Correlations between working memory impairment and neurometabolites of prefrontal cortex and lenticular nucleus in patients with major depressive disorder

Shan, Yanyan; Jia, Yanbin; Zhong, Shuming; Li, Xueguo; Zhao, Hui; Chen, Junhao; Lu, Qianyi; Zhang, Lu; Li, Zhinan; Lai, Shunkai; Wang, Ying

doi:10.1016/j.jad.2017.10.030

Cited by 27 publications

(6 citation statements)

References 51 publications

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“…Ketamine administration is accepted as a rapid and persistent antidepressant treatment for MDD 22 , 30 , 31 . MDD is associated with altered neuronal and structural plasticity and neurogenesis in brain regions, including the hypothalamus, hippocampus, and PFC 32 – 34 . However, whether miR-29a/b/c-3p responds to ketamine treatment in the hypothalamus, hippocampus, and PFC is still unknown.…”

Section: Resultsmentioning

confidence: 99%

“…Brain imaging and postmortem studies suggest that reductions in dendrite arborization and complexity and the number of neurons and glia in brain regions, including the hippocampus, PFC, cingulate cortex, nucleus accumbens, and amygdala, could contribute to depressive symptoms 32 – 34 . Therefore, we investigated the function of miR-29b-3p in neuron cell survival and cytodendrite growth.…”

Section: Resultsmentioning

confidence: 99%

“…MDD is a prevalent central nervous system disorder associated with differential brain regions, including the hypothalamus, hippocampus, and PFC 32 – 34 . According to recent research, ketamine has a rapid and persistent antidepressant effect 3 – 5 and influences the hypothalamus 41 , hippocampus 18 , and PFC 42 .…”

Section: Discussionmentioning

confidence: 99%

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Prefrontal cortex miR-29b-3p plays a key role in the antidepressant-like effect of ketamine in rats

Wan

Feng

et al. 2018

Exp Mol Med

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Ketamine has a rapid, obvious, and persistent antidepressant effect, but its underlying molecular mechanisms remain unknown. Recently, microRNAs (miRNAs) have emerged as important modulators of ketamine’s antidepressant effect. We investigated the alteration in miR-29b-3p in the brain of rats subjected to ketamine administration and chronic unpredictable mild stress (CUMS), and a sucrose preference test and forced swimming test were used to evaluate the rats’ depressive-like state. We used recombination adeno-associated virus (rAAV) or lentivirus-expressing miR-29b-3p to observe the change in metabotropic glutamate receptor 4 (GRM4). Cell culture and electrophysiological recordings were used to evaluate the function of miR-29b-3p. Ketamine dramatically increased miR-29b-3p expression in the prefrontal cortex of the normal rats. The dual luciferase reporter test confirmed that GRM4 was the target of miR-29b-3p. The miR-29b-3p levels were downregulated, while the GRM4 levels were upregulated in the prefrontal cortex of the depressive-like rats. The ketamine treatment increased miR-29b-3p expression and decreased GRM4 expression in the prefrontal cortex of the depressive-like rats and primary neurons. By overexpressing and silencing miR-29b-3p, we further validated that miR-29b-3p could negatively regulate GRM4. The silencing of miR-29b-3p suppressed the Ca2+ influx in the prefrontal cortex neurons. The miR-29b-3p overexpression contributed to cell survival, cytodendrite growth, increases in extracellular glutamate concentration, and cell apoptosis inhibition. The overexpression of miR-29b-3p by rAAV resulted in a noticeable relief of the depressive behaviors of the CUMS rats and a lower expression of GRM4. The miR-29b-3p/GRM4 pathway acts as a critical mediator of ketamine’s antidepressant effect in depressive-like rats and could be considered a potential therapeutic target for treating major depression disorder.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Prefrontal cortex miR-29b-3p plays a key role in the antidepressant-like effect of ketamine in rats

Wan

Feng

et al. 2018

Exp Mol Med

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“…Furthermore, working memory is the basis for individuals to successfully perform various cognitive tasks, also plays an important role in complex cognitive activities [ 5 ]. Our and other’s previous studies suggested that decreased working memory performance in bipolar and unipolar disorder reflected neurofunctional deficits [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 77%

Differences in verbal and spatial working memory in patients with bipolar II and unipolar depression: an MSI study

