• Neuroscience · Aug 2016

    Single exposure to cocaine impairs aspartate uptake in the pre-frontal cortex via dopamine D1-receptor dependent mechanisms.

    • Matheus Figueiredo Sathler, Bernardo Stutz, Robertta Silva Martins, Maurício Dos Santos Pereira, Ney Roner Pecinalli, Luis E Santos, Rosilane Taveira-da-Silva, Jennifer Lowe, Isis Grigorio de Freitas, Ricardo Augusto de Melo Reis, Alex C Manhães, and Regina C C Kubrusly.
    • Laboratório de Neurofarmacologia, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, Brazil. Electronic address: msathler@id.uff.br.
    • Neuroscience. 2016 Aug 4; 329: 326-36.

    AbstractDopamine 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.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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