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Jackson Laboratory cre dependent hm4di dreadd mice

(A–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A, B) and <t>NaV1.8:hM4Di</t> (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.33; time×treatment interaction p = 0.22. n = 16, paired design. (C) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.92; time×treatment interaction, p = 0.43. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (E, F) and NaV1.8:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001, n = 10 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 17 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Cre Dependent Hm4di Dreadd Mice, supplied by Jackson Laboratory, 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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cre dependent hm4di dreadd mice - by Bioz Stars, 2026-06

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1) Product Images from "IL-1β engages distinct peripheral sensory circuits to suppress feeding across time"

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

Journal: bioRxiv

doi: 10.64898/2026.02.23.707454

(A–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A, B) and NaV1.8:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.33; time×treatment interaction p = 0.22. n = 16, paired design. (C) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.92; time×treatment interaction, p = 0.43. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (E, F) and NaV1.8:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001, n = 10 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 17 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A, B) and NaV1.8:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.33; time×treatment interaction p = 0.22. n = 16, paired design. (C) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.92; time×treatment interaction, p = 0.43. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (E, F) and NaV1.8:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001, n = 10 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 17 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Injection

(A–F) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A–C) and NaV1.8:hM4Di (D–F) mice following i.p. injection with PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (A) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (D) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (G–I) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (J–L) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment (all p < 0.0001). n = 16 mice, paired design. (A–L) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A–F) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A–C) and NaV1.8:hM4Di (D–F) mice following i.p. injection with PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (A) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (D) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (G–I) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (J–L) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment (all p < 0.0001). n = 16 mice, paired design. (A–L) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Injection

(A–D) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (A, B) and Phox2b:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.96; time×treatment interaction p = 0.67. n = 13 mice, paired design. (C) Two-way repeated measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.75; time×treatment interaction, p = 0.84. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (E, F) and Phox2b:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 8 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 12 mice, paired design. (I–K) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (I) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (A–K) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A–D) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (A, B) and Phox2b:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.96; time×treatment interaction p = 0.67. n = 13 mice, paired design. (C) Two-way repeated measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.75; time×treatment interaction, p = 0.84. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (E, F) and Phox2b:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 8 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 12 mice, paired design. (I–K) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (I) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (A–K) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Injection

(A) AAV-Ctrl-mediated EGFP expression in the nodose ganglion of a NaV1.8-Cre/+ (NaV1.8:AAV-Ctrl) mouse. (B, C) Scn10a (B) and CHRM4 (C) mRNA expression in nodose ganglia measured by RT-qPCR (2^–ΔCt values normalized to Gapdh) in NaV1.8-Cre mice injected bilaterally into nodose ganglia with AAV-Ctrl (n = 4) or AAV-hM4Di (n = 5). (B) Mann–Whitney test, p = 0.557. (C) Two-tailed Fisher’s exact test, adjusted p = 0.0079. Filled symbols indicate detectable values, hollow symbols indicate non-detected amplification (set at limit of detection). (D, E) Cumulative chow intake at the indicated time point in fasted NaV1.8:AAV-Ctrl (D) or NaV1.8:AAV-hM4Di (E) nodose mice after i.p. injection of PBS or DCZ (100 μg/kg). (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.95; time×treatment interaction, p = 0.76. n = 9 mice, paired design. (E) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0187; time×treatment interaction, p = 0.0095. n = 16 mice, paired design. (F–K) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (F–H) or NaV1.8:AAV-hM4Di nodose mice (I–K) following i.p. injection of PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (F) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0014; time×treatment interaction, p = 0.0003. n = 9 mice, paired design. (I) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (L–N) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (L) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9 mice, paired design. (B–N) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A) AAV-Ctrl-mediated EGFP expression in the nodose ganglion of a NaV1.8-Cre/+ (NaV1.8:AAV-Ctrl) mouse. (B, C) Scn10a (B) and CHRM4 (C) mRNA expression in nodose ganglia measured by RT-qPCR (2^–ΔCt values normalized to Gapdh) in NaV1.8-Cre mice injected bilaterally into nodose ganglia with AAV-Ctrl (n = 4) or AAV-hM4Di (n = 5). (B) Mann–Whitney test, p = 0.557. (C) Two-tailed Fisher’s exact test, adjusted p = 0.0079. Filled symbols indicate detectable values, hollow symbols indicate non-detected amplification (set at limit of detection). (D, E) Cumulative chow intake at the indicated time point in fasted NaV1.8:AAV-Ctrl (D) or NaV1.8:AAV-hM4Di (E) nodose mice after i.p. injection of PBS or DCZ (100 μg/kg). (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.95; time×treatment interaction, p = 0.76. n = 9 mice, paired design. (E) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0187; time×treatment interaction, p = 0.0095. n = 16 mice, paired design. (F–K) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (F–H) or NaV1.8:AAV-hM4Di nodose mice (I–K) following i.p. injection of PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (F) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0014; time×treatment interaction, p = 0.0003. n = 9 mice, paired design. (I) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (L–N) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (L) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9 mice, paired design. (B–N) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Expressing, Quantitative RT-PCR, Injection, MANN-WHITNEY, Two Tailed Test, Amplification

