Changes in the expression level of MAPK pathway components induced by monosodium glutamate-administration produce neuronal death in the hippocampus from neonatal rats

Rivera-Carvantes, Martha Catalina; Jarero-Basulto, Jose J.; Feria‐Velasco, Alfredo; Beas‐Zárate, Carlos; Navarro-Meza, Mónica; González-López, Mariana Berenice; Gudiño-Cabrera, Graciela; García-Rodríguez, Julio César

doi:10.1016/j.neuroscience.2017.09.029

Cited by 15 publications

(14 citation statements)

References 87 publications

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“…The hippocampus is the limbic system of the brain, and it is related functions of the central nervous system such as learning and memory [ 21 22 ]. Meanwhile, hippocampal tissue is composed of a large number of neural stem cells, with structure of neat, relatively independent cells.…”

Section: Discussionmentioning

confidence: 99%

Collapsin Response Mediator Protein-2 Ameliorates Sevoflurane-Mediated Neurocyte Injury by Targeting PI3K-mTOR-S6K Pathway

Zhu

2018

Med Sci Monit

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BackgroundCollapsin response mediator protein-2 (CRMP-2) is the first member of the CRMP family that has been identified in primary neuronal cells; it was originally found and identified in the regulation of microtubule dimerization into microtubules.Material/MethodsIn the present study, we aimed to investigate the roles and mechanisms of CRMP-2 in sevoflurane-induced neurocyte injury. Cell viability, proliferation, and apoptosis were measured by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Colorimetry was performed to measure the activity of caspase-3. Western blot and quantitative real-time reverse transcription assays were used to evaluate the related mRNAs and proteins expression.ResultsWe found that CRMP-2 reversed the inhibitory effect of sevoflurane on the viability of nerve cells. Moreover, CRMP-2 accelerated the proliferation and suppressed the apoptosis of sevoflurane-induced nerve cells. CRMP-2 modulated the expression levels of apoptosis-associated protein in sevoflurane-induced nerve cells. Furthermore, it was demonstrated that CRMP-2 impacted the PI3K-mTOR-S6K pathway.ConclusionsCRMP2 ameliorated sevoflurane-mediated neurocyte injury by targeting the PI3K-mTOR-S6K pathway. Thus, CRMP2 might be an effective target for sevoflurane-induced neurocyte injury therapies.

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Section: Discussionmentioning

confidence: 99%

Collapsin Response Mediator Protein-2 Ameliorates Sevoflurane-Mediated Neurocyte Injury by Targeting PI3K-mTOR-S6K Pathway

Zhu

2018

Med Sci Monit

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“…It has been broadly demonstrated that extracellular Glu levels are significantly increased in precipitant conditions of neuronal damage and during the seizures [ 122 , 127 , 128 ] that Glu-mediated excessive neuronal excitation leads to neuronal damage through a process known as excitotoxicity, which has been widely resembled in the hippocampus with several Glu analogues ( Figure 2 ) [ 61 , 62 , 122 , 127 , 129 , 130 , 131 ]. Subsequently, neuronal damage and seizures may self-promote and regulate reciprocally in a positive feedback mechanism, wherein Glu is the neurotransmitter clearly implied.…”

Section: Changes In the Neurotransmission Systems By Seizures Relamentioning

confidence: 99%

“…Nissl stain. Scale bars correspond to 500 and 50 µm in upper and lower panels, respectively (for methodological details see: Rivera-Cervantes [ 131 ]).…”

Section: Figurementioning

confidence: 99%

Interactions Between Epilepsy and Plasticity

et al. 2018

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Undoubtedly, one of the most interesting topics in the field of neuroscience is the ability of the central nervous system to respond to different stimuli (normal or pathological) by modifying its structure and function, either transiently or permanently, by generating neural cells and new connections in a process known as neuroplasticity. According to the large amount of evidence reported in the literature, many stimuli, such as environmental pressures, changes in the internal dynamic steady state of the organism and even injuries or illnesses (e.g., epilepsy) may induce neuroplasticity. Epilepsy and neuroplasticity seem to be closely related, as the two processes could positively affect one another. Thus, in this review, we analysed some neuroplastic changes triggered in the hippocampus in response to seizure-induced neuronal damage and how these changes could lead to the establishment of temporal lobe epilepsy, the most common type of focal human epilepsy.

