| First Author | Sathler MF | Year | 2016 |
| Journal | Neuroscience | Volume | 329 |
| Pages | 326-36 | PubMed ID | 27208619 |
| Mgi Jnum | J:299319 | Mgi Id | MGI:6492416 |
| Doi | 10.1016/j.neuroscience.2016.05.022 | Citation | Sathler MF, et al. (2016) Single exposure to cocaine impairs aspartate uptake in the pre-frontal cortex via dopamine D1-receptor dependent mechanisms. Neuroscience 329:326-36 |
| abstractText | Dopamine and glutamate play critical roles in the reinforcing effects of cocaine. We demonstrated that a single intraperitoneal administration of cocaine induces a significant decrease in [(3)H]-d-aspartate uptake in the pre-frontal cortex (PFC). This decrease is associated with elevated dopamine levels, and requires dopamine D1-receptor signaling (D1R) and adenylyl cyclase activation. The effect was observed within 10min of cocaine administration and lasted for up to 30min. This rapid response is related to D1R-mediated cAMP-mediated activation of PKA and phosphorylation of the excitatory amino acid transporters EAAT1, EAAT2 and EAAT3. We also demonstrated that cocaine exposure increases extracellular d-aspartate, l-glutamate and d-serine in the PFC. Our data suggest that cocaine activates dopamine D1 receptor signaling and PKA pathway to regulate EAATs function and extracellular EAA level in the PFC. |
