Striatal modulation of <scp>BDNF</scp> expression using micro<scp>RNA</scp>124a‐expressing lentiviral vectors impairs ethanol‐induced conditioned‐place preference and voluntary alcohol consumption

Bahí, Amine; Dreyer, Jean-Luc

doi:10.1111/ejn.12228

Cited by 85 publications

(75 citation statements)

References 83 publications

(114 reference statements)

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“…To the best of our knowledge, we are the first who could demonstrate a negative correlation between levels of BDNF and the expression of miR124a. Indeed, we have shown in previous report that BDNF is a direct target of miR124a (Bahi and Dreyer, 2013;Chandrasekar and Dreyer, 2009). Our findings are in line with those of O'Connor and coworkers who found using microarray and RT-PCR, that earlylife stress affected the expression of multiple hippocampal miRNAs (O'Connor et al, 2013).…”

Section: Discussionsupporting

confidence: 93%

“…Reactions were essentially carried out as described previously (Bahi and Dreyer, 2013;Chandrasekar and Dreyer, 2009). In brief, total RNA from brain regions was isolated using the TRizol according to the manufacturer instructions.…”

Section: Tissue Collection and Quantification Of Bdnf And Mir124a Aftmentioning

confidence: 99%

“…For qPCR, 20 ml of amplification mixture with SYBRGreen Kit was used containing 3 ml of cDNA and 100 nM primers. Primer sequences used were: GAPDH: 5 0 -ATG ACT CTA CCC ACG GCA AG-3 0 and 5 0 -CAT ACT CAG CAC CAG CAT CAC-3 0 ; miR124a: 5 0 -TCC GTG TTC ACA GCG GAC-3 0 and 5 0 -CAT TCA CCG CGT GCC TTA-3 0 and BDNF: 5 0 -GGT TCG AGA GGT CTG ACG AC-3 0 and 5 0 -CAA AGG CAC TTG ACT GCT GA-3 0 (Bahi et al, 2008a;Bahi and Dreyer, 2013). The PCR protocol used consisted of a 45-s denaturation at 94 8C followed by 45-s annealing and extension at 64 8C for 40 cycles.…”

Section: Tissue Collection and Quantification Of Bdnf And Mir124a Aftmentioning

confidence: 99%

“…Our lentivirus derived plasmid (pTK431), driven by the cytomegalovirus (CMV) promoter, carried the transgenes for BDNF, miR124a or siR124a described in our previous studies (Bahi et al, 2008a;Bahi and Dreyer, 2013;Chandrasekar and Dreyer, 2009). The empty vector (LV-Mock) was used as negative control.…”

Section: Lentiviral Constructions and Productionmentioning

confidence: 99%

“…Among them, miR124a is strongly expressed in the brain; miR124a regulates adult neurogenesis (Cao et al, 2007), and promotes neuronal differentiation (Makeyev et al, 2007) and it is involved in several brain disorders (Qi et al, 2012). In addition, miR124a also strongly affects the expression of several neurotransmitters, including mainly BDNF (Bahi and Dreyer, 2013;Dreyer, 2009, 2011). This prompted us to investigate the potential role of miR124a in the ethiology of depression.…”

Section: Introductionmentioning

confidence: 99%

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Selective lentiviral-mediated suppression of microRNA124a in the hippocampus evokes antidepressants-like effects in rats

Bahí

Chandrasekar

Dreyer

2014

Psychoneuroendocrinology

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Summary Several lines of evidences suggest that the brain-derived neutrophic factor (BDNF) is implicated in the pathophysiology of depression. However, the molecular mechanisms are not fully understood. In the current study we aimed to investigate how genetic modulation of BDNF in the hippocampus using microRNa124a (miR124a)-expressing lentiviral vectors (LV) might affect depression-like behavior in adult rats. For this purpose, we assessed the expression level of miR124a and its direct target BDNF in the hippocampus and the cortex after 21-days exposure to social defeat stress. Results demonstrated that miR124a was up-regulated in the hippocampus but not in the cortex. In contrast, and as expected, BDNF transcripts were down-regulated. In a different set of experiments, male Wistar rats received bilateral intra-hippocampal or intracortical infusions of BDNF-and miR124a-expressing lentiviral vectors and depression-like behavior was assessed after 21-days social defeat stress using the novelty suppressed feeding, the sucrose preference and the forced swim tests. The results indicated that miR124a overexpression exacerbated depression-like behavior. However, an anti-depressant like effect was observed when BDNF or miR124a-silencers (siR124a) were injected into the hippocampus. Importantly, when expressed into the cortex, LV-miR124a, LV-siR124a and LV-BDNF had no effect on depression. Our findings indicate that hippocampal miR124a and its direct target BDNF play an important role in depression-like behavior. Taken together, the current results reveal, for the first time, a potential molecular regulation of miR124a on BDNF, and the pronounced behavioral consequences of this regulation shed light on the mechanisms underlying BDNF anti-depressant potential. #