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“…Various lines of evidence support the idea that in several neurological diseases, extracellular Glu accumulation overactivates GluR and induces excitotoxic cell death (Meldrum, 2000; Fan and Raymond, 2007; Besancon et al, 2008; Dabrowska et al, 2017). Additionally, the apoptotic cell death that occurs during normal development and/or under pathological conditions shares similar morphological features and a great variety of signaling cascades that induce both of biochemical and molecular events that produce neuronal damage; particularly in susceptible regions such as the hippocampus (Arundine and Tymianski, 2004; Rivera-Cervantes et al, 2004, 2015, 2017; Kwak and Weiss, 2006; Forder and Tymianski, 2009; Zhou et al, 2017). Accordingly, an understanding of the mechanisms that activate these events could allow the design of therapeutic strategies more efficient than the existing ones.…”

Section: Introductionmentioning

confidence: 99%

“…For the above reasons, the aim of this study was to investigate the expressional changes of signaling molecules through which rhEPO could achieve its neuroprotective effect in the hippocampus of neonatal rats with excitotoxic brain injury induced by MSG administration (Rivera-Cervantes et al, 2009; Rivera-Carvantes et al, 2017). With this finality, we first established the optimally efficient dose of rhEPO with the greatest neuroprotective effect and then evaluated the changes in gene expression levels induced by this molecule, particularly in key molecules at the onset of EPO-mediated signaling, such as EPO, EPOR and the postulated βcR.…”

Section: Introductionmentioning

confidence: 99%

The Recombinant Human Erythropoietin Administered in Neonatal Rats After Excitotoxic Damage Induces Molecular Changes in the Hippocampus

et al. 2019

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In vitro and in vivo experimental evidence has contributed important knowledge regarding the antiapoptotic effect mediated by EPO signaling in the damaged brain, particularly through different models with a hypoxic component. However, little emphasis has been placed on the effectiveness of rhEPO administration against cellular alterations caused by in vivo excitotoxicity or on the molecular mechanism that regulates this effect. In this study, we investigated the effects of a single dose of rhEPO on hippocampal damage induced by subcutaneous application of monosodium glutamate (MSG) on postnatal days 1, 3, 5 and 7 in neonatal rats. We found that a dose of 1000 IU/kg of b.w. administered 24 h after MSG had the greatest protective effect. In addition, we analyzed changes in gene expression, particularly in 3 key molecules involved in EPO-mediated signaling (EPO, EPOR and βcR). We observed that the expression of EPO and EPOR was differentially modified at both the mRNA and protein levels under the evaluated conditions, while the expression of the βcR gene was substantially increased. Our data suggest that a low dose of rhEPO is sufficient to induce cellular protection under these experimental conditions and that the molecular changes could be a positive feedback mechanism, mediated by reactive astrocytes in association with in vivo neuroprotective mechanisms.

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Changes in the expression level of MAPK pathway components induced by monosodium glutamate-administration produce neuronal death in the hippocampus from neonatal rats

Cited by 15 publications

References 87 publications

Collapsin Response Mediator Protein-2 Ameliorates Sevoflurane-Mediated Neurocyte Injury by Targeting PI3K-mTOR-S6K Pathway

Collapsin Response Mediator Protein-2 Ameliorates Sevoflurane-Mediated Neurocyte Injury by Targeting PI3K-mTOR-S6K Pathway

Interactions Between Epilepsy and Plasticity

The Recombinant Human Erythropoietin Administered in Neonatal Rats After Excitotoxic Damage Induces Molecular Changes in the Hippocampus

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