(A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (A, E) , PGD2 (250 μg/kg) (B, F) , PGF2α (1 mg/kg) (C, G) , or PGI2 (250 μg/kg) (D, H) , with or without DCZ (100 μg/kg). (A–C) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0012; time×treatment interaction, p = 0.0025. n = 13-16 mice, paired design. (I–P) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (I, M) , PGD2 (250 μg/kg) (J, N) , PGF2α (1 mg/kg) (K, O) , or PGI2 (250 μg/kg) (L, P) , with or without DCZ (100 μg/kg) pretreatment. (I–L) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 10-14 mice, paired design. (A–P) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Figure Legend Snippet: (A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (A, E) , PGD2 (250 μg/kg) (B, F) , PGF2α (1 mg/kg) (C, G) , or PGI2 (250 μg/kg) (D, H) , with or without DCZ (100 μg/kg). (A–C) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0012; time×treatment interaction, p = 0.0025. n = 13-16 mice, paired design. (I–P) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (I, M) , PGD2 (250 μg/kg) (J, N) , PGF2α (1 mg/kg) (K, O) , or PGI2 (250 μg/kg) (L, P) , with or without DCZ (100 μg/kg) pretreatment. (I–L) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 10-14 mice, paired design. (A–P) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Techniques Used: Injection

(A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (A, B, E, F) or NaV1.8:AAV-hM4Di (C, D, G, H) nodose mice following i.p. injection with PBS, PGE2 (250 μg/kg ) (A–D) or PGD2 (250 μg/kg) (E–H) , with or without DCZ (100 μg/kg) pretreatment (A, C, E, G) . Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9–16 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (A, B, E, F) or NaV1.8:AAV-hM4Di (C, D, G, H) nodose mice following i.p. injection with PBS, PGE2 (250 μg/kg ) (A–D) or PGD2 (250 μg/kg) (E–H) , with or without DCZ (100 μg/kg) pretreatment (A, C, E, G) . Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9–16 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Injection

(A) Experimental schematic for experiments. (B–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (Ket, 15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (B) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (E–G) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL1β. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (H–J) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (H) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 16 mice, paired design. (B–J) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Figure Legend Snippet: (A) Experimental schematic for experiments. (B–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (Ket, 15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (B) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (E–G) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL1β. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (H–J) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (H) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 16 mice, paired design. (B–J) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques Used: Injection

