Primary hippocampal neurons as suitable model to evaluate the influence of neurotoxicants on neuronal development

2017 ◽  
Vol 280 ◽  
pp. S278
Author(s):  
Natalia Marchetti ◽  
Laura Gerosa ◽  
Mariaserena Boraso ◽  
Barbara Viviani
Keyword(s):  
Hippocampal Neurons ◽  
Neuronal Development ◽  
Suitable Model ◽  
Primary Hippocampal Neurons

scholarly journals Roles of Lycopene During Neurite Development of Primary Hippocampal Neurons

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 923-923
Author(s):  
Madison Scott ◽  
Joseph Jansen ◽  
Mary Margaret Hayden ◽  
Katheryn Broman ◽  
Han-A Park
Keyword(s):  
Hippocampal Neurons ◽  
Developmental Disorders ◽  
Neuronal Development ◽  
Stage Iv ◽  
Neurite Growth ◽  
Redox Balance ◽  
University Of Alabama ◽  
Mitochondrial Superoxide ◽  
Primary Hippocampal Neurons ◽  
Neurite Development

Abstract Objectives Neurite outgrowth and branching is critical during neuronal development. Failure to achieve proper neurite complexity is highly associated with developmental disorders. We have previously shown that oxidative stress contributes to alteration of neurite morphology. Therefore, nutrients capable of regulating neuronal redox balance may help maintain normal neurite development. We have recently found that lycopene, a nutritional antioxidant, protects mitochondria by preventing generation of mitochondrial superoxide. In this study, we hypothesize that treatment with lycopene improves development of primary hippocampal neurons under physiological conditions. Methods Primary hippocampal neurons were grown in neurobasal media with or without 0.1 μM lycopene for 1, 3, 5, 7, and 14 days, and imaged using a Zeiss Axio Vert.A1 microscope. Neurons were classified into 4 different categories: stage I, circular and non-polar neurons; stage II, presence of minor neurites without polarity; stage III, neurons with polarity; and stage IV, neurons with dendritic branches. We also performed Sholl analysis to quantify intersections of neurites evaluating neurite complexity. Results Primary hippocampal neurons grown in media containing lycopene showed advanced neuronal development. In particular, lycopene treatment significantly advanced polarity and dendritic arborization in immature neurons. In addition, neurons grown in lycopene showed improved neurite branching at their maturity. Conclusions This study shows that lycopene supports neurite growth and branching during development. Therefore, we suggest novel role of lycopene during physiological development of the brain, or potential therapeutic effect against developmental disorders. Funding Sources RGC Program (University of Alabama) Crenshaw Research Fund (University of Alabama).

scholarly journals Dynein activator Hook1 is required for trafficking of BDNF-signaling endosomes in neurons

2018 ◽  
Vol 218 (1) ◽  
pp. 220-233 ◽  
Author(s):  
Mara A. Olenick ◽  
Roberto Dominguez ◽  
Erika L.F. Holzbaur
Keyword(s):  
Axonal Transport ◽  
Hippocampal Neurons ◽  
Neuronal Development ◽  
Molecular Motor ◽  
Cytoplasmic Dynein ◽  
Differential Association ◽  
Primary Hippocampal Neurons ◽  
Bdnf Signaling ◽  
Microfluidic Chambers

Axonal transport is required for neuronal development and survival. Transport from the axon to the soma is driven by the molecular motor cytoplasmic dynein, yet it remains unclear how dynein is spatially and temporally regulated. We find that the dynein effector Hook1 mediates transport of TrkB–BDNF-signaling endosomes in primary hippocampal neurons. Hook1 comigrates with a subpopulation of Rab5 endosomes positive for TrkB and BDNF, which exhibit processive retrograde motility with faster velocities than the overall Rab5 population. Knockdown of Hook1 significantly reduced the motility of BDNF-signaling endosomes without affecting the motility of other organelles. In microfluidic chambers, Hook1 depletion resulted in a significant decrease in the flux and processivity of BDNF-Qdots along the mid-axon, an effect specific for Hook1 but not Hook3. Hook1 depletion inhibited BDNF trafficking to the soma and blocked downstream BDNF- and TrkB-dependent signaling to the nucleus. Together, these studies support a model in which differential association with cargo-specific effectors efficiently regulates dynein in neurons.

