control of mood and emotion.

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“…Changes in spine density in CA1 have been reported to be correlated with stress exposure (Shors et al, 2001; Pawlak et al, 2005; Donohue et al, 2006), learning and memory (Moser et al, 1994, 1997), and anti-depressant effects (Wang et al, 2013) in rodents. Moreover, given that activity-regulated genes are implied to contribute to plasticity (Leslie and Nedivi, 2011), and the recent suggestions that NgRs are regulated by various forms of activity stimuli (Guo et al, 2013; Karlsson et al, 2013), we next examined whether the alterations in spine distribution seen in NgR2 −/− mice may also affect behavioral tasks in the adult, such as learning and memory.…”

Section: Resultsmentioning

confidence: 99%

Loss of Nogo receptor homolog NgR2 alters spine morphology of CA1 neurons and emotionality in adult mice

Borrie

Sartori

Lehmann

et al. 2014

Front. Behav. Neurosci.

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Molecular mechanisms which stabilize dendrites and dendritic spines are essential for regulation of neuronal plasticity in development and adulthood. The class of Nogo receptor proteins, which are critical for restricting neurite outgrowth inhibition signaling, have been shown to have roles in developmental, experience and activity induced plasticity. Here we investigated the role of the Nogo receptor homolog NgR2 in structural plasticity in a transgenic null mutant for NgR2. Using Golgi-Cox staining to analyze morphology, we show that loss of NgR2 alters spine morphology in adult CA1 pyramidal neurons of the hippocampus, significantly increasing mushroom-type spines, without altering dendritic tree complexity. Furthermore, this shift is specific to apical dendrites in distal CA1 stratum radiatum (SR). Behavioral alterations in NgR2−/− mice were investigated using a battery of standardized tests and showed that whilst there were no alterations in learning and memory in NgR2−/− mice compared to littermate controls, NgR2−/− displayed reduced fear expression in the contextual conditioned fear test, and exhibited reduced anxiety- and depression-related behaviors. This suggests that the loss of NgR2 results in a specific phenotype of reduced emotionality. We conclude that NgR2 has role in maintenance of mature spines and may also regulate fear and anxiety-like behaviors.

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Systematic correlation between spine plasticity and the anxiety/depression-like phenotype induced by corticosterone in mice

Cited by 38 publications

References 16 publications

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Spine synapse remodeling in the pathophysiology and treatment of depression

Loss of Nogo receptor homolog NgR2 alters spine morphology of CA1 neurons and emotionality in adult mice

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Systematic correlation between spine plasticity and the anxiety/depression-like phenotype induced by corticosterone in mice

Cited by 38 publications

References 16 publications

H&lt;sub&gt;2&lt;/sub&gt;S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H&lt;sub&gt;2&lt;/sub&gt;S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Spine synapse remodeling in the pathophysiology and treatment of depression

Loss of Nogo receptor homolog NgR2 alters spine morphology of CA1 neurons and emotionality in adult mice

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H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway