Article Figures & Data
Figures
- Figure 1.
Experimental timeline showing each of the imaging sessions in relation to periods of cocaine or sucrose self-administration and abstinence.
- Figure 2.
Self-administration behavior. A, Rats increased their cocaine intake across 14 d of self-administration with daily 6 h access. B, Both the cocaine and sucrose self-administration groups preferred the active nose poke over the inactive nose poke. Data are presented as the mean ± SEM.
- Figure 3.
Seed-based functional connectivity maps illustrating left and right hemisphere seeds for striatal and cortical regions. Maps are composite statistical maps from the chamber exposure control group at baseline. Regions showing significant functional connectivity with the seed region are displayed (uncorrected threshold, t > 2.4, p < 0.05). Green arrows indicate the seed region in each map. Each region shows 2 contiguous slices of 12 total coronal slices scanned from rostral to caudal in the brain.
- Figure 4.
Three-dimensional functional connectivity maps of the rat brain illustrating significant effects of sucrose or cocaine self-administration and Abs. A, Chamber exposure controls showed no change at 1d Abs and an increase in cortical functional connectivity at 14d Abs. B, The sucrose group largely showed increased connectivity in subcortical areas at 1d Abs. C, The cocaine group showed increased functional connectivity in subcortical areas, including thalamic, hypothalamic, and forebrain regions at 1d Abs, whereas decreases were observed at 14d Abs. All maps are composites of n = 5-8 rats and are set at a correlation threshold (edge weight) value of 0.3. Spheres represent node strength, and line thicknesses represent edge weights.
- Figure 5.
Cocaine self-administration increases modularity, clustering, and small worldness at 1d Abs. A, Node strength. B, Clustering coefficient. C, Modularity. D, Average path length. E, Small worldness. All data are the mean ± SE. *Cocaine group vs control; **sucrose group vs control at 14 Abs. Two-way repeated-measures ANOVA used with Tukey’s multiple-comparison post hoc test (α < 0.05).
- Figure 6.
Cocaine or sucrose self-administration increased clustering across limbic, cortical, and thalamic regions at 1d Abs. *Cocaine group vs chamber exposure controls at 1d Abs; **sucrose group vs chamber exposure controls at 1d Abs. Repeated-measures ANOVA with Tukey’s multiple-comparison test (α < 0.05).
- Figure 7.
No correlation between cocaine self-administration and global and regional brain clustering coefficient was observed. A, Cocaine intake data for global clustering coefficient in chamber exposure controls and cocaine-treated rats. B, Nose-poke data for the same groups as in A. C, D, Nose-poke and cocaine intake correlations with regional clustering coefficients of cocaine rats. Blue circles, Baseline day; red squares, 1d Abs; black triangles, 14d Abs.
Tables
- Table 1.
Regions showing significant bilateral group × session interactions for clustering coefficient
