Figure 2. Microglia depletion during cocaine withdrawal prevents dendritic spines changes and CP-AMPAR accumulation in the nucleus accumbens shell.

(A) Representative images of Golgi-stained dendritic segments containing spines of NAc shell MSNs at WD21 under the indicated conditions. (B) Dendritic spine density in distal dendritic segments was higher in cocaine control mice at WD21 (interaction Diet x Drug: F_{(1, 108)} = 5.357, p<0.05; N=24–32 segments/6–8 mice per group). (C) The cumulative distribution of the spine head diameter shows a significant rightward shift for the cocaine control group, indicative of wider spine diameters across the distribution, while it shows a significant leftward shift in the cocaine PLX group, indicative of smaller spine diameters across the distribution (K–S test (1949 spines/6–8 mice per group): cocaine control vs saline control (D=0.08258, p<0.05), cocaine control vs saline PLX (D=0.08281, p<0.05), cocaine control vs cocaine PLX (D=0.1290, p<0.05), cocaine PLX vs saline control (D=0.06191, p<0.05), cocaine PLX vs saline PLX (D=0.08297, p<0.05). (D) The average spine head diameter in MSNs distal dendritic segments at WD21 differs between cocaine control and cocaine PLX (Group: F_{(3, 7792)} = 22.74, p<0.05). (E) Schematic depicting whole-cell patch clamp recordings from NAc shell MSNs. (F) Example traces of AMPA EPSCs evoked at −70 mV, 0 mV, and +40 mV for rectification index. (G) Average current-voltage relationship curves of evoked AMPAR-EPSCs. (H) The rectification index is higher in NAc MSNs of cocaine control mice (interaction Drug x Diet: F_{(1, 63)} = 9,184, p<0.05; N= 11–16 cells/6–7 mice group). Data are presented as mean ± SEM. Scale bars = 5 μm. The symbols indicate, * p<0.05 compared to saline control, saline PLX and cocaine PLX, ⨍ p<0.05 compared to saline control, saline PLX and cocaine control.