Image Search Results

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A, B) and NaV1.8:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.33; time×treatment interaction p = 0.22. n = 16, paired design. (C) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.92; time×treatment interaction, p = 0.43. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (E, F) and NaV1.8:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001, n = 10 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 17 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Article Snippet: Chemogenetic manipulation of IL-1β and prostaglandin-induced feeding suppression involved NaV1.8-Cre (B6.129(Cg)- Scn10a tm2(cre)Jwo /TjpJ, 036564, Jackson Laboratory) and Phox2b-Cre (B6(Cg)-Tg(Phox2b-cre)3Jke/J, 016223, Jackson Laboratory) expressing mice crossed with Cre-dependent hM4Di DREADD mice (B6.129- Gt(ROSA)26Sor tm1(CAG-CHRM4*,-mCitrine)Ute /J, 026219, Jackson Laboratory) to yield double transgenic NaV1.8:hM4Di or Phox2b:hM4Di mice.

Techniques: Injection

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A–F) Cumulative chow intake at the indicated time points in fasted NaV1.8:Ctrl (A–C) and NaV1.8:hM4Di (D–F) mice following i.p. injection with PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (A) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (D) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (G–I) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (J–L) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment (all p < 0.0001). n = 16 mice, paired design. (A–L) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Techniques: Injection

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A–D) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (A, B) and Phox2b:hM4Di (C, D) mice following i.p. injection with PBS or DCZ (100 μg/kg). (A) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.96; time×treatment interaction p = 0.67. n = 13 mice, paired design. (C) Two-way repeated measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.75; time×treatment interaction, p = 0.84. n = 17 mice, paired design. (E–H) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl (E, F) and Phox2b:hM4Di (G, H) mice following i.p. injection with PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 8 mice, paired design. (G) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment, p < 0.0001. n = 12 mice, paired design. (I–K) Cumulative chow intake at the indicated time points in fasted Phox2b:Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (I) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 13 mice, paired design. (A–K) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: **p<0.01, ***p<0.001, ****p<0.0001

Techniques: Injection

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A) AAV-Ctrl-mediated EGFP expression in the nodose ganglion of a NaV1.8-Cre/+ (NaV1.8:AAV-Ctrl) mouse. (B, C) Scn10a (B) and CHRM4 (C) mRNA expression in nodose ganglia measured by RT-qPCR (2^–ΔCt values normalized to Gapdh) in NaV1.8-Cre mice injected bilaterally into nodose ganglia with AAV-Ctrl (n = 4) or AAV-hM4Di (n = 5). (B) Mann–Whitney test, p = 0.557. (C) Two-tailed Fisher’s exact test, adjusted p = 0.0079. Filled symbols indicate detectable values, hollow symbols indicate non-detected amplification (set at limit of detection). (D, E) Cumulative chow intake at the indicated time point in fasted NaV1.8:AAV-Ctrl (D) or NaV1.8:AAV-hM4Di (E) nodose mice after i.p. injection of PBS or DCZ (100 μg/kg). (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.95; time×treatment interaction, p = 0.76. n = 9 mice, paired design. (E) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0187; time×treatment interaction, p = 0.0095. n = 16 mice, paired design. (F–K) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (F–H) or NaV1.8:AAV-hM4Di nodose mice (I–K) following i.p. injection of PBS, CCK (10 μg/kg), or DCZ (100 μg/kg)+CCK. (F) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0014; time×treatment interaction, p = 0.0003. n = 9 mice, paired design. (I) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (L–N) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl mice following i.p. injection of PBS, IL-1β (5 μg/kg), or DCZ (100 μg/kg)+IL-1β. (L) Two-way repeated measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9 mice, paired design. (B–N) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques: Expressing, Quantitative RT-PCR, Injection, MANN-WHITNEY, Two Tailed Test, Amplification

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (A, E) , PGD2 (250 μg/kg) (B, F) , PGF2α (1 mg/kg) (C, G) , or PGI2 (250 μg/kg) (D, H) , with or without DCZ (100 μg/kg). (A–C) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. (D) Two-way repeated-measures ANOVA: main effect of time, p < 0.0001; main effect of treatment, p = 0.0012; time×treatment interaction, p = 0.0025. n = 13-16 mice, paired design. (I–P) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, PGE2 (250 μg/kg) (I, M) , PGD2 (250 μg/kg) (J, N) , PGF2α (1 mg/kg) (K, O) , or PGI2 (250 μg/kg) (L, P) , with or without DCZ (100 μg/kg) pretreatment. (I–L) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 10-14 mice, paired design. (A–P) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Techniques: Injection