Regions Baseline 1d Abs 14d Abs Chamber control Sucrose SA Cocaine SA Chamber control Sucrose SA Cocaine SA Chamber control Sucrose SA Cocaine SA CeA 0.27 ± 0.02 0.33 ± 0.06 0.35 ± 0.02 0.29 ± 0.03 0.47 ± 0.06 0.43 ± 0.04* 0.41 ± 0.05 0.31 ± 0.02 0.39 ± 0.06 BaA 0.28 ± 0.02 0.35 ± 0.04 0.35 ± 0.03 0.28 ± 0.03 0.41 ± 0.05 0.41 ± 0.05* 0.36 ± 0.04 0.30 ± 0.01 0.31 ± 0.04 NAc 0.25 ± 0.04 0.33 ± 0.06 0.30 ± 0.03 0.31 ± 0.05 0.42 ± 0.05 0.49 ± 0.08* 0.41 ± 0.06 0.28 ± 0.03 0.33 ± 0.03 dHPC 0.32 ± 0.04 0.42 ± 0.07 0.34 ± 0.04 0.32 ± 0.05 0.45 ± 0.11 0.46 ± 0.03* 0.41 ± 0.03 0.38 ± 0.04 0.31 ± 0.02 VP 0.28 ± 0.02 0.34 ± 0.05 0.36 ± 0.05 0.30 ± 0.06 0.43 ± 0.04 0.50 ± 0.08* 0.42 ± 0.04 0.31 ± 0.02 0.35 ± 0.04 GP 0.28 ± 0.03 0.31 ± 0.04 0.37 ± 0.04 0.34 ± 0.05 0.43 ± 0.01 0.47 ± 0.07 0.39 ± 0.05 0.27 ± 0.03 0.30 ± 0.05 LH 0.28 ± 0.02 0.34 ± 0.03 0.40 ± 0.03 0.30 ± 0.02 0.39 ± 0.05 0.45 ± 0.05* 0.35 ± 0.04 0.31 ± 0.03 0.32 ± 0.04 PV Thal 0.31 ± 0.02 0.41 ± 0.05 0.39 ± 0.05 0.34 ± 0.05 0.51 ± 0.04 0.55 ± 0.07* 0.42 ± 0.04 0.30 ± 0.02 0.34 ± 0.05 AP Thal 0.31 ± 0.01 0.45 ± 0.06 0.40 ± 0.04 0.32 ± 0.04 0.46 ± 0.08 0.58 ± 0.06* 0.40 ± 0.03 0.30 ± 0.04 0.33 ± 0.03 RN Thal 0.29 ± 0.04 0.33 ± 0.07 0.39 ± 0.04 0.32 ± 0.05 0.43 ± 0.05 0.41 ± 0.04 0.45 ± 0.06 0.28 ± 0.04 0.34 ± 0.05 MD Thal 0.35 ± 0.03 0.42 ± 0.04 0.33 ± 0.03 0.32 ± 0.05 0.41 ± 0.05 0.48 ± 0.06* 0.36 ± 0.03 0.32 ± 0.02 0.30 ± 0.02 VL Thal 0.32 ± 0.02 0.35 ± 0.03 0.38 ± 0.03 0.32 ± 0.04 0.45 ± 0.04* 0.47 ± 0.05* 0.40 ± 0.03 0.30 ± 0.00 0.38 ± 0.01 VPM Thal 0.27 ± 0.04 0.35 ± 0.06 0.35 ± 0.03 0.32 ± 0.03 0.57 ± 0.06* 0.39 ± 0.08* 0.38 ± 0.05 0.32 ± 0.03 0.34 ± 0.04 LP Thal 0.33 ± 0.02 0.41 ± 0.08 0.35 ± 0.04 0.31 ± 0.03 0.47 ± 0.10* 0.54 ± 0.04* 0.37 ± 0.03 0.26 ± 0.04 0.31 ± 0.02 Pf Thal 0.30 ± 0.03 0.39 ± 0.05 0.31 ± 0.03 0.29 ± 0.04 0.46 ± 0.01* 0.51 ± 0.06* 0.42 ± 0.07 0.32 ± 0.01 0.34 ± 0.02 LG Thal 0.33 ± 0.03 0.41 ± 0.04 0.33 ± 0.05 0.33 ± 0.05 0.47 ± 0.04 0.52 ± 0.04* 0.40 ± 0.06 0.33 ± 0.03 0.37 ± 0.04 PrL 0.33 ± 0.02 0.36 ± 0.05 0.30 ± 0.02 0.31 ± 0.05 0.41 ± 0.02 0.40 ± 0.03 0.43 ± 0.06 0.31 ± 0.02 0.36 ± 0.04 IL 0.30 ± 0.03 0.28 ± 0.02 0.30 ± 0.01 0.31 ± 0.06 0.49 ± 0.12 0.43 ± 0.06 0.43 ± 0.08 0.28 ± 0.03 0.32 ± 0.04 M2 0.29 ± 0.03 0.28 ± 0.00 0.39 ± 0.05 0.29 ± 0.05 0.33 ± 0.07 0.46 ± 0.06 0.50 ± 0.08 0.31 ± 0.03 0.36 ± 0.03 S1 jw 0.29 ± 0.03 0.39 ± 0.04 0.28 ± 0.02 0.31 ± 0.04 0.42 ± 0.04 0.38 ± 0.08 0.43 ± 0.04 0.30 ± 0.03 0.34 ± 0.05 S1 ul 0.28 ± 0.02 0.31 ± 0.01 0.37 ± 0.05 0.29 ± 0.03 0.38 ± 0.05 0.44 ± 0.07* 0.40 ± 0.03 0.30 ± 0.04 0.35 ± 0.04 S1 Sh 0.29 ± 0.02 0.36 ± 0.03 0.33 ± 0.03 0.33 ± 0.05 0.44 ± 0.05 0.49 ± 0.07* 0.38 ± 0.04 0.29 ± 0.02 0.32 ± 0.04 S2 0.28 ± 0.03 0.33 ± 0.02 0.39 ± 0.05 0.31 ± 0.05 0.39 ± 0.06 0.48 ± 0.05* 0.40 ± 0.03 0.26 ± 0.04 0.33 ± 0.06 Data are shown as the mean ± SEM for sucrose or cocaine SA rats and chamber exposure controls at baseline, 1d Abs, and 14d Abs. CeA, Central amygdala; BaA, basal amygdala; dHPC, dorsal hippocampus; VP, ventral pallidum; GP, globus pallidus; LH, lateral hypothalamus; Thal, thalamus; PV, paraventricular; AP, anteroposterior; RN, reticular nucleus; MD, mediodorsal; VL, ventrolateral; VPM, ventroposteromedial; LP, lateroposterior; Pf, parafascicular; LG, lateral genticulate; PrL, prelimbic; IL, infralimbic; M2, secondary motor; S1, primary somatosensory cortex; jw, jaw region, ul, upper lip; Sh, shoulder; S2, secondary somatosensory cortex. All regions in the table showed significant group × session interactions with a repeated-measures two-factor ANOVA (α < 0.05).
Asterisks represent the results of Tukey’s multiple-comparison post hoc test: *difference from chamber exposure controls; **difference between cocaine and sucrose groups.
- Table 2.