Chen

Feng

et al. 2021

BMC Psychiatry

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Background Depressive symptoms could be similarly expressed in bipolar and unipolar disorder. However, changes in cognition and brain networks might be quite distinct. We aimed to find out the difference in the neural mechanism of impaired working memory in patients with bipolar and unipolar disorder. Method According to diagnostic criteria of bipolar II disorder of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and assessments, 13 bipolar II depression (BP II), 8 unipolar depression (UD) patients and 15 healthy controls (HC) were recruited in the study. We used 2-back tasks and magnetic source imaging (MSI) to test working memory functions and get the brain reactions of the participants. Results Compared with HC, only spatial working memory tasks accuracy was significantly worse in both UD and BP II (p = 0.001). Pearson correlation showed that the stronger the FCs’ strength of MFG-IPL and IPL-preSMA, the higher accuracy of SWM task within left FPN in patients with UD (r = 0.860, p = 0.006; r = 0.752, p = 0.031). However, the FC strength of IFG-IPL was negatively correlated with the accuracy of SWM task within left FPN in patients with BP II (r = − 0.591, p = 0.033). Conclusions Our study showed that the spatial working memory of patients with whether UD or BP II was impaired. The patterns of FCs within these two groups of patients were different when performing working memory tasks.

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“…These changes in synchrony are important not only for understanding the mechanism of the underlying pathology, but also as a potential non-invasive biological diagnostic ( Gandal et al, 2012 ), which may be detectable early in the disease process, and for developing treatments ( Strüber and Herrmann, 2020 ). As a core cognitive function, the impairment of WM appears in many different disorders including schizophrenia ( Park and Holzman, 1992 ; Goldman-Rakic, 1994 ; Roitman et al, 2000 ; Peled et al, 2001 ; Kim et al, 2003 ; Micheloyannis et al, 2006 ; Basar-Eroglu et al, 2007 ; Haenschel et al, 2007 , 2009 ; Badcock et al, 2008 ; Pachou et al, 2008 ; Barr et al, 2010 , 2017 ; Griesmayr et al, 2014 ; Lett et al, 2014 ; Wu et al, 2014 ; Pinal et al, 2015 ; Senkowski and Gallinat, 2015 ; Van Snellenberg et al, 2016 ; Kang et al, 2018 ; Ma et al, 2018 ; Appaji et al, 2020 ; Murphy N. et al, 2020 ), bipolar disorder ( Wu et al, 2014 ; Appaji et al, 2020 ), autism spectrum disorder ( Bangel et al, 2014 ; Rabiee et al, 2018 ), Parkinson’s disease ( Siegert et al, 2008 ; Cools and D’Esposito, 2011 ; Zhao et al, 2018 ; Harrington et al, 2020 ), psychosis ( Gold et al, 2019 ), Attention-deficit/hyperactivity disorder (ADHD; Martinussen et al, 2005 ; Wolf et al, 2009 ; Matt Alderson et al, 2013 ; Bédard et al, 2014 ; Wu et al, 2017 ; Zammit et al, 2018 ; Jang et al, 2020 ), and depression ( Shan et al, 2018 ). The role of synchronized oscillations in different brain disorders has been thoroughly examined elsewhere ( Uhlhaas and Singer, 2006 ), and there is much recent interest in identifying non-invasive and quantitative signatures for different disorders ( Başar, 2013 ; Nimmrich et al, 2015 ; Asllani et al, 2018 ).…”

Section: Dysfunctions In Oscillations and Synchrony During Working Memory Occur In Brain Disordersmentioning

confidence: 99%

Dependence of Working Memory on Coordinated Activity Across Brain Areas

Rezayat

Clark

Dehaqani

et al. 2022

Front. Syst. Neurosci.

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Neural signatures of working memory (WM) have been reported in numerous brain areas, suggesting a distributed neural substrate for memory maintenance. In the current manuscript we provide an updated review of the literature focusing on intracranial neurophysiological recordings during WM in primates. Such signatures of WM include changes in firing rate or local oscillatory power within an area, along with measures of coordinated activity between areas based on synchronization between oscillations. In comparing the ability of various neural signatures in any brain area to predict behavioral performance, we observe that synchrony between areas is more frequently and robustly correlated with WM performance than any of the within-area neural signatures. We further review the evidence for alteration of inter-areal synchrony in brain disorders, consistent with an important role for such synchrony during behavior. Additionally, results of causal studies indicate that manipulating synchrony across areas is especially effective at influencing WM task performance. Each of these lines of research supports the critical role of inter-areal synchrony in WM. Finally, we propose a framework for interactions between prefrontal and sensory areas during WM, incorporating a range of experimental findings and offering an explanation for the observed link between intra-areal measures and WM performance.

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Correlations between working memory impairment and neurometabolites of prefrontal cortex and lenticular nucleus in patients with major depressive disorder

Cited by 27 publications

References 51 publications

Prefrontal cortex miR-29b-3p plays a key role in the antidepressant-like effect of ketamine in rats

Prefrontal cortex miR-29b-3p plays a key role in the antidepressant-like effect of ketamine in rats

Differences in verbal and spatial working memory in patients with bipolar II and unipolar depression: an MSI study

Dependence of Working Memory on Coordinated Activity Across Brain Areas

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