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118 | Acetylcholine and dopamine interact in the medial prefrontal cortex to modulate cocaine-associated memory

Cognition, Behavior, and Memory

Author: VERONICA PASTOR PASTOR | email: verpastor@fmed.uba.ar


Verónica Pastor , Juliana F Dalto , Marta C Antonelli , Jorge H  Medina

1° CONICET-Universidad de Buenos Aires, Instituto de Biología Celular y Neurociencia “Prof. Eduardo De Robertis” (IBCN), Buenos Aires, Argentina.

Neuromodulation of the medial prefrontal cortex (mPFC) is essential for cortical control of behaviors induced by appetitive stimuli, such as cue-induced seeking behavior after the formation of drug-context associative memories. We have recently reported that the antagonism of mPFC alpha 7 nicotinic receptors (nAChRs) by methyllycaconitine (MLA) blocked cue-induced cocaine memory retrieval in a non-transient manner. However, the interaction between modulatory systems in the mPFC and their role in memory processing is a question which remains unanswered. Previous work showed that the activation of alpha 7 nAChRs in the mPFC increases dopamine release and that dopamine signaling through D1 receptors (D1R) is necessary for cocaine memory retrieval. Thus, we hypothesized that cholinergic signaling through alpha 7 nAChRs is needed in the mPFC to allow cue-induced cocaine memory retrieval by interacting with dopaminergic D1R activation. Using pharmacologic and behavioral techniques we demonstrate that D1R activation reversed MLA-induced blockade of cocaine CPP retrieval. Moreover, the modulatory role of D1R was evident only in the presence of nAChRs antagonism. These results suggest that alpha 7 nAChRs and D1R signaling interact in the mPFC for allowing cue-induced cocaine memory retrieval. Acknowledgements: International Society for Neurochemistry, CAEN grant (VP)

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