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A–H) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-Ctrl (A, B, E, F) or NaV1.8:AAV-hM4Di (C, D, G, H) nodose mice following i.p. injection with PBS, PGE2 (250 μg/kg ) (A–D) or PGD2 (250 μg/kg) (E–H) , with or without DCZ (100 μg/kg) pretreatment (A, C, E, G) . Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 9–16 mice, paired design. (A–H) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques: Injection

Journal: bioRxiv

Article Title: IL-1β engages distinct peripheral sensory circuits to suppress feeding across time

doi: 10.64898/2026.02.23.707454

Figure Lengend Snippet: (A) Experimental schematic for experiments. (B–D) Cumulative chow intake at the indicated time points in fasted NaV1.8:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (Ket, 15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (B) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 15 mice, paired design. (E–G) Cumulative chow intake at the indicated time points in fasted Phox2b:hM4Di mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL1β. (E) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 17 mice, paired design. (H–J) Cumulative chow intake at the indicated time points in fasted NaV1.8:AAV-hM4Di nodose mice following i.p. injection with PBS, IL-1β (5 μg/kg), ketorolac (15 mg/kg)+IL-1β, or DCZ (100 μg/kg)+ketorolac+IL-1β. (H) Two-way repeated-measures ANOVA: main effects of time, treatment, and time×treatment interaction, p < 0.0001. n = 16 mice, paired design. (B–J) Error bars indicate mean ± SEM. Lines represent individual mice. Holm–Šídák post hoc comparisons: *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

Techniques: Injection

Gi designer receptors exclusively activated by designer drugs (DREADD) inhibition of microglia blocks alcohol-induced neuronal cell death. A – D: Organotypic brain slice cultures (OBSCs) from CX3CR1.Cre ERT2 .hM4di.mCitrine (+/–) mice were used to assess the role of microglia on neuronal death ex vivo. A: Representative image with or without addition of 4-hydroxy-tamoxifen (4-OH-TAM; 10 ng/mL) to induce Cre recombination, which caused a robust increase in mCitrine within ionized calcium-binding adapter molecule 1 (Iba-1) + microglia, consistent with microglial DREADD expression. Arrowheads denote colocalization between Iba-1 and mCitrine. B: Representative images of propidium iodide (PI) labeling of cell death in OBSC in response to ethanol. C: Ethanol (EtOH; 100 mmol/L; 4 days) caused a robust increase in cell death 24 hours into withdrawal, which was significantly blocked by microglial Gi signaling induced by clozapine N-oxide [CNO; two-way analysis of variance (ANOVA) main effect of ethanol F 1,20 = 11.37, P = 0.003; Sidak post test]. D and E: Induction of hM4Di Gi DREADD inhibition of microglia in vivo . CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (5 g/kg per day; intragastric) with or without CNO (3 mg/kg; intraperitoneally; 10 hours after ethanol). Assessments were performed 24 hours following the final treatment. D: Representative images of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) cell death stain in orbitofrontal cortex. E: Ethanol increased TUNEL + cell death by approximately threefold, which was prevented by Gi DREADD inhibition of proinflammatory microglia (two-way ANOVA, EtOH × CNO interaction F 1,16 = 8.5, P = 0.01; Sidak post test). N = 3 control and CNO slices ( C ); N = 10 ethanol slices ( C ); N = 8 ethanol + CNO slices ( C ); N = 4 water + phosphate-buffered saline (PBS) mice and water + CNO mice ( D and E ); N = 6 ethanol + PBS mice and ethanol + CNO mice ( D and E ). ∗ P < 0.05, ∗∗ P < 0.01. Scale bars: 20 μm ( A ); 500 μm ( B ); 25 μm ( D ).