scholarly journals Tissue-based metabolic labeling of polysialic acids in living primary hippocampal neurons

2015 ◽  
Vol 112 (3) ◽  
pp. E241-E248 ◽  
Author(s):  
Kyungtae Kang ◽  
Sunghoon Joo ◽  
Ji Yu Choi ◽  
Sujeong Geum ◽  
Seok-Pyo Hong ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Hippocampal Neurons ◽  
Neuronal Development ◽  
Polysialic Acid ◽  
Metabolic Labeling ◽  
Primary Hippocampal Neurons ◽  
Polysialic Acids ◽  
Conventional Cell ◽  
Vitro Analysis

The posttranslational modification of neural cell-adhesion molecule (NCAM) with polysialic acid (PSA) and the spatiotemporal distribution of PSA-NCAM play an important role in the neuronal development. In this work, we developed a tissue-based strategy for metabolically incorporating an unnatural monosaccharide, peracetylated N-azidoacetyl-d-mannosamine, in the sialic acid biochemical pathway to present N-azidoacetyl sialic acid to PSA-NCAM. Although significant neurotoxicity was observed in the conventional metabolic labeling that used the dissociated neuron cells, neurotoxicity disappeared in this modified strategy, allowing for investigation of the temporal and spatial distributions of PSA in the primary hippocampal neurons. PSA-NCAM was synthesized and recycled continuously during neuronal development, and the two-color labeling showed that newly synthesized PSA-NCAMs were transported and inserted mainly to the growing neurites and not significantly to the cell body. This report suggests a reliable and cytocompatible method for in vitro analysis of glycans complementary to the conventional cell-based metabolic labeling for chemical glycobiology.

ATRA-induced increase in intracellular Ca2+concentration in primary hippocampal neurons

2010 ◽  
Vol 34 (8) ◽  
pp. S74-S74
Author(s):  
Tingyu Li ◽  
Xiaojuan Zhang ◽  
Xuan Zhang ◽  
Jian Hea ◽  
Yang Bi Youxue Liu ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Primary Hippocampal Neurons

Spastin Interacts with CRMP2 to Regulate Neurite Outgrowth by Controlling Microtubule Dynamics through Phosphorylation Modifications

2020 ◽  
Vol 19 ◽  
Author(s):  
Sumei Li ◽  
Jifeng Zhang ◽  
Jiaqi Zhang ◽  
Jiong Li ◽  
Longfei Cheng ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Hippocampal Neurons ◽  
Neuronal Development ◽  
Phosphorylation Site ◽  
Microtubule Dynamics ◽  
Microtubule Assembly ◽  
C Terminus ◽  
Mediator Protein ◽  
Branch Formation

