NGF, BDNF and Arc mRNA Expression in the Hippocampus of Rats After Administration of Morphine

Rouhani, Fatemeh; Khodarahmi, Parvin; Naseh, Vahid

doi:10.1007/s11064-019-02851-z

Cited by 16 publications

(8 citation statements)

References 52 publications

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“…When neurons in the brain are damaged in PD, a large amount of NSE enters the blood circulation; thus, the elevated level of NSE in plasma is related to disease severity. Brain tissue BDNF and NGF are neurotrophic factors (nutrients required for neuronal differentiation and development in the brain) that play roles in repairing damaged neurons and regulating synaptic functions, and participate in memory and learning; therefore, their deficiency is also closely related to the progression of neurodegenerative diseases and the occurrence of cognitive dysfunction (21,22). We found that the H&Y stage and NMSS score were negatively correlated with NGF and BDNF levels, and were positively correlated with NSE levels.…”

Section: Discussionmentioning

confidence: 76%

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

et al. 2020

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Objective: To investigate the expression level of the maternally expressed gene-3 (MEG3) of the free long non-coding RNA (lncRNAs) in the plasma of Parkinson's disease (PD) patients and its relationship with the disease.Methods: Thirty PD patients (PD group) who treated at Xuanwu Hospital of Capital University of Medical Sciences between January 2017 and December 2019 were selected as the research objects and 30 healthy subjects were enrolled in the study during the same period as the control group. Cognitive function was assessed according to the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) were used to evaluate cognitive function, Non-Motor Symptoms Scale (NMSS) was used to evaluate severity of non-motor symptoms. The relative expression of lncRNAs MEG3 in plasma was measured by PCR, and the levels of neuron-specific enolase (NSE), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in plasma were measured by ELISA, and the relationship with these all indexes was analyzed.Results: The NMSS score of PD group was significantly higher than that of the control group, while the MMSE and MoCA scores were significantly lower than that of the control group (P < 0.05); The relative expression of lncRNAs MEG3, NGF and BDNF levels of PD group were significantly lower than that of the control group, and NSE level was significantly higher than that of the control group (P < 0.05); The H&Y stage and NMSS score in PD group were negatively correlated with the relative expression of lncRNAs MEG3, the levels of NGF and BDNF (P < 0.05), and positively correlated with NSE (P < 0.05); The MMSE and MoCA scores in PD group were positively correlated with the relative expression of lncRNAs MEG3, NGF, BDNF levels (P < 0.05), and negatively correlated with NSE (P < 0.05); The relative expression of lncRNAs MEG3 in PD group was positively correlated with NGF, BDNF levels (P < 0.05), and negatively correlated with NSE (P < 0.05).Conclusion: The expression of lncRNAs MEG3 in the plasma of PD patients was downregulated compared to that of healthy control subjects, and its expression level was closely related to the aggravation of non-motor symptoms, cognitive decline, and PD stage. These associations may reflect the synergism of the increase of NSE and decrease of NGF and BDNF levels, highlighting plasma lncRNA MEG3 as a new candidate biomarker of PD.

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Section: Discussionmentioning

confidence: 76%

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

et al. 2020

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“…In rodents, BDNF administration into the ventral tegmental area induces an opiate‐dependent behavioral (Vargas‐Perez et al., 2009). Morphine administration increases BDNF expression in different brain areas (Bolanos & Nestler, 2004; Hatami et al., 2007; Rouhani et al., 2019), whereas morphine withdrawal decreases BDNF levels by inhibiting its processing from proBDNF (Bachis et al., 2017) or through a histone modification of the BDNF promoter (Mashayekhi et al., 2012). Here we show that withdrawal by up‐regulating p75NTR and decreasing TrkB in synapses causes an imbalance in the expression of these two receptors.…”

Section: Discussionmentioning

confidence: 99%

“…The hippocampus has been considered a key brain area for cognitive and social behavior (Anacker & Hen, 2017; Nadel et al., 2013; Rubin et al., 2014). Remarkably, loss of cognitive function and synaptic remodeling observed in OUD occur despite the increased expression of the brain‐derived neurotrophic factor (BDNF) in the hippocampus of animals (Alvandi et al., 2017; Rouhani et al., 2019) or in human serum (Heberlein et al., 2011). Thus, the molecular mechanisms whereby opioid abuse reduces cognitive abilities remain to be fully understood.…”

