Effects of Aberrant miR-384-5p Expression on Learning and Memory in a Rat Model of Attention Deficit Hyperactivity Disorder

Xu, Qin; Tang, Ranran; Wang, Jing; Qin, Hong; Guo, Xirong; Tong, Meiling; Yang, Lei; Chi, Xia

doi:10.3389/fneur.2019.01414

Cited by 10 publications

(7 citation statements)

References 44 publications

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“…D1-like receptor (DRD1) was a potential target regulated by miR-384-5p. The inhibition or overexpression of miR-384-5p in the prefrontal cortex in a rat model of attention deficit hyperactivity disorder affected DRD1 gene expression and changed the protein level of the dopamine transporter (DAT) [31,32]. Changes in DAT expression affected the reuptake of DA by the presynaptic membrane, changed the DA level, and regulated the learning and memory level of rats [32].…”

Section: Mirnas and Neurotransmission-related Receptorsmentioning

confidence: 99%

“…The inhibition or overexpression of miR-384-5p in the prefrontal cortex in a rat model of attention deficit hyperactivity disorder affected DRD1 gene expression and changed the protein level of the dopamine transporter (DAT) [31,32]. Changes in DAT expression affected the reuptake of DA by the presynaptic membrane, changed the DA level, and regulated the learning and memory level of rats [32]. Furthermore, miR-504 in the nucleus accumbens in a rat model of CUMS was shown to target and regulate the DRD1 level [33] similar to the function of miR-384-5p.…”

Section: Mirnas and Neurotransmission-related Receptorsmentioning

confidence: 99%

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A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

Gao

Zhang

Wang

et al. 2022

IJMS

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Depression is a psychiatric disorder that presents with a persistent depressed mood as the main clinical feature and is accompanied by cognitive impairment. Changes in neuroplasticity and neurogenesis greatly affect depression. Without genetic changes, epigenetic mechanisms have been shown to function by regulating gene expression during the body’s adaptation to stress. Studies in recent years have shown that as important regulatory factors in epigenetic mechanisms, microRNAs (miRNAs) play important roles in the development and progression of depression through the regulation of protein expression. Herein, we review the mechanisms of miRNA-mediated neuroplasticity in depression and discus synaptic structural plasticity, synaptic functional plasticity, and neurogenesis. Furthermore, we found that miRNAs regulate neuroplasticity through several signalling pathways to affect cognitive functions. However, these pathways do not work independently. Therefore, we try to identify synergistic correlations between miRNAs and multiple signalling pathways to broaden the potential pathogenesis of depression. In addition, in the future, dual-function miRNAs (protection/injury) are promising candidate biomarkers for the diagnosis of depression, and their regulated genes can potentially be used as target genes for the treatment of depression.

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Section: Mirnas and Neurotransmission-related Receptorsmentioning

confidence: 99%

Section: Mirnas and Neurotransmission-related Receptorsmentioning

confidence: 99%

A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

Gao

Zhang

Wang

et al. 2022

IJMS

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“…Knockdown of miR-384 inhibits the apoptosis of hippocampal neurons induced by chronic cerebral ischemia (Liu et al, 2019). Similarly, miR-384-5p promotes neurotoxicity and attenuates learning and memory in rats (Jiang et al, 2016;Q. Xu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Knockdown of miR‐384 inhibits the apoptosis of hippocampal neurons induced by chronic cerebral ischemia (Liu et al., 2019 ). Similarly, miR‐384‐5p promotes neurotoxicity and attenuates learning and memory in rats (Jiang et al., 2016 ; Q. Xu et al., 2019 ). However, whether the roles of miRNA‐384‐3p are consistent with those of miR‐384‐5p in neurotoxicity remains obscure.…”

Section: Introductionmentioning

confidence: 99%

miRNA‐384‐3p alleviates sevoflurane‐induced nerve injury by inhibiting Aak1 kinase in neonatal rats

