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neural tissue dissociation kit postnatal neurons  (Miltenyi Biotec)


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    Miltenyi Biotec neural tissue dissociation kit postnatal neurons
    Neural Tissue Dissociation Kit Postnatal Neurons, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 119 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/neuronal/Neural+Tissue+Dissociation+Kit+-+Postnatal+Neurons/bio_rxiv__64898__2026__07__02__735775-309-6-11
    Average 97 stars, based on 119 article reviews
    neural tissue dissociation kit postnatal neurons - by Bioz Stars, 2026-09
    97/100 stars

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    Article Title: Minimizing the ex vivo confounds of cell-isolation techniques on transcriptomic -profiles of purified microglia
    Article Snippet: .. To test the effect of transcription and translation inhibitors on the relative abundance of cell types following cell preparation, aliquots of cells were stained with: 1) Microglial (Cd11b-APC (M1/70, #130-113-793, Miltenyi Biotec) / Cd45-Vioblue (REA737, #130-110-802, Miltenyi Biotec)), 2) Neuronal (Cd24-Vioblue (REA743, #130-110-831, Miltenyi Biotec)), 3) Astrocytic (ACSA2-APC (REA969, #130-116-245, Miltenyi Biotec)), or 4) Oligodendrocytic (O4-APC (REA576, #130-119-982, Miltenyi Biotec)) fluorophore-conjugated antibodies, according to manufacturer’s instructions. ..

    Article Title: Minimizing the <i>Ex Vivo</i> Confounds of Cell-Isolation Techniques on Transcriptomic and Translatomic Profiles of Purified Microglia
    Article Snippet: .. To test the effect of cell preparation method on the relative abundance of cell types, aliquots of cells were stained with the following: (1) microglial [CD11b-APC (M1/70, #130-113-793, Miltenyi Biotec)/CD45-VioBlue (REA737, #130-110-802, Miltenyi Biotec)]; (2) neuronal [CD24-VioBlue March/April 2022, 9(2) ENEURO.0348-21.2022 eNeuro.org (REA743, #130-110-831, Miltenyi Biotec)]; (3) astrocytic [ACSA2-APC (REA969, #130-116-245, Miltenyi Biotec)]; or (4) Oligodendrocytic [O4-APC (REA576, #130-119-982, Miltenyi Biotec)] fluorophore-conjugated antibodies, according to manufacturer’s instructions. ..

    Article Title: Minimizing the Ex Vivo Confounds of Cell-Isolation Techniques on Transcriptomic and Translatomic Profiles of Purified Microglia
    Article Snippet: .. To test the effect of cell preparation method on the relative abundance of cell types, aliquots of cells were stained with the following: (1) microglial [CD11b-APC (M1/70, #130-113-793, Miltenyi Biotec)/CD45-VioBlue (REA737, #130-110-802, Miltenyi Biotec)]; (2) neuronal [CD24-VioBlue (REA743, #130-110-831, Miltenyi Biotec)]; (3) astrocytic [ACSA2-APC (REA969, #130-116-245, Miltenyi Biotec)]; or (4) Oligodendrocytic [O4-APC (REA576, #130-119-982, Miltenyi Biotec)] fluorophore-conjugated antibodies, according to manufacturer’s instructions. ..



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    Miltenyi Biotec neural tissue dissociation kit postnatal neurons
    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 <t>against</t> <t>Tuj-1</t> 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.
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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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    (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