Journal: The American Journal of Pathology

Article Title: Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol

doi: 10.1016/j.ajpath.2025.10.005

Figure Lengend Snippet: Gi designer receptors exclusively activated by designer drugs (DREADD) inhibition of microglia blocks alcohol-induced neuronal cell death. A – D: Organotypic brain slice cultures (OBSCs) from CX3CR1.Cre ERT2 .hM4di.mCitrine (+/–) mice were used to assess the role of microglia on neuronal death ex vivo. A: Representative image with or without addition of 4-hydroxy-tamoxifen (4-OH-TAM; 10 ng/mL) to induce Cre recombination, which caused a robust increase in mCitrine within ionized calcium-binding adapter molecule 1 (Iba-1) + microglia, consistent with microglial DREADD expression. Arrowheads denote colocalization between Iba-1 and mCitrine. B: Representative images of propidium iodide (PI) labeling of cell death in OBSC in response to ethanol. C: Ethanol (EtOH; 100 mmol/L; 4 days) caused a robust increase in cell death 24 hours into withdrawal, which was significantly blocked by microglial Gi signaling induced by clozapine N-oxide [CNO; two-way analysis of variance (ANOVA) main effect of ethanol F 1,20 = 11.37, P = 0.003; Sidak post test]. D and E: Induction of hM4Di Gi DREADD inhibition of microglia in vivo . CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (5 g/kg per day; intragastric) with or without CNO (3 mg/kg; intraperitoneally; 10 hours after ethanol). Assessments were performed 24 hours following the final treatment. D: Representative images of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) cell death stain in orbitofrontal cortex. E: Ethanol increased TUNEL + cell death by approximately threefold, which was prevented by Gi DREADD inhibition of proinflammatory microglia (two-way ANOVA, EtOH × CNO interaction F 1,16 = 8.5, P = 0.01; Sidak post test). N = 3 control and CNO slices ( C ); N = 10 ethanol slices ( C ); N = 8 ethanol + CNO slices ( C ); N = 4 water + phosphate-buffered saline (PBS) mice and water + CNO mice ( D and E ); N = 6 ethanol + PBS mice and ethanol + CNO mice ( D and E ). ∗ P < 0.05, ∗∗ P < 0.01. Scale bars: 20 μm ( A ); 500 μm ( B ); 25 μm ( D ).

Article Snippet: For Gi DREADD inhibition, CX3CR1.Cre ERT2 .hM4di mice were bred in-house from CX3CR1.Cre ERT2 (JAX strain 020940; 129P2 background) and DIO.hm4di mice (JAX strain 026219; 129S background) obtained from Jackson Laboratory.

Techniques: Inhibition, Slice Preparation, Ex Vivo, Binding Assay, Expressing, Labeling, In Vivo, End Labeling, TUNEL Assay, Staining, Control, Saline

Gi designer receptors exclusively activated by designer drugs inhibition of microglia fails to attenuate alcohol-induced negative affect in males. A: Experimental design. Male CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (EtOH; 5 g/kg per day; intragastric) with or without clozapine N-oxide (CNO) 10 hours after treatment. Mice underwent open field testing for anxiety-like behavior 3 days into withdrawal and conditioned fear for acquisition and extinction at 34 days into abstinence. B: hM4di expression was measured by RT-PCR. Males showed approximately 25% of the level hM4di expression as females. t- Test was used. C and D: Microglial inhibition failed to prevent the induction of anxiety-like behavior caused by alcohol seen change in the distance traveled in the center of the open field [one-way analysis of variance (ANOVA) F 2,18 = 2.0, P = 0.16; C ] and a reduction in the time spent in the center of the open field (one-way ANOVA F 2,17 = 3.99, P = 0.038; Sidak post test; D ). E: Fine motor movement was significantly reduced in the EtOH + CNO group (one-way ANOVA F 2,18 = 3.5, P = 0.05; Sidak post test). F: Ethanol had no impact on conditioned fear memory acquisition. G: Neither ethanol nor microglial inhibition had any effect on contextual fear memory (two-way ANOVA time × treatment F 8,72 = 0.9, P = 0.5). H: Microglial inhibition had no impact on fear memory extinction (one-way repeated measures ANOVAs: control F 2.86,16.19 = 3.2, P = 0.053; ethanol F 2.999,17.99 = 0.38, P = 0.77; ethanol + CNO F 1.94,11.7 = 0.9, P = 0.43). I: No robust proinflammatory gene induction signature was seen with ethanol in the hM4di mice, with little impact of microglial inhibition. ∗ P < 0.05. GFAP, glial fibrillary acidic protein; NS, not significant; TLR, toll-like receptor; TNF, tumor necrosis factor.

