Association of N‐cadherin levels and downstream effectors of Rho GTPases with dendritic spine loss induced by chronic stress in rat hippocampal neurons

Castañeda, Patricia; Muñoz, Mauricio; García-Rojo, Gonzalo; Ulloa, José Luis; Bravo, Javier A.; Márquez, Ruth; García-Pérez, María A.; Arancibia, Damaris; Araneda, Karina; Rojas, Paulina S.; Mondaca‐Ruff, David; Dı́az-Véliz, Gabriela; Mora, Sergio; Aliaga, Esteban; Fiedler, Jenny L.

doi:10.1002/jnr.23635

Cited by 12 publications

(16 citation statements)

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“…Cofilin is a crucial regulator of actin dynamics and has important roles in dendritic spine remodeling, synaptic plasticity, and ultimately behavior (Rust, 2015). Cofilin has been implicated in the pathogenesis of neurodegenerative diseases (Garvalov et al, 2007;Minamide et al, 2000), the formation and maintenance of memories (Kramar et al, 2013;Wang et al, 2013), and stress-induced spine loss (Castaneda et al, 2015). Cofilin activity is regulated by phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

EphB2 in the Medial Prefrontal Cortex Regulates Vulnerability to Stress

Zhang

Han

Chen

et al. 2016

Neuropsychopharmacol

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The ephrin B2 (EphB2) receptor is a tyrosine kinase receptor that is associated with synaptic development and maturation. It has recently been implicated in cognitive deficits and anxiety. However, still unknown is the involvement of EphB2 in the vulnerability to stress. In the present study, we observed decreases in EphB2 levels and their downstream molecules in the medial prefrontal cortex (mPFC) but not in the orbitofrontal cortex (OFC) in mice that were susceptible to chronic social defeat stress. The activation of EphB2 receptors with EphrinB1-Fc in the mPFC produced stress-resistant and antidepressant-like behavioral effects in susceptible mice that lasted for at least 10 days. EphB2 receptor knockdown by short-hairpin RNA in the mPFC increased the susceptibility to stress and induced depressive-like behaviors in a subthreshold chronic social defeat stress paradigm. These behavioral effects were associated with changes in the phosphorylation of cofilin and membrane α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) trafficking and the expression of some synaptic proteins in the mPFC. We also found that EphB2 regulated stress-induced spine remodeling in the mPFC. Altogether, these results indicate that EphB2 is a critical regulator of stress vulnerability and might be a potential target for the treatment of depression.

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Section: Discussionmentioning

confidence: 99%

EphB2 in the Medial Prefrontal Cortex Regulates Vulnerability to Stress

Zhang

Han

Chen

et al. 2016

Neuropsychopharmacol

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“…The formation, growth, and elimination of the dendritic spines are precisely controlled, which requires the reorganization of the neural network in response to acute stress or learning processes. These processes are commonly dysregulated or disrupted in chronically stressed animals [ 46 , 79 ]. Therefore, understanding dendritic spines is fundamental in uncovering the mechanisms underlying depression.…”

Section: The Plasticity Of Dendritic Spinesmentioning

confidence: 99%

“…These increases and decreases in spine density are dependent on NMDA receptor activation [ 35 ]. Similar to acute stress, the same CRS regimen causes a decrease in spine density in the apical dendrites of hippocampal CA1 pyramidal neurons in male rat and male mouse [ 40 , 43 , 46 , 48 ] but causes an increase in spine density in the same region in female rats [ 37 , 38 , 42 ]. One recent study shows that CRS decreases spine density in basal dendrites, while it increases apical dendritic arbors in the CA1 pyramidal neurons of the ventral hippocampus in female but not in male rats [ 47 ].…”

Section: The Effects Of Chronic Stress On Dendritic Spines In Diffmentioning

confidence: 99%

Dendritic Spines in Depression: What We Learned from Animal Models

et al. 2016

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Depression, a severe psychiatric disorder, has been studied for decades, but the underlying mechanisms still remain largely unknown. Depression is closely associated with alterations in dendritic spine morphology and spine density. Therefore, understanding dendritic spines is vital for uncovering the mechanisms underlying depression. Several chronic stress models, including chronic restraint stress (CRS), chronic unpredictable mild stress (CUMS), and chronic social defeat stress (CSDS), have been used to recapitulate depression-like behaviors in rodents and study the underlying mechanisms. In comparison with CRS, CUMS overcomes the stress habituation and has been widely used to model depression-like behaviors. CSDS is one of the most frequently used models for depression, but it is limited to the study of male mice. Generally, chronic stress causes dendritic atrophy and spine loss in the neurons of the hippocampus and prefrontal cortex. Meanwhile, neurons of the amygdala and nucleus accumbens exhibit an increase in spine density. These alterations induced by chronic stress are often accompanied by depression-like behaviors. However, the underlying mechanisms are poorly understood. This review summarizes our current understanding of the chronic stress-induced remodeling of dendritic spines in the hippocampus, prefrontal cortex, orbitofrontal cortex, amygdala, and nucleus accumbens and also discusses the putative underlying mechanisms.

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“…Formation, growth, and elimination of dendritic spines are under a precise control, requiring reorganization of the neural network in response to acute stress or learning processes. These processes are frequently dysregulated or disrupted in chronically stressed animals [82,83]. Therefore, understanding dendritic spines is fundamental in uncovering the mechanisms underlying depression and also anti-depressant activities.…”

Section: Sex Differences In the Anti-depressant Activity Of Ketaminementioning

confidence: 99%

Sex Differences in the Antidepressant Effects of Ketamine in Animal Models of Depression

Adu-Nti¹,

Ghartey‐Kwansah²,

Aboagye³

2019

Int J Depress Anxiety

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Major depressive disorder (MDD) is the most common psychiatric disease and it affects millions of people across the world. Patients suffering from MDD consistently complain about cognitive disturbances, significantly worsening the burden of this illness. The second most frequent mental illness in Europe is mood disorders and they are dominated by MDD, a-ecting 7% of the population. The recent discovery that the N-methyl-D-aspartate receptor (NMDAR) antagonist; ketamine; a revolutionary novel antidepressant, rapidly relieves depressive symptoms and suicidal imaginations, particularly amongst those with treatment-resistant depression have generated a new wave of excitement. This article discusses the sex differences that exist in depressive patients, summarizes the antidepressant activity of ketamine and reviews the mechanisms underlying the rapid antidepressant effects of ketamine. It further discusses the sexual differences in the antidepressant activity of ketamine in preclinical studies.

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Association of N‐cadherin levels and downstream effectors of Rho GTPases with dendritic spine loss induced by chronic stress in rat hippocampal neurons

Cited by 12 publications

References 0 publications

EphB2 in the Medial Prefrontal Cortex Regulates Vulnerability to Stress

EphB2 in the Medial Prefrontal Cortex Regulates Vulnerability to Stress

Dendritic Spines in Depression: What We Learned from Animal Models

Sex Differences in the Antidepressant Effects of Ketamine in Animal Models of Depression

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