Article Figures & Data
Figures
- Figure 1.
Ca2+-permeable AMPARs are present in NAc synapses after prolonged withdrawal from extended-access cocaine self-administration. A, Timeline: On WD35–WD49 after the end of self-administration (SA) of cocaine or saline, rats were killed (without any further drug exposure) for electrophysiology experiments. B, Location of recorded cells in NAc core and shell. Numbers on sections are distance (in millimeters) from bregma. C, Representative traces showing AMPAR EPSCs recorded at −70 and +40 mV. Dotted line indicates peak of current in saline-pretreated rat to facilitate comparison with cocaine-pretreated rat. Groups are as indicated in D. D, The average rectification index of AMPAR EPSCs was greater in NAc cells from cocaine-pretreated rats relative to saline-pretreated rats in both core and shell. Each circle represents one cell. Lines are means for each group. **p < 0.01 versus saline.
- Figure 2.
Locomotor sensitization to cocaine persists through WD44. A, Timeline: Rats were treated with saline or cocaine (15 mg/kg) for 8 d. On WD41, rats received a challenge injection of cocaine (15 mg/kg); 3 d later (WD44), they were challenged with a lower dose of cocaine (7.5 mg/kg). B, Locomotor activity in response to 15 mg/kg cocaine on treatment days 1 and 8, and WD41. Data are mean number of beam breaks for 5 min intervals during the first 40 min after cocaine injection (left) and total beam breaks summed over this period (right). **p < 0.01, *p < 0.05 versus day 1. C, Locomotor activity in response to 7.5 mg/kg cocaine on WD44. Data are plotted as in B. The cocaine group showed a greater locomotor response during the 40 min after cocaine (Coc) injection compared with the saline (Sal) group. **p < 0.01 versus saline. n = 11/group.
- Figure 3.
AMPAR subunit distribution in NAc core and shell after 41 d of withdrawal from noncontingent cocaine injections. A, Timeline: Rats were treated with saline or cocaine (15 mg/kg) for 8 d. On WD41, rats were killed (without any further drug exposure) for analysis of AMPAR subunits using a protein cross-linking assay. B, Schematic of core and shell dissections. C, Cell surface, intracellular (Intra), and total levels of GluA1, GluA2, and GluA3 in core and shell. Rats treated with repeated noncontingent cocaine injections did not differ significantly from saline controls. Data from the cocaine group were normalized to the mean of the saline group. Error bars show SEM. *p < 0.05 versus saline. n = 16–18/group.
- Figure 4.
Ca2+-permeable AMPARs are not added to NAc synapses after prolonged withdrawal from noncontingent cocaine. A, Timeline: On WD35–WD49, after noncontingent cocaine or saline, rats were killed (without any further drug exposure) for electrophysiology experiments. B, Location of recorded cells in NAc core and shell. Numbers on sections are distance (in millimeters) from bregma. C, Representative traces showing AMPAR EPSCs recorded at −70 and +40 mV. Dotted line indicates peak of current in saline rats. Groups are as indicated in D. D, No difference was observed between saline- and cocaine-pretreated rats in the rectification index of AMPAR EPSCs from NAc cells in NAc core or shell. Each circle represents one cell. Lines are means for each group.
