dopamine-induced plasticity, phospholipase d (pld) activity and cocaine-cue behavior depend on pld-linked metabotropic glutamate receptors in amygdala由多巴胺带来的对可塑性,磷脂酶d(骑士)活动和cocaine-cue行为取决于pld-linked metabotropic谷氨酸受体在杏仁核.pdfVIP

Dopamine-Induced Plasticity, Phospholipase D (PLD) Activity and Cocaine-Cue Behavior Depend on PLD- Linked Metabotropic Glutamate Receptors in Amygdala 1. 1. 1 1,2 1 Balaji Krishnan *, Kathy M. Genzer , Sebastian W. Pollandt , Jie Liu , Joel P. Gallagher , Patricia Shinnick-Gallagher1 1 Department of Pharmacology and Toxicology, University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America, 2 Department of Anesthesiology, Presbyterian Hospital, Columbia University, New York, New York, United States of America Abstract Cocaine-cue associations induce synaptic plasticity with long lasting molecular and cellular changes in the amygdala, a site crucial for cue-associated memory mechanisms. The underlying neuroadaptations can include marked alterations in signaling via dopamine (DA) receptors (DRs) and metabotropic glutamate (Glu) receptors (mGluRs). Previously, we reported that DR antagonists blocked forms of synaptic plasticity in amygdala slices of Sprague-Dawley rats withdrawn from repeated cocaine administration. In the present study, we investigated synaptic plasticity induced by exogenous DA and its dependence on mGluR signaling and a potential role for phospholipase D (PLD) as a downstream element linked to mGluR and DR signaling. Utilizing a modified conditioned place preference (CPP) paradigm as a functional behavioral measure, we studied the neurophysiological effects after two-weeks to the last cocaine conditioning. We recorded, electrophysiolog- ically, a DR-induced synaptic potentiation in the basolateral to lateral capsula central amygdala (BLA-lcCeA) synaptic pathway t