Aims: Our work aims to revealing the underlying microtubule mechanism of neurites outgrowth during neuronal development, and also proposes a feasible intervention pathway for reconstructing neural network connections after nerve injury. Background: Microtubule polymerization and severing are the basis for the neurite outgrowth and branch formation. Collapsin response mediator protein 2 (CRMP2) regulates axonal growth and branching as a binding partner of the tubulin heterodimer to promote microtubule assembly. And spastin participates in the growth and regeneration of neurites by severing microtubules into small segments. However, how CRMP2 and spastin cooperate to regulate neurite outgrowth by controlling the microtubule dynamics needs to be elucidated. Objective: To explore whether neurite outgrowth was mediated by coordination of CRMP2 and spastin. Method: Hippocampal neurons were cultured in vitro in 24-well culture plates for 4 days before being used to perform the transfection. Calcium phosphate was used to transfect the CRMP2 and spastin constructs and their control into the neurons. An interaction between CRMP2 and spastin was examined by using pull down, CoIP and immunofluorescence colocalization assays. And immunostaining was also performed to determine the morphology of neurites. Result: We first demonstrated that CRMP2 interacted with spastin to promote the neurite outgrowth and branch formation. Furthermore, our results identified that phosphorylation modification failed to alter the binding affinities of CRMP2 for spastin, but inhibited their binding to microtubules. CRMP2 interacted with the MTBD domain of spastin via its C-terminus, and blocking the binding sites of them inhibited the outgrowth and branch formation of neurites. In addition, we confirmed one phosphorylation site S210 at spastin in hippocampal neurons and phosphorylation spastin at site S210 promoted the neurite outgrowth but not branch formation by remodeling microtubules. Conclusion: Taken together, our data demonstrated that the interaction of CRMP2 and spastin is required for neurite outgrowth and branch formation and their interaction is not regulated by their phosphorylation.

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

Neurotrophic Properties of Silexan, an Essential Oil from the Flowers of Lavender-Preclinical Evidence for Antidepressant-Like Properties

2020 ◽  
Vol 54 (01) ◽  
pp. 37-46
Author(s):  
Kristina Friedland ◽  
Giacomo Silani ◽  
Anita Schuwald ◽  
Carola Stockburger ◽  
Egon Koch ◽  
...  
Keyword(s):  
Essential Oil ◽  
Hippocampal Neurons ◽  
Day Treatment ◽  
Neuronal Cell ◽  
Antidepressant Activity ◽  
In Vivo Models ◽  
Antidepressant Effects ◽  
Primary Hippocampal Neurons

Abstract Background Silexan, a special essential oil from flowering tops of lavandula angustifolia, is used to treat subsyndromal anxiety disorders. In a recent clinical trial, Silexan also showed antidepressant effects in patients suffering from mixed anxiety-depression (ICD-10 F41.2). Since preclinical data explaining antidepressant properties of Silexan are missing, we decided to investigate if Silexan also shows antidepressant-like effects in vitro as well as in vivo models. Methods We used the forced swimming test (FST) in rats as a simple behavioral test indicative of antidepressant activity in vivo. As environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology—resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function—we investigated the neurotrophic properties of Silexan in neuronal cell lines and primary hippocampal neurons. Results The antidepressant activity of Silexan (30 mg/kg BW) in the FST was comparable to the tricyclic antidepressant imipramine (20 mg/kg BW) after 9-day treatment. Silexan triggered neurite outgrowth and synaptogenesis in 2 different neuronal cell models and led to a significant increase in synaptogenesis in primary hippocampal neurons. Silexan led to a significant phosphorylation of protein kinase A and subsequent CREB phosphorylation. Conclusion Taken together, Silexan demonstrates antidepressant-like effects in cellular as well as animal models for antidepressant activity. Therefore, our data provides preclinical evidence for the clinical antidepressant effects of Silexan in patients with mixed depression and anxiety.

Impact of manganese on primary hippocampal neurons from rodents

Hippocampus ◽  
2014 ◽  
Vol 24 (5) ◽  
pp. 598-610 ◽  
Author(s):  
Alexia Daoust ◽  
Yasmina Saoudi ◽  
Jacques Brocard ◽  
Nora Collomb ◽  
Cécile Batandier ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Primary Hippocampal Neurons

Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric β-amyloid 1-42-induced neurotoxicity

2013 ◽  
Vol 554 ◽  
pp. 64-69 ◽  
Author(s):  
Xueling Dai ◽  
Ping Chang ◽  
Qingzhu Zhu ◽  
Wenjuan Liu ◽  
Yaxuan Sun ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Chitosan Oligosaccharides ◽  
Primary Hippocampal Neurons ◽  
Β Amyloid
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