Chen

Gao²,

Pei

2022

Brain and Behavior

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Objective: Sevoflurane is a common anesthetic and is widely used in pediatric clinical surgery to induce and maintain anesthesia through inhalation. Increasing studies have revealed that sevoflurane has neurotoxic effects on neurons, apoptosis, and memory impairment. miR-384 is involved in the process of neurological diseases.However, the role of miRNA-384-3p in sevoflurane-induced nerve injury is not clear.This study focused on exploring the roles and mechanisms of miRNA-384-3p in sevoflurane-induced nerve injury.Methods: Seven-day-old rats were exposed to 2.3% sevoflurane to induce nerve injury.The morphological changes in neurons in the hippocampal CA1 region were detected by HE staining and Nissl staining. Neuronal apoptosis was detected by TUNEL and Western blot assays. Spatial memory and learning ability were detected by the Morris water maze assay. The target gene of miRNA-384-3p was verified through a luciferase reporter assay. A rescue experiment was used to confirm the miRNA-384-3p pathway in sevoflurane-induced nerve injury.Results: Sevoflurane reduced miRNA-384-3p expression in the rat hippocampus. miRNA-384-3p alleviated sevoflurane-induced morphological changes in hippocampal neurons and apoptosis of neurons in the hippocampal CA1 region. Meanwhile, miRNA-384-3p attenuated the decline in spatial memory and learning ability induced by sevoflurane. miRNA-384-3p alleviated sevoflurane-induced nerve injury by inhibiting the expression of adaptor-associated kinase 1 (Aak1). Conclusion:Our findings revealed the role and mechanism of miRNA-384-3p in sevoflurane-induced nerve injury, suggesting that miRNA-384-3p could be a novel and promising strategy for reducing sevoflurane-induced neurotoxicity.

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“…For the mechanisms underlying the association between ADHD and miRNAs, animal studies have investigated whether miRNA (i.e., rno-let-7d) expression or miRNA target genes (i.e., Homer 1a ) are related to an ADHD phenotype [ 25 – 29 ]. A rat model revealed that miR-1-b, miR-182, miR-183-5p, miR-206-3p, miR-211-5p, miR-384-5p, miR-471-5p, and miR-741-3p may be involved in learning and memory deficits in ADHD [ 30 , 31 ]. Dopamine deficiency has been proposed as an underlying cause of ADHD, and upregulation of miR-140-5p and miR-140-3p was observed in dopamine neurons [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs serve as prediction and treatment-response biomarkers of attention-deficit/hyperactivity disorder and promote the differentiation of neuronal cells by repressing the apoptosis pathway

et al. 2022

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Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder. This study aimed to examine whether miRNA expression abundance in total white blood cells (WBCs) facilitated the identification of ADHD and reflected its response to treatment. Furthermore, whether miRNA markers facilitated the growth of the human cortical neuronal (HCN-2) cells was also investigated. Total WBC samples were collected from 145 patients and 83 controls, followed by RNA extraction and qPCR assays. Subsequently, WBC samples were also collected at the endpoint from ADHD patients who had undergone 12 months of methylphenidate treatment. The determined ΔCt values of 12 miRNAs were applied to develop an ADHD prediction model and to estimate the correlation with treatment response. The prediction model applying the ΔCt values of 12 examined miRNAs (using machine learning algorithm) demonstrated good validity in discriminating ADHD patients from controls (sensitivity: 96%; specificity: 94.2%). Among the 92 ADHD patients completing the 12-month follow-up, miR-140-3p, miR-27a-3p, miR-486-5p, and miR-151-5p showed differential trends of ΔCt values between treatment responders and non-responders. In addition, the in vitro cell model revealed that miR-140-3p and miR-126-5p promoted the differentiation of HCN-2 cells by enhancing the length of neurons and the number of junctions. Microarray and flow cytometry assays confirmed that this promotion was achieved by repressing apoptosis and/or necrosis. The findings of this study suggest that the expression levels of miRNAs have the potential to serve as both diagnostic and therapeutic biomarkers for ADHD. The possible biological mechanisms of these biomarker miRNAs in ADHD pathophysiology were also clarified.

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Effects of Aberrant miR-384-5p Expression on Learning and Memory in a Rat Model of Attention Deficit Hyperactivity Disorder

Cited by 10 publications

References 44 publications

A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

miRNA‐384‐3p alleviates sevoflurane‐induced nerve injury by inhibiting Aak1 kinase in neonatal rats

MicroRNAs serve as prediction and treatment-response biomarkers of attention-deficit/hyperactivity disorder and promote the differentiation of neuronal cells by repressing the apoptosis pathway

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