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The Journal of Neuroscience, November 15, 2000, 20(22):8443-8451
Dopamine and cAMP-Regulated Phosphoprotein 32 kDa Controls Both Striatal Long-Term Depression and Long-Term Potentiation, Opposing Forms of Synaptic Plasticity
Paolo Calabresi1, 2, Paolo Gubellini1, Diego Centonze1, 2, Barbara Picconi1, Giorgio Bernardi1, 2, Karima Chergui3, Per Svenningsson3, Allen A. Fienberg3, and Paul Greengard3 1 Clinica Neurologica, Dipartimento di Neuroscienze, Università di Tor Vergata, Rome, Italy, 2 Istituto di Ricovero e Cura a Carattