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primary neurons  (MedChemExpress)


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    Structured Review

    MedChemExpress primary neurons
    Primary Neurons, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/neurons/MTCO2+Antibody/pm41518198-272-0-45
    Average 97 stars, based on 36 article reviews
    primary neurons - by Bioz Stars, 2026-09
    97/100 stars

    Images

    Related Articles

    Activity Assay:

    Article Title: Pharmacological suppression of lactate mitigates postoperative cognitive dysfunction.
    Article Snippet: Hippocampal metabolic reprogramming from oxidative phosphorylation to glycolysis is a pathological feature in postoperative cognitive dysfunction (POCD).. However, the relationship between elevated lactate levels and cognitive deficits following surgical trauma needs to be further illuminated.. The lactate dehydrogenase-A (LDHA) inhibitor oxamate (OXA) and the lactate transporter inhibitor α -cyano-4-hydroxycinnamate (4-CIN) were delivered by intraperitoneal administration before POCD modeling.

    Article Title: Targeting p75NTR activity alleviates the neurotoxic effect of high glucose on iPSC-derived dopaminergic neurons
    Article Snippet: To investigate the induction of osmotic stress, neurons were treated with 100 mM l -glucose (Sigma, G5500), 100 mM mannitol (Sigma, M4125), or 100 mM d -glucose (Sigma, G8769) for 48 h. .. To inhibit p75NTR activity, neurons were treated with 2.5 ng/ml p75NTR MC-192 (Abcam, ab6172) or 400nM LM11A-31 (MedChemExpress, HY-117088) for 48 h. For sortilin inhibition, neurons were treated with 1 μM AF38469 (MedChemExpress, HY-12802) for 48 h. .. The Amyloid-β (1–42) peptide was purchased from AnaSpec (AS-20276, AnaSpec, Fremont, CA, USA) and oligomers were prepared according to the manufacturer’s instructions and previously described protocols [ , ].

    Saline:

    Article Title: Pharmacological suppression of lactate mitigates postoperative cognitive dysfunction.
    Article Snippet: Hippocampal metabolic reprogramming from oxidative phosphorylation to glycolysis is a pathological feature in postoperative cognitive dysfunction (POCD).. However, the relationship between elevated lactate levels and cognitive deficits following surgical trauma needs to be further illuminated.. The lactate dehydrogenase-A (LDHA) inhibitor oxamate (OXA) and the lactate transporter inhibitor α -cyano-4-hydroxycinnamate (4-CIN) were delivered by intraperitoneal administration before POCD modeling.

    Membrane:

    Article Title: Extracellular Vesicle–Mediated O-GlcNAcase Transfer Drives Neuronal Necroptosis to Facilitate Gallbladder Cancer Perineural Invasion
    Article Snippet: .. To assess membrane integrity and cell damage in neurons and BMDMs, LDH release was quantified using a commercial LDH Assay Kit (MedChemExpress, HY-K1090). ..

    Lactate Dehydrogenase Assay:

    Article Title: Extracellular Vesicle–Mediated O-GlcNAcase Transfer Drives Neuronal Necroptosis to Facilitate Gallbladder Cancer Perineural Invasion
    Article Snippet: .. To assess membrane integrity and cell damage in neurons and BMDMs, LDH release was quantified using a commercial LDH Assay Kit (MedChemExpress, HY-K1090). ..

    Phospho-proteomics:

    Article Title: Excessive mitochondrial stress response triggers neuronal injury through the persistent eIF2α phosphorylation in mice exposed to manganese.
    Article Snippet: • Excessive MSR is involved in neurocognitive abnormalities following Mn

    Cell Culture:

    Article Title: USP5-C-MAF Axis Regulates Autophagy-Dependent Neuronal Ferroptosis in Spinal Cord Injury Therapeutics.
    Article Snippet: .. Cultured neurons were incubated with PI (5 μg/mL, HY- D0815, MedChemExpress) at 37°C for 10 min. After incubation, the cells were washed with PBS to remove excess dye. ..

    Incubation:

    Article Title: USP5-C-MAF Axis Regulates Autophagy-Dependent Neuronal Ferroptosis in Spinal Cord Injury Therapeutics.
    Article Snippet: .. Cultured neurons were incubated with PI (5 μg/mL, HY- D0815, MedChemExpress) at 37°C for 10 min. After incubation, the cells were washed with PBS to remove excess dye. ..

