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    Hello Bio Inc clozapine n oxide
    Clozapine N Oxide, supplied by Hello Bio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
    Recombinant Proteins Clozapine N Oxide Sigma Aldrich C0832 Hoechst 33342 Thermo Fisher Scientific H3507 Experimental Models, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., <t>Days</t> <t>4–6);</t> <t>clozapine-N-oxide</t> (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.
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    (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., Days 4–6); clozapine-N-oxide (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.

    Journal: bioRxiv

    Article Title: Microglial pruning of extinction-ensemble synapses preserves fear memory

    doi: 10.64898/2026.05.05.722833

    Figure Lengend Snippet: (A) Experimental design. FosTRAP2 mice received intracerebroventricular (ICV) injection of AAV-hSyn-DIO-hM3Dq-mCherry or control AAV-hSyn-DIO-mCherry (Day –28). Fear ensemble neurons were TRAP-labeled by 4-OHT immediately after conditioning (Cond., Day 1), restricting hM3Dq-mCherry or mCherry expression to conditioning-activated neurons. Mice then underwent extinction training (Ext., Days 4–6); clozapine-N-oxide (CNO) was delivered intraperitoneally immediately after each extinction session to engage hM3Dq during the post-session window, followed by an extinction retrieval test (Ext. Retr., Day 7). (B) Chemogenetic validation. Representative mPFC images showing mCherry control expression (top) or hM3Dq-mCherry expression (bottom). Right, representative whole-cell current-clamp recordings from an hM3Dq + neuron showing robust depolarization and high-frequency firing in response to bath-applied CNO (100 μM). Scale bar, 20 μm. (C) Behavioral effects. Freezing during CS presentations across Cond., Ext., and Ext. Retr. in mCherry controls ( n = 8 mice) and hM3Dq-mCherry mice ( n = 10 mice). Post-session chemogenetic activation of fear-ensemble neurons accelerated extinction learning and reduced freezing at extinction retrieval. Data are mean ± s.e.m. * P < 0.05, ** P < 0.01, two-way repeated-measures ANOVA for Ext. and unpaired Student’s t test at Ext. Retr.

    Article Snippet: Designer receptors exclusively activated by designer drugs (DREADDs; hM3Dq or hM4Di) were manipulated in vivo with clozapine-N-oxide (CNO; MedChemExpress, HY-17366A).

    Techniques: Injection, Control, Labeling, Expressing, Biomarker Discovery, Activation Assay