Regions showing significant lateralized group × session interactions for clustering coefficient
Regions Baseline 1d Abs 14d Abs Chamber control Sucrose SA Cocaine SA Chamber control Sucrose SA Cocaine SA Chamber control Sucrose SA Cocaine SA LaA (R) 0.29 ± 0.03 0.32 ± 0.04 0.30 ± 0.04 0.30 ± 0.02 0.40 ± 0.06 0.47 ± 0.06* 0.40 ± 0.05 0.33 ± 0.02 0.34 ± 0.03 MeA (R) 0.31 ± 0.03 0.38 ± 0.06 0.41 ± 0.02 0.32 ± 0.03 0.43 ± 0.04 0.49 ± 0.06* 0.41 ± 0.06 0.27 ± 0.02 0.32 ± 0.04 DMS (L) 0.30 ± 0.04 0.29 ± 0.05 0.39 ± 0.05 0.31 ± 0.05 0.46 ± 0.04 0.49 ± 0.05* 0.44 ± 0.04 0.28 ± 0.02 0.37 ± 0.04 LSept (R) 0.30 ± 0.02 0.29 ± 0.03 0.39 ± 0.04 0.35 ± 0.08 0.37 ± 0.09 0.56 ± 0.07* 0.42 ± 0.04 0.26 ± 0.01 0.32 ± 0.04 AHA (R) 0.28 ± 0.03 0.35 ± 0.03 0.34 ± 0.03 0.30 ± 0.03 0.49 ± 0.04* 0.51 ± 0.07* 0.41 ± 0.06 0.34 ± 0.05 0.36 ± 0.05 MB (R) 0.28 ± 0.03 0.37 ± 0.05 0.32 ± 0.02 0.31 ± 0.03 0.41 ± 0.09 0.51 ± 0.09* 0.42 ± 0.05 0.32 ± 0.02 0.36 ± 0.04 VM Thal (R) 0.34 ± 0.03 0.43 ± 0.04 0.40 ± 0.03 0.31 ± 0.03 0.51 ± 0.05* 0.52 ± 0.07* 0.40 ± 0.06 0.28 ± 0.04 0.36 ± 0.03 PThal (R) 0.34 ± 0.03 0.36 ± 0.07 0.38 ± 0.03 0.32 ± 0.03 0.45 ± 0.08 0.47 ± 0.04* 0.35 ± 0.03 0.29 ± 0.02 0.33 ± 0.03 MG Thal (L) 0.31 ± 0.02 0.38 ± 0.04 0.41 ± 0.04 0.36 ± 0.07 0.45 ± 0.05 0.52 ± 0.05 0.45 ± 0.09 0.38 ± 0.04 0.35 ± 0.04 cRSC (L) 0.39 ± 0.04 0.34 ± 0.03 0.35 ± 0.05 0.38 ± 0.05 0.60 ± 0.07* 0.51 ± 0.05 0.46 ± 0.04 0.36 ± 0.05 0.36 ± 0.02 M1 (L) 0.26 ± 0.02 0.29 ± 0.02 0.29 ± 0.03 0.31 ± 0.04 0.40 ± 0.07 0.38 ± 0.05 0.45 ± 0.05 0.32 ± 0.02 0.33 ± 0.04 S1 Tr (R) 0.31 ± 0.03 0.44 ± 0.09 0.40 ± 0.06 0.26 ± 0.04 0.43 ± 0.07 0.48 ± 0.06* 0.48 ± 0.09 0.38 ± 0.03 0.32 ± 0.02 PRhC (L) 0.30 ± 0.02 0.27 ± 0.04 0.30 ± 0.03 0.34 ± 0.02 0.60 ± 0.10* 0.41 ± 0.04** 0.39 ± 0.05 0.28 ± 0.02 0.36 ± 0.04 MRN (L) 0.35 ± 0.03 0.35 ± 0.05 0.38 ± 0.04 0.37 ± 0.04 0.44 ± 0.03 0.53 ± 0.04* 0.38 ± 0.03 0.43 ± 0.03 0.34 ± 0.03 Cer2 (L) 0.38 ± 0.04 0.39 ± 0.04 0.33 ± 0.02 0.33 ± 0.05 0.49 ± 0.02* 0.46 ± 0.05* 0.51 ± 0.05 0.32 ± 0.02* 0.35 ± 0.03* Data are shown as the mean ± SEM for sucrose or cocaine SA rats and chamber exposure controls at baseline, 1d Abs, and 14d Abs. R, Right; L, left; LaA, lateral amygdala; MeA, medial amygdala; DMS, dorsomedial striatum; LSept, lateral septum; AHA, anterior hypothalamic area; MB, mammillary bodies; Thal, thalamus; VM, ventromedial; Pthal, posterior thalamus; MG, medial genticulate; cRSC, caudal retrosplenial cortex; M1, primary motor cortex; S1, primary somatosensory cortex; Tr, trunk region; PRhC, perirhinal cortex; MRN, midbrain reticular nucleus; Cer2, 2nd cerebellar lobule. All regions in table showed significant group x session interactions with a repeated-measures two factor ANOVA (α < 0.05).
Asterisks represent results of Tukey’s multiple-comparison post hoc test: *difference from chamber exposure controls; **difference between cocaine and sucrose groups..
In this issue