    Inhibition:

    Article Title: Targeting p75NTR activity alleviates the neurotoxic effect of high glucose on iPSC-derived dopaminergic neurons
    Article Snippet: To investigate the induction of osmotic stress, neurons were treated with 100 mM l -glucose (Sigma, G5500), 100 mM mannitol (Sigma, M4125), or 100 mM d -glucose (Sigma, G8769) for 48 h. .. To inhibit p75NTR activity, neurons were treated with 2.5 ng/ml p75NTR MC-192 (Abcam, ab6172) or 400nM LM11A-31 (MedChemExpress, HY-117088) for 48 h. For sortilin inhibition, neurons were treated with 1 μM AF38469 (MedChemExpress, HY-12802) for 48 h. .. The Amyloid-β (1–42) peptide was purchased from AnaSpec (AS-20276, AnaSpec, Fremont, CA, USA) and oligomers were prepared according to the manufacturer’s instructions and previously described protocols [ , ].

    Imaging:

    Article Title: Triggering action potentials of a single neuron by multiphoton excitation elicits visually guided behavior
    Article Snippet: The neurons were processed with YM-58483 (10 μM; Y4895, Sigma) for 20 minutes to block the SOC channels. .. Further, the neurons were processed with Caloxin 2A1 (400 μM; HY-P3278A, MedChemExpress) until the end of imaging to block the PMCA. ..

    Blocking Assay:

    Article Title: Triggering action potentials of a single neuron by multiphoton excitation elicits visually guided behavior
    Article Snippet: The neurons were processed with YM-58483 (10 μM; Y4895, Sigma) for 20 minutes to block the SOC channels. .. Further, the neurons were processed with Caloxin 2A1 (400 μM; HY-P3278A, MedChemExpress) until the end of imaging to block the PMCA. ..



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    (A) Experimental design for <t>chemogenetic</t> suppression of excitatory neurons during in vivo imaging of ATP dynamics and microglial morphology. AAV-CaMKII-Cre, AAV-hSyn-DIO-hM4D(Gi)-mCherry, and AAV-hSyn-GRAB-ATP1.0 were injected into the motor cortex of Cx3cr1 GFP/+ mice, followed by DCZ administration. (B) Representative time-lapse images showing ATP events and microglial morphology near mCherry-positive Gi-DREADD-expressing neurons after DCZ administration. Dashed lines indicate mCherry-positive neuronal somata. The arrowhead indicates an ATP hotspot, and the arrow indicates a newly formed BE. (C and D) Quantification of ATP hotspot frequency (C) and ATP hotspot size (D) before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (E) Nearest-neighbor distance between ATP hotspots and mCherry-positive Gi-DREADD-expressing neurons compared with a random spatial model (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (F) Quantification of BEs per ATP hotspot before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (G) Correlation between BE number and ATP hotspot area after DCZ administration (simple linear regression; n = 30 ATP hotspots; data collected from 4 mice). (H) Experimental design for freely moving miniature two-photon imaging combined with EEG and EMG recordings to monitor ATP dynamics across sleep-wake states. (I) Representative EEG spectrograms, EMG traces, and vigilance-state classifications during dark and light phases. W, wake; N, NREM sleep; R, REM sleep. (J) Quantification of time spent in wake, NREM sleep, and REM sleep during dark and light phases (n = 6 mice). (K) Representative GRAB-ATP fluorescence images during dark and light phases. Arrowheads indicate ATP hotspots. (L) Quantification of ATP hotspot event frequency during dark and light phases (two-sided paired t-test, n = 6 mice). (M) Quantification of ATP hotspot area during dark and light phases (two-sided unpaired t-test; dark, n = 24 ATP hotspots; light, n = 57 ATP hotspots; data collected from 6 mice). (N) Representative images showing microglial BEs during awake and NREM sleep states. Insets show BE dynamics over time. (O) Quantification of BE number during awake and NREM sleep states (two-sided paired t-test, n = 5 mice). Data are shown as mean ± SEM. Individual points represent mice, ATP hotspots, or BEs as indicated. ns, not significant.
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    Image Search Results


    Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

    Journal: Bioactive Materials

    Article Title: A cell motility-based selective hydrogel enables rapid generation of nerve-repairing blood clots

    doi: 10.1016/j.bioactmat.2026.05.015

    Figure Lengend Snippet: Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

    Article Snippet: Then, the samples were fixed and stained with astrocyte marker GFAP (1:500, CST, Rabbit mAb #80788) and neuron marker Tuj-1 (1:200, HUABIO, SP06-00) to assess differentiation.

