Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE80656 | GEO | 2016/10/04
SECONDARY ACCESSION(S): PRJNA319581
REPOSITORIES: GEO
Similar Datasets
Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children’s health. Here we examined the effects of long-term (14 days) and low dose (1 μM) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ≥1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.
2016-10-04 | GSE80653 | GEO
Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children’s health. Here we examined the effects of long-term (14 days) and low dose (1 μM) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ≥1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.
2016-10-04 | GSE80638 | GEO
Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children’s health. Here we examined the effects of long-term (14 days) and low dose (1 μM) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ≥1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.
2016-10-04 | GSE80652 | GEO
Project description:Alteration of gene expression profile of cerebelllar neuron-enriched cultures from neonatal rats by nicotine, acetamiprid, or imidacloprid treatment
| PRJNA319581 | ENA
Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children's health. Here we examined the effects of longterm (14 days) and low dose (1 ?M) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ?1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.
| S-EPMC5086726 | biostudies-literature
Project description:BackgroundAcetamiprid (ACE) and imidacloprid (IMI) belong to a new, widely used class of pesticide, the neonicotinoids. With similar chemical structures to nicotine, neonicotinoids also share agonist activity at nicotinic acetylcholine receptors (nAChRs). Although their toxicities against insects are well established, their precise effects on mammalian nAChRs remain to be elucidated. Because of the importance of nAChRs for mammalian brain function, especially brain development, detailed investigation of the neonicotinoids is needed to protect the health of human children. We aimed to determine the effects of neonicotinoids on the nAChRs of developing mammalian neurons and compare their effects with nicotine, a neurotoxin of brain development.Methodology/principal findingsPrimary cultures of cerebellar neurons from neonatal rats allow for examinations of the developmental neurotoxicity of chemicals because the various stages of neurodevelopment-including proliferation, migration, differentiation, and morphological and functional maturation-can be observed in vitro. Using these cultures, an excitatory Ca(2+)-influx assay was employed as an indicator of neural physiological activity. Significant excitatory Ca(2+) influxes were evoked by ACE, IMI, and nicotine at concentrations greater than 1 µM in small neurons in cerebellar cultures that expressed the mRNA of the α3, α4, and α7 nAChR subunits. The firing patterns, proportion of excited neurons, and peak excitatory Ca(2+) influxes induced by ACE and IMI showed differences from those induced by nicotine. However, ACE and IMI had greater effects on mammalian neurons than those previously reported in binding assay studies. Furthermore, the effects of the neonicotinoids were significantly inhibited by the nAChR antagonists mecamylamine, α-bungarotoxin, and dihydro-β-erythroidine.Conclusions/significanceThis study is the first to show that ACE, IMI, and nicotine exert similar excitatory effects on mammalian nAChRs at concentrations greater than 1 µM. Therefore, the neonicotinoids may adversely affect human health, especially the developing brain.
| S-EPMC3290564 | biostudies-literature
Project description:Summary We present here an optimized protocol to obtain primary neuron-enriched cultures from embryonic chicken brains with no need for an animal facility. The protocol details the steps to isolate a neuron-enriched cell fraction from chicken embryos, followed by characterization of the chicken neurons with mass spectrometry proteomics and cell staining. Because of the high homology between chicken and human amyloid precursor protein processing machinery, these chicken neurons can be used as an alternative to rodent models for studying Alzheimer disease. Graphical abstract Highlights • An in vitro model that can be used for Alzheimer disease studies• Fast and accessible protocol with no need for an animal facility• Isolation of a neuron-enriched cell fraction from chicken embryos• Characterization of the neuronal model using proteomics and cell staining approaches Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics. We present here an optimized protocol to obtain primary neuron-enriched cultures from embryonic chicken brains with no need for an animal facility. The protocol details the steps to isolate a neuron-enriched cell fraction from chicken embryos, followed by characterization of the chicken neurons with mass spectrometry proteomics and cell staining. Because of the high homology between chicken and human amyloid precursor protein processing machinery, these chicken neurons can be used as an alternative to rodent models for studying Alzheimer disease.
| S-EPMC9558106 | biostudies-literature
Project description:To test the potential of canonical Wnt signalling to modulate nociception via transcriptional regulation in dorsal root ganglion (DRG) neurons, we performed a genome-wide transcriptome analysis of neuron-enriched DRG cultures treated with Wnt3a or vehicle for 6 hours.
2014-07-07 | GSE56880 | GEO
Project description:To test the potential of canonical Wnt signalling to modulate nociception via transcriptional regulation in dorsal root ganglion (DRG) neurons, we performed a genome-wide transcriptome analysis of neuron-enriched DRG cultures treated with Wnt3a or vehicle for 6 hours. Total RNA obtained from neuron-enriched mouse DRG culture subjected to Wnt3a treatment for 6 hours was compared to a matched control (vehicle-treated) DRG culture.
2014-07-07 | E-GEOD-56880 | biostudies-arrayexpress
Project description:Anaerobic enriched-cultures Raw sequence reads
| PRJNA818155 | ENA