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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. <t>hM4Di</t> labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos <t>PVN</t> <t>neurons.</t> <t>rAAV-F-RAM-d2tTA-hM4Di</t> was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).
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Image Search Results


( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. hM4Di labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos PVN neurons. rAAV-F-RAM-d2tTA-hM4Di was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).

Journal: Science Advances

Article Title: Hcn1-dependent engram neurons in the PVN encode gastric inflammatory sensitization

doi: 10.1126/sciadv.aeb6961

Figure Lengend Snippet: ( A ) Schematic of the calcium imaging experimental setup. ( B ) Representative calcium signal from PVN neurons in the gastritis group and the saline group. ( C and D ) Gastritis-induced increase in amplitude (Δ F / F ) and frequency of the calcium signal in PVN neurons (saline versus gastritis; n = 6 mice; two-tailed t test). ( E ) RAM (receptor-activated mapping) activity tagging system. hM4Di labels neurons activated after DOX withdrawal. ( F ) Schematic of chemogenetic inhibition targeting gastritis-activated Fos PVN neurons. rAAV-F-RAM-d2tTA-hM4Di was injected into the mouse PVN region. The mice were then maintained on DOX-containing diet for 2 weeks before modeling to label gastritis-activated Fos PVN neurons. After a 3-week recovery period, intraperitoneal (ip) injection of CNO (3 mg/kg) was administered to inhibit Fos PVN neurons before gastritis modeling. ( G and H ) Chemogenetic suppression significantly reduced Fos expression in PVN compared to controls ( n = 6 mice; two-tailed t test). ( I to K ) Gastric tissue injury scores and representative H&E-stained sections ( n = 6; two-tailed t test). ( L ) Chemogenetic inhibition of Fos PVN neurons attenuated gastritis-associated inflammatory cytokine levels versus controls ( n = 6; two-tailed t test). ( M ) Schematic of optogenetic inhibition of Fos PVN neurons. ( N to P ) Gastric injury scores and H&E staining ( n = 6; two-tailed t test). ( Q ) Optogenetic inhibition reduced inflammatory cytokines compared to the control group ( n = 6; two-tailed t test).

Article Snippet: rAAV-F-RAM-d2tTA-hM4Di (200 nl per side, GeneChem) was injected bilaterally into the PVN or PSTh.

Techniques: Imaging, Saline, Two Tailed Test, Activity Assay, Inhibition, Injection, Expressing, Staining, Control