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Involvement of cannabinoid CB1 receptor in stress-induced enhancement of extracellular glutamate in nucleus accumbens core after extinction of cocaine-conditioned place preference

Andrea Susana Guzman

  • Córdoba,
  • Argentina
  • Andrea Susana Guzman ¹
  • , María Paula Avalos, ¹
  • , Pia Valentina Euliarte ¹
  • , Marianela Adela Sanchez ¹
  • , Daiana Rigoni ¹
  • , Julieta Boezio ¹
  • , Flavia Andrea Bollati ¹
  • , Miriam Beatriz Virgolini ¹
  • , Liliana Marina Cancela ¹
  • 1 IFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.

Previous findings from our lab have demonstrated pharmacologically the role of the cannabinoid CB1 receptors (CB1Rs) within nucleus accumbens core (NAcC) in restraint stress-induced reinstatement of extinguished cocaine-conditioned place preference (CPP). Given the well-established role of glutamatergic transmission within NAcC in reinstatement of cocaine seeking, we evaluated the effects of AM251, a highly selective CB1R antagonist, and ACEA, a highly selective agonist, on stress-induced changes in extracellular glutamate levels within NAcC under reinstatement conditions. In vivo microdialysis experiment in male Wistar rats, combined with HPLC and electrochemical detection was used. Firstly, a reinstating stress session (30 min of restraint), but not a non-reinstating stress session (15 min of restraint), increased the extracellular glutamate levels within NAcC in animals that were re-exposed to the drug-paired compartment after extinction of cocaine-CPP. Interestingly, the microinjection of AM251 directly into NAcC inhibited this stress-induced increase of glutamate, and the microinjection of ACEA potentiated it when combined with the non-reinstating stress. These data suggest that CB1Rs in NAcC modulate the context-specific enhancement of glutamate after restraint stress. These findings may be explained in the framework of a dysregulation of glutamate homeostasis in NAcC and provide neurochemical basis to investigate in vivo mechanisms underpinning stress-induced relapse.