Figure 7.

Schematic model illustrating the proposed mechanism for the impairment of group II mGluR-mediated LTD induction in the mPFC after repeated cocaine administration. According to this model, repeated cocaine administration increases levels of dopamine (DA) in the mPFC and then leads to increased formation of cAMP via the activation of D₁ receptors. Extracellular cAMP is then metabolized to adenosine by phosphodiesterase and ecto 5′-nucleotidase and acts on the adenosine A₃ receptors. The activation of adenosine A₃ receptors would increase PKC activity and thereby triggers an impairment of group II mGluR function, resulting in an impairment of LTD induced by DCG-IV or LY379268.