Journal: The American Journal of Pathology

Article Title: Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol

doi: 10.1016/j.ajpath.2025.10.005

Figure Lengend Snippet: Gi designer receptors exclusively activated by designer drugs inhibition of microglia fails to attenuate alcohol-induced negative affect in males. A: Experimental design. Male CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (EtOH; 5 g/kg per day; intragastric) with or without clozapine N-oxide (CNO) 10 hours after treatment. Mice underwent open field testing for anxiety-like behavior 3 days into withdrawal and conditioned fear for acquisition and extinction at 34 days into abstinence. B: hM4di expression was measured by RT-PCR. Males showed approximately 25% of the level hM4di expression as females. t- Test was used. C and D: Microglial inhibition failed to prevent the induction of anxiety-like behavior caused by alcohol seen change in the distance traveled in the center of the open field [one-way analysis of variance (ANOVA) F 2,18 = 2.0, P = 0.16; C ] and a reduction in the time spent in the center of the open field (one-way ANOVA F 2,17 = 3.99, P = 0.038; Sidak post test; D ). E: Fine motor movement was significantly reduced in the EtOH + CNO group (one-way ANOVA F 2,18 = 3.5, P = 0.05; Sidak post test). F: Ethanol had no impact on conditioned fear memory acquisition. G: Neither ethanol nor microglial inhibition had any effect on contextual fear memory (two-way ANOVA time × treatment F 8,72 = 0.9, P = 0.5). H: Microglial inhibition had no impact on fear memory extinction (one-way repeated measures ANOVAs: control F 2.86,16.19 = 3.2, P = 0.053; ethanol F 2.999,17.99 = 0.38, P = 0.77; ethanol + CNO F 1.94,11.7 = 0.9, P = 0.43). I: No robust proinflammatory gene induction signature was seen with ethanol in the hM4di mice, with little impact of microglial inhibition. ∗ P < 0.05. GFAP, glial fibrillary acidic protein; NS, not significant; TLR, toll-like receptor; TNF, tumor necrosis factor.

Techniques: Inhibition, Expressing, Reverse Transcription Polymerase Chain Reaction, Control

