Cocaine hcl

Cocaine HCl, nifedipine (Nif), (±)-BayK-8644 (BayK), and Naspm were obtained from Sigma (St. Louis, MO). NBQX was obtained from Tocris Bioscience (Minneapolis, MN). Nif and BayK were dissolved in 0.9% saline containing 1.5% DMSO and 1.5% Tween80. Naspm and NBQX were dissolved in 0.9% saline. Antibodies listed in Supplementary Table 1.

Cocaine-HCl, (+)-MK-801 hydrogen maleate, and memantine-HCl were purchased from Sigma-Aldrich (St. Louis, Missouri, USA) and dissolved in saline (0.9% NaCl). For training, Cocaine-HCl was dissolved to a final concentration of 12 mg/ml (of the salt) and administered in a volume of 1 ml/kg body weight. MK-801 and memantine (0.2 and 10 mg/kg, respectively; doses as free-base) and 0.9% saline were given at 2 ml/kg body weight. All drug treatments and saline were administered intraperitoneally (i.p.). The two NMDA receptor antagonists were used to ensure that any effects were due to common actions on this receptor system. Both MK-801 and memantine function as open-channel antagonists that block NMDA receptors only when these channels are activated (Chen et al. 1992 (link)). However, MK-801 and memantine interact with the NMDA receptor complex in distinct ways. Memantine is a low-affinity blocker with rapid blocking kinetics (Ribeiro Do Couto et al. 2004 ; Tzschentke and Schmidt 1999 (link)), while MK-801 is a high-affinity blocker with slower kinetics (Parsons et al. 1999 (link)). Additionally, these compounds differ in their binding site. MK-801 binds to the PCP site inside the pore of the receptor (Moring et al. 1994 (link); Sakurada et al. 1993 (link)), whereas memantine is believed to bind at or near the Mg2+ binding site (Chen and Lipton 1997 (link); Chen et al. 1992 (link)).

Cocaine HCl was purchased from Sigma-Aldrich (St. Louis, MO, USA), dissolved in physiologic saline, and administered IP in a volume of 10 ml/kg.