Fig 1: Plasma concentrations of CXCL12 [stromal cell-derived factor-1 (SDF-1)], CX3CL1 (fractalkine), and CCL11 (eotaxin-1) in male Wistar rats exposed to ethanol and acute stress. (A) CXCL12 (SDF-1) and (B) CX3CL1 (fractalkine) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle. (C) CCL11 (eotaxin-1) concentrations were determined in rats exposed to ethanol (3 g/kg, i.g.) during 4 weeks or vehicle with/without acute stress before ethanol exposure. Bars are means and SEM (nanograms per milliliter). CXCL12 and CX3CL1 concentrations were analyzed by Student’s t-test and &&p < 0.01 denotes significant differences compared to the vehicle group. CCL11 concentrations were analyzed by two-way analysis of variance (ANOVA) and **p < 0.01 and ***p < 0.001 denote significant main effect of “stress” and “ethanol exposure,” respectively. (D) CXCL12 (SDF-1); (E) CX3CL1 (fractalkine); and (F) CCL11 (eotaxin-1) concentrations were determined in rats exposed to acute ethanol (3 g/kg, i.g.) at 0, 30, 60, 120, and 240 min after ethanol exposure. Circles are means and SEM (nanograms per milliliter). CXCL12, CX3CL1, and CCL11 concentrations were analyzed by one-way ANOVA and *p < 0.05, **p < 0.01, and ***p < 0.001 denote significant main effect of “time.” +p < 0.05 and ++p < 0.01 denote significant differences compared to t = 0 min. White circles are means and SEM (nanograms per milliliter) at t = 240 min with no ethanol exposure and concentrations were analyzed by Student’s t-test. &p < 0.05 denotes significant differences compared to t = 0 or 240 min with no ethanol.
Fig 2: Brain mRNA expression levels of inflammatory markers, neurotrophic factors, and the α7 nAChR in young, and cognitively unimpaired (AU) or impaired (AI) aged rats. (A-C) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) IL-1β mRNA levels. (D-F) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) MIP-1α mRNA levels. (G-I) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) CX3CL1 mRNA levels. (J-L) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) ICAM-1 mRNA levels. (M-O) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) CNTF mRNA levels. (P-R) Neocortical (nyoung = 5, nAU = 5, nAI = 5), striatal (nyoung = 5, nAU = 5, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) BDNF mRNA levels. (S-U) Neocortical (nyoung = 5, nAU = 4, nAI = 5), striatal (nyoung = 5, nAU = 4, nAI = 5), and hippocampal (nyoung = 5, nAU = 5, nAI = 5) α7 nAChR mRNA levels. Asterisks mark significant changes in mRNA expression levels compared to young animals: ***P < .001, **P < .01, *P < .05 (univariate ANOVA + post hoc LSD). CHRNA7, α7 nicotinic acetylcholine receptors; BDNF, brain-derived neurotrophic factor; CNTF, ciliary neurotrophic factor; ICAM-1, intercellular adhesion molecule 1; IL-1β, interleukin-1β; MIP-1α, macrophage inflammatory protein 1α.
Fig 3: Effects of repeated cocaine exposure on the relative mRNA expression of Cx3cl1 and Cx3cr1 in the hippocampus of rats.Basal Cx3cl1 mRNA levels in male and female control rats at different time points after vehicle administration (fold change vs. males, dose 0) (A). Relative Cx3cl1 mRNA levels in male (B) and female rats (C) 2, 72, and 240 h after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats at different time points after vehicle administration (fold change vs. males, dose 0) (D). Relative Cx3cr1 mRNA levels in male (E) and female rats (F) 2, 72, and 240 h after vehicle or cocaine treatment. Relative mRNA levels were analyzed by two-way ANOVA. Bars represent the mean ± SEM (6–8 rats/group). (*) p < 0.05 indicates significant differences compared with their respective vehicle group.
Fig 4: Effects of acute cocaine exposure on the relative mRNA expression of Cx3cl1 and Cx3cr1 in the hippocampus of rats.Basal Cx3cl1 mRNA levels in male and female control rats 30 min after vehicle administration (fold change vs. males, dose 0) (A). Relative Cx3cl1 mRNA levels in male (B) and female rats (C) 30 min after vehicle or cocaine treatment. Basal Cx3cl1 mRNA levels in male and female control rats 240 min after vehicle administration (fold change vs. males, dose 0) (D). Relative Cx3cl1 mRNA levels in male (E) and female rats (F) 240 min after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats 30 min after vehicle administration (fold change vs. males, dose 0) (G). Relative Cx3cr1 mRNA levels in male (H) and female rats (I) 30 min after vehicle or cocaine treatment. Basal Cx3cr1 mRNA levels in male and female control rats 240 min after vehicle administration (fold change vs. males, dose 0) (J). Relative Cx3cr1 mRNA levels in male (K) and female rats (L) 240 min after vehicle or cocaine treatment. Basal mRNA levels were analyzed using Student’s t-test (Fig. 3A, 3D, 3G, and 3J). Relative mRNA levels were analyzed by one-way ANOVA in male and female rats. Bars represent the mean ± SEM (6–7 rats/group). (^) p < 0.05 and (^^^) p < 0.001 indicate significant differences compared with control males/dose 0. (*) p < 0.05, (**) p < 0.01, and (***) p < 0.001 indicate significant differences compared with the vehicle group. (#) p < 0.05 and (###) p < 0.001 indicates significant differences compared with the group treated with 5 mg/kg.
Fig 5: Effects of acute and repeated cocaine exposure on plasma CX3CL1 concentrations in rats.Basal CX3CL1 concentrations in male and female control rats 30 min after vehicle administration (A). Plasma CX3CL1 concentrations in male (B) and female rats (C) 30 min after vehicle or cocaine treatment. Basal CX3CL1 concentrations in male and female control rats 240 min after vehicle administration (D). Plasma CX3CL1 concentrations in male (E) and female rats (F) 240 min after vehicle or cocaine treatment. Basal CX3CL1 concentrations in male and female control rats at different time points after vehicle administration (G). Plasma CX3CL1 concentrations in male (H) and female rats (I) 2, 72, and 240 h after vehicle or cocaine treatment. Basal CX3CL1 concentrations were analyzed using Student’s t-test (Fig. 5A and 5D) or by two-way ANOVA (Fig. 5G). CX3CL1 concentrations from acute treatment in male and female rats were analyzed by one-way ANOVA (.Fig. 5B, 5C, 5E, and 5F). CX3CL1 concentrations from repeated treatment in male and female rats were analyzed by two-way ANOVA (Fig. 5H and 5I). Bars represent the mean ± SEM (6–8 rats/group). (^) p < 0.05 indicates significant differences compared with control males. (+) p < 0.05 indicates significant differences compared with control females at 2 h. (*) p < 0.05 indicates significant differences compared with the vehicle group and (#) p < 0.05 indicates significant differences compared with the group treated with 5 mg/kg.
Supplier Page from Abcam for Rat Fractalkine ELISA Kit (CX3CL1)