Gi designer receptors exclusively activated by designer drugs (DREADD) inhibition of microglia attenuates alcohol-induced negative affect in females. A: Experimental design. Female CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (EtOH; 5 g/kg per day; intragastric) with or without clozapine N-oxide (CNO) 10 hours after treatment. Mice underwent open field testing for anxiety-like behavior 3 days into withdrawal and conditioned fear for acquisition and extinction at 34 days into abstinence. B and C: Microglial inhibition prevented the induction of anxiety-like behavior caused by alcohol seen as a reduction in the distance traveled in the center of the open field [one-way analysis of variance (ANOVA) F 2,20 = 3.95, P = 0.036; Sidak post test; B ] and reduced time spent in the center of the open field (one-way ANOVA F 2,20 = 7.1, P = 0.0046; Sidak post test; C ). D: Microglial inhibition prevented the trend toward a reduction in fine motor movement in the open field caused by ethanol (one-way ANOVA F 2,21 = 2.16, P = 0.14). E: Ethanol had no impact on conditioned fear learning acquisition. F: In contextual fear memory assessments, ethanol increased freezing in the last minute of assessment that was prevented by microglial inhibition with CNO (two-way ANOVA time × treatment F 8,84 = 3.7, P < 0.0001; Sidak post test). G: Ethanol disrupted the extinction of conditioned fear memory, which was restored by microglial inhibition (one-way repeated measures ANOVAs: control F 2.4,13.5 = 2.1, P = 0.16; ethanol F 2.8,19.8 = 0.9, P = 0.45; ethanol + CNO F 3.0,17.6 = 6.6, P = 0.0035). H: The persistent induction of multiple proinflammatory genes in the cortex 5 weeks into abstinence was prevented by Gi DREADD inhibition of microglia (two-way ANOVA F 2,231 = 6.921, P = 0.001). I: A negative correlation between IFNA gene expression and time spent in the center of the open field was found. IFN gene expression failed a normality test; thus, a Spearman correlation coefficient was calculated. R = -0.45, P = 0.039. N = 8 female water + vehicle, ethanol + vehicle, and ethanol + CNO ( B – I ). ∗ P < 0.05, ∗∗ P < 0.01. GFAP, glial fibrillary acidic protein; NS, not significant; TNF, tumor necrosis factor.

Journal: The American Journal of Pathology

Article Title: Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol

doi: 10.1016/j.ajpath.2025.10.005

Figure Lengend Snippet: Gi designer receptors exclusively activated by designer drugs (DREADD) inhibition of microglia attenuates alcohol-induced negative affect in females. A: Experimental design. Female CX3CR1.Cre ERT2 .hM4Di (+/–) mice received 10 days of water or binge ethanol (EtOH; 5 g/kg per day; intragastric) with or without clozapine N-oxide (CNO) 10 hours after treatment. Mice underwent open field testing for anxiety-like behavior 3 days into withdrawal and conditioned fear for acquisition and extinction at 34 days into abstinence. B and C: Microglial inhibition prevented the induction of anxiety-like behavior caused by alcohol seen as a reduction in the distance traveled in the center of the open field [one-way analysis of variance (ANOVA) F 2,20 = 3.95, P = 0.036; Sidak post test; B ] and reduced time spent in the center of the open field (one-way ANOVA F 2,20 = 7.1, P = 0.0046; Sidak post test; C ). D: Microglial inhibition prevented the trend toward a reduction in fine motor movement in the open field caused by ethanol (one-way ANOVA F 2,21 = 2.16, P = 0.14). E: Ethanol had no impact on conditioned fear learning acquisition. F: In contextual fear memory assessments, ethanol increased freezing in the last minute of assessment that was prevented by microglial inhibition with CNO (two-way ANOVA time × treatment F 8,84 = 3.7, P < 0.0001; Sidak post test). G: Ethanol disrupted the extinction of conditioned fear memory, which was restored by microglial inhibition (one-way repeated measures ANOVAs: control F 2.4,13.5 = 2.1, P = 0.16; ethanol F 2.8,19.8 = 0.9, P = 0.45; ethanol + CNO F 3.0,17.6 = 6.6, P = 0.0035). H: The persistent induction of multiple proinflammatory genes in the cortex 5 weeks into abstinence was prevented by Gi DREADD inhibition of microglia (two-way ANOVA F 2,231 = 6.921, P = 0.001). I: A negative correlation between IFNA gene expression and time spent in the center of the open field was found. IFN gene expression failed a normality test; thus, a Spearman correlation coefficient was calculated. R = -0.45, P = 0.039. N = 8 female water + vehicle, ethanol + vehicle, and ethanol + CNO ( B – I ). ∗ P < 0.05, ∗∗ P < 0.01. GFAP, glial fibrillary acidic protein; NS, not significant; TNF, tumor necrosis factor.

Techniques: Inhibition, Control, Gene Expression

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