Section: Introductionmentioning

confidence: 99%

Neuronal apoptosis induced by morphine withdrawal is mediated by the p75 neurotrophin receptor

Asuni

Speidell

Mocchetti

2021

Journal of Neurochemistry

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Morphine withdrawal evokes neuronal apoptosis through mechanisms that are still under investigation. We have previously shown that morphine withdrawal increases the levels of pro-brain-derived neurotrophic factor (BDNF), a proneurotrophin that promotes neuronal apoptosis through the binding and activation of the panneurotrophin receptor p75 (p75NTR). In this work, we sought to examine whether morphine withdrawal increases p75NTR-driven signaling events. We employed a repeated morphine treatment-withdrawal paradigm in order to investigate biochemical and histological indicators of p75NTR-mediated neuronal apoptosis in mice. We found that repeated cycles of spontaneous morphine withdrawal promote an accumulation of p75NTR in hippocampal synapses. At the same time, TrkB, the receptor that is crucial for BDNF-mediated synaptic plasticity in the hippocampus, was decreased, suggesting that withdrawal alters the neurotrophin receptor environment to favor synaptic remodeling and apoptosis. Indeed, we observed evidence of neuronal apoptosis in the hippocampus, including activation of c-Jun N-terminal kinase (JNK) and increased active caspase-3. These effects were not seen in saline or morphinetreated mice which had not undergone withdrawal. To determine whether p75NTR was necessary in promoting these outcomes, we repeated these experiments in p75NTR heterozygous mice. The lack of one p75NTR allele was sufficient to prevent the increases in phosphorylated JNK and active caspase-3. Our results suggest that p75NTR participates in the neurotoxic and proinflammatory state evoked by morphine withdrawal. Because p75NTR activation negatively influences synaptic repair and promotes cell death, preventing opioid withdrawal is crucial for reducing neurotoxic mechanisms accompanying opioid use disorders.

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“…The analysis of AKT, ACO3 and SMOX mRNA expression was conducted as described by Rouhani et al 16 : total RNA was extracted with TRIzol reagent (Shanghai Pufei Biotech, Shanghai, China), according to the manufacturer's instructions. Nucleic acid-protein complexes were extracted with chloroform and precipitated in isopropanol.…”

Section: Rt-pcr Analysis Of Akt Aco3 and Smox Mrna Expressionmentioning

confidence: 99%

The involvement of ACO3 protein in diabetic retinopathy through the PI3k/Akt signaling pathway

2022

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Background. Diabetic retinopathy (DR) is one of the most common complications of diabetic microvascular disease and its pathogenesis is complicated. The PI3k/Akt signaling pathway plays an important role in the angiogenesis of DR. Objectives.To explore the molecular mechanisms of the ACO3 protein and related proteins in DR, in order to provide a scientific theoretical basis for the clinical treatment of this disease. Materials and methods.A DR rat model was used in this study. One group (anti-ACO3 group, n = 10) was injected with protein ACO3 antagonist; the 2 nd study group (the DR group, n = 10) was injected with the same amount of normal saline; the control group (n = 10) did not undergo any procedures. We used hematoxylin and eosin (H&E) staining to observe the pathological features of the eye tissues. Immunohistochemistry was used to analyze the expression of ACO3 and AKT. Western blot was used to analyze the expression of ANGPT1, ANGPT4 and KDR; reverse transcription polymerase chain reaction (RT-PCR) was used to assess the mRNA expression of AKT, ACO3 and SMOX in the eye tissues of the rats.Results. In the anti-ACO3 group, the results of H&E staining showed that there was a decrease in retinal edema and no obvious abnormality in the blood vessels. The immunohistochemistry analysis of proteins proved that ACO3 and AKT were strongly expressed in the DR group. The western blot analysis of ANGPT1, ANGPT4 and KDR expression showed that in the DR group, the expression of all 3 proteins was higher than in the anti-ACO3 group, and much higher than in the control group. Conclusions.The mRNA expression of AKT, ACO3 and SMOX was strong in the DR group, but decreased in the anti-ACO3 group.

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NGF, BDNF and Arc mRNA Expression in the Hippocampus of Rats After Administration of Morphine

Cited by 16 publications

References 52 publications

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

Association of the Plasma Long Non-coding RNA MEG3 With Parkinson's Disease

Neuronal apoptosis induced by morphine withdrawal is mediated by the p75 neurotrophin receptor

The involvement of ACO3 protein in diabetic retinopathy through the PI3k/Akt signaling pathway

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