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Ceftriaxone rescues the reduced colocalization of PSD-95 and CaMKIIα induced by Poly I:C. (A) Representative image used for colocalization analysis. The red box denotes the zoomed-in ROI highlighting a primary dendrite of a single neuron. Scale bars: 20 μm (overview) and 2 μm (zoom). (B,C) Quantification of normalized expression levels at 48 h post-treatment: PSD-95 ( B , red) and CaMKIIα ( C , green). (D) Pearson’s R coefficients for colocalization of CaMKIIα and PSD-95 within primary dendrites. (E) Representative immunocytochemical staining of AMPA-receptor subunits GluA1 and <t>GluA2.</t> Scale bar: 100 μm. (F,G) Normalized expression levels of GluA1 (F) and GluA2 (G) at 48 h post-treatment. Data are presented as mean ± SEM. ** p < 0.01, **** p < 0.0001; ns, not significant.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit <t>GluA2.</t> (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.
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Image Search Results


Ceftriaxone rescues the reduced colocalization of PSD-95 and CaMKIIα induced by Poly I:C. (A) Representative image used for colocalization analysis. The red box denotes the zoomed-in ROI highlighting a primary dendrite of a single neuron. Scale bars: 20 μm (overview) and 2 μm (zoom). (B,C) Quantification of normalized expression levels at 48 h post-treatment: PSD-95 ( B , red) and CaMKIIα ( C , green). (D) Pearson’s R coefficients for colocalization of CaMKIIα and PSD-95 within primary dendrites. (E) Representative immunocytochemical staining of AMPA-receptor subunits GluA1 and GluA2. Scale bar: 100 μm. (F,G) Normalized expression levels of GluA1 (F) and GluA2 (G) at 48 h post-treatment. Data are presented as mean ± SEM. ** p < 0.01, **** p < 0.0001; ns, not significant.

Journal: Frontiers in Cellular Neuroscience

Article Title: Ceftriaxone attenuates Poly I:C–induced neuroinflammation in vitro by modulating glutamate transport, synaptic integrity, and immunometabolic reprogramming

doi: 10.3389/fncel.2025.1684398

Figure Lengend Snippet: Ceftriaxone rescues the reduced colocalization of PSD-95 and CaMKIIα induced by Poly I:C. (A) Representative image used for colocalization analysis. The red box denotes the zoomed-in ROI highlighting a primary dendrite of a single neuron. Scale bars: 20 μm (overview) and 2 μm (zoom). (B,C) Quantification of normalized expression levels at 48 h post-treatment: PSD-95 ( B , red) and CaMKIIα ( C , green). (D) Pearson’s R coefficients for colocalization of CaMKIIα and PSD-95 within primary dendrites. (E) Representative immunocytochemical staining of AMPA-receptor subunits GluA1 and GluA2. Scale bar: 100 μm. (F,G) Normalized expression levels of GluA1 (F) and GluA2 (G) at 48 h post-treatment. Data are presented as mean ± SEM. ** p < 0.01, **** p < 0.0001; ns, not significant.

Article Snippet: The primary antibodies used were CaMKIIα (goat, 1:750, Abcam, ab111890), COX4 (rabbit, 1:500, Synaptic Systems, AB_2620041), Connexin 43 (rabbit, 1:500, Sigma-Aldrich, C6219), EAAT1/GLAST-1/SLC1A3 (rabbit, 1:500, Novus Biologicals, NB100-1869), EAAT2/GLT-1 (rabbit, 1:500, Novus Biologicals, NBP1-20136), GFAP (mouse, 1:1000, Sigma-Aldrich, G3893), GluR1 (GluA1) (guinea pig, 1:400, Alomone Labs, AGP-009), GluR2 (GluA2) (rabbit, 1:400, Alomone Labs, AGC-005), IBA-1 (mouse, 1:1000, Synaptic Systems, 234011), PSD-95 (mouse, 1:750, Novus Biologicals, NB300-556), and MAP2 (chicken, 1:1000, Synaptic Systems, 188006).

Techniques: Expressing, Staining

EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit GluA2. (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.

Journal: Journal of Neurochemistry

Article Title: Extracellular Vesicles Released From Cortical Neurons Influence Spontaneous Activity of Recipient Neurons

doi: 10.1111/jnc.70231

Figure Lengend Snippet: EVs isolated from primary cultures contain AMPA receptor subunits. (A) Glutamate receptor subunits are present in EVs isolated from primary cultures, in combination with the EV‐marker CD63. (B) Immunoelectron microscopy of EVs isolated from cultured neurons support the presence of the glutamate receptor subunit GluA2. (C) EVs isolated from mouse brains ( n = 4 mice) and validated qualitatively by the presence of the EV markers Flotillin‐1 and CD81, contain both AMPA receptor subunits and Nr2b subunit of NMDA receptors. SIgnificance use of * indicates GluA2‐negative EV.

Article Snippet: Grids with EVs were incubated with the primary antibody GluA2 (AGC‐005, Alomone Labs) for 2 h. Protein A coupled to 10 nm colloidal gold particles was used to target the primary antibody (G. Posthuma, University Medical Center Utrecht) (1:50).

Techniques: Isolation, Marker, Immuno-Electron Microscopy, Cell Culture