    Techniques: Derivative Assay, Membrane, Staining, CCK-8 Assay, Immunostaining, Control, Migration

    (A) Experimental design for chemogenetic suppression of excitatory neurons during in vivo imaging of ATP dynamics and microglial morphology. AAV-CaMKII-Cre, AAV-hSyn-DIO-hM4D(Gi)-mCherry, and AAV-hSyn-GRAB-ATP1.0 were injected into the motor cortex of Cx3cr1 GFP/+ mice, followed by DCZ administration. (B) Representative time-lapse images showing ATP events and microglial morphology near mCherry-positive Gi-DREADD-expressing neurons after DCZ administration. Dashed lines indicate mCherry-positive neuronal somata. The arrowhead indicates an ATP hotspot, and the arrow indicates a newly formed BE. (C and D) Quantification of ATP hotspot frequency (C) and ATP hotspot size (D) before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (E) Nearest-neighbor distance between ATP hotspots and mCherry-positive Gi-DREADD-expressing neurons compared with a random spatial model (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (F) Quantification of BEs per ATP hotspot before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (G) Correlation between BE number and ATP hotspot area after DCZ administration (simple linear regression; n = 30 ATP hotspots; data collected from 4 mice). (H) Experimental design for freely moving miniature two-photon imaging combined with EEG and EMG recordings to monitor ATP dynamics across sleep-wake states. (I) Representative EEG spectrograms, EMG traces, and vigilance-state classifications during dark and light phases. W, wake; N, NREM sleep; R, REM sleep. (J) Quantification of time spent in wake, NREM sleep, and REM sleep during dark and light phases (n = 6 mice). (K) Representative GRAB-ATP fluorescence images during dark and light phases. Arrowheads indicate ATP hotspots. (L) Quantification of ATP hotspot event frequency during dark and light phases (two-sided paired t-test, n = 6 mice). (M) Quantification of ATP hotspot area during dark and light phases (two-sided unpaired t-test; dark, n = 24 ATP hotspots; light, n = 57 ATP hotspots; data collected from 6 mice). (N) Representative images showing microglial BEs during awake and NREM sleep states. Insets show BE dynamics over time. (O) Quantification of BE number during awake and NREM sleep states (two-sided paired t-test, n = 5 mice). Data are shown as mean ± SEM. Individual points represent mice, ATP hotspots, or BEs as indicated. ns, not significant.

    Journal: bioRxiv

    Article Title: Astrocyte-to-microglia purinergic signaling mediates synaptic shielding and promotes neuronal activity

    doi: 10.64898/2026.07.05.735345

    Figure Lengend Snippet: (A) Experimental design for chemogenetic suppression of excitatory neurons during in vivo imaging of ATP dynamics and microglial morphology. AAV-CaMKII-Cre, AAV-hSyn-DIO-hM4D(Gi)-mCherry, and AAV-hSyn-GRAB-ATP1.0 were injected into the motor cortex of Cx3cr1 GFP/+ mice, followed by DCZ administration. (B) Representative time-lapse images showing ATP events and microglial morphology near mCherry-positive Gi-DREADD-expressing neurons after DCZ administration. Dashed lines indicate mCherry-positive neuronal somata. The arrowhead indicates an ATP hotspot, and the arrow indicates a newly formed BE. (C and D) Quantification of ATP hotspot frequency (C) and ATP hotspot size (D) before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (E) Nearest-neighbor distance between ATP hotspots and mCherry-positive Gi-DREADD-expressing neurons compared with a random spatial model (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (F) Quantification of BEs per ATP hotspot before and after DCZ administration (one-way ANOVA with Dunnett’s multiple-comparisons test, n = 4 mice). (G) Correlation between BE number and ATP hotspot area after DCZ administration (simple linear regression; n = 30 ATP hotspots; data collected from 4 mice). (H) Experimental design for freely moving miniature two-photon imaging combined with EEG and EMG recordings to monitor ATP dynamics across sleep-wake states. (I) Representative EEG spectrograms, EMG traces, and vigilance-state classifications during dark and light phases. W, wake; N, NREM sleep; R, REM sleep. (J) Quantification of time spent in wake, NREM sleep, and REM sleep during dark and light phases (n = 6 mice). (K) Representative GRAB-ATP fluorescence images during dark and light phases. Arrowheads indicate ATP hotspots. (L) Quantification of ATP hotspot event frequency during dark and light phases (two-sided paired t-test, n = 6 mice). (M) Quantification of ATP hotspot area during dark and light phases (two-sided unpaired t-test; dark, n = 24 ATP hotspots; light, n = 57 ATP hotspots; data collected from 6 mice). (N) Representative images showing microglial BEs during awake and NREM sleep states. Insets show BE dynamics over time. (O) Quantification of BE number during awake and NREM sleep states (two-sided paired t-test, n = 5 mice). Data are shown as mean ± SEM. Individual points represent mice, ATP hotspots, or BEs as indicated. ns, not significant.

    Article Snippet: For chemogenetic neuronal silencing experiments, deschloroclozapine (DCZ; #HY-42110, MedChemExpress) was administered intraperitoneally at 100 μg/kg during in vivo imaging.

    Techniques: In Vivo Imaging, Injection, Expressing, Imaging, Fluorescence