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Section: Discussionsupporting

confidence: 93%

Section: Tissue Collection and Quantification Of Bdnf And Mir124a Aftmentioning

confidence: 99%

Section: Tissue Collection and Quantification Of Bdnf And Mir124a Aftmentioning

confidence: 99%

Section: Lentiviral Constructions and Productionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Selective lentiviral-mediated suppression of microRNA124a in the hippocampus evokes antidepressants-like effects in rats

Bahí

Chandrasekar

Dreyer

2014

Psychoneuroendocrinology

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Molecular mechanisms of alcohol's effects on the human body: A review and update

Renu,

Myakala,

Chakraborty

et al. 2023

J Biochem & Molecular Tox

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Alcohol consumption has been linked to numerous negative health outcomes although it has some beneficial effects on moderate dosages, the most severe of which being alcohol‐induced hepatitis. The number of people dying from this liver illness has been shown to climb steadily over time, and its prevalence has been increasing. Researchers have found that alcohol consumption primarily affects the brain, leading to a wide range of neurological and psychological diseases. High‐alcohol‐consumption addicts not only experienced seizures, but also ataxia, aggression, social anxiety, and variceal hemorrhage that ultimately resulted in death, ascites, and schizophrenia. Drugs treating this liver condition are limited and can cause serious side effects like depression. Serine‐threonine kinases, cAMP protein kinases, protein kinase C, ERK, RACK 1, Homer 2, and more have all been observed to have their signaling pathways disrupted by alcohol, and alcohol has also been linked to epigenetic changes. In addition, alcohol consumption induces dysbiosis by changing the composition of the microbiome found in the gastrointestinal tract. Although more studies are needed, those that have been done suggest that probiotics aid in keeping the various microbiota concentrations stable. It has been argued that reducing one's alcohol intake may seem less harmful because excessive drinking is a lifestyle disorder.

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microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1

Yang

Guo

et al. 2019

Journal Cellular Physiology

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Isoflurane anesthesia induces neuroapoptosis in the development of the brain. In this study, neonatal rats and hippocampal neurons were subjected to isoflurane exposure, in which the effect of miR-124 on the neurological deficits induced by isoflurane was evaluated. Isoflurane anesthesia models were induced in neonatal SD rats aged 7 days and then treated with miR-124 agomir, miR-124 antagomir, or LV-CMV-early growth response 1 (EGR1) plasmids. Then, the spatial learning and memory ability of rats were evaluated by Morris water maze. Furthermore, primary hippocampal neurons cultured 7 days were also exposed to isoflurane and transfected with miR-124 agomir, miR-124 antagomir, or LV-CMV-EGR1 plasmids. The targeting relationship of miR-124 and EGR1 was verified by the dual-luciferase reporter gene assay. To identify the effect of miR-124 on neuron activities, the viability and apoptosis of hippocampal neurons were assessed. In response to isoflurane exposure, miR-124 expression was reduced and EGR1 expression was increased in the hippocampal tissues and neurons. The isoflurane anesthesia damaged rats' spatial learning and memory ability, and reduced viability, and promoted apoptosis of hippocampal neurons. EGR1 was targeted and negatively regulated by miR-124. The treatment of miR-124 agomir improved rats' spatial learning and memory ability and notably increased hippocampal neuron viability and resistance to apoptosis, corresponding to an increased brain-derived neurotrophic factor (BDNF) expression, inhibited expression of proapoptotic factors (cleaved-Caspase-3 and Bax), and enhanced the expression of antiapoptotic factor (Bcl-2). Upregulated miR-124 inhibited the expression of EGR1, by which mechanism miR-124 reduced the neurological deficits induced by isoflurane in neonatal rats through inhibiting apoptosis of hippocampal neurons.

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Striatal modulation of BDNF expression using microRNA124a‐expressing lentiviral vectors impairs ethanol‐induced conditioned‐place preference and voluntary alcohol consumption

Cited by 85 publications

References 83 publications

Selective lentiviral-mediated suppression of microRNA124a in the hippocampus evokes antidepressants-like effects in rats

Selective lentiviral-mediated suppression of microRNA124a in the hippocampus evokes antidepressants-like effects in rats

Molecular mechanisms of alcohol's effects on the human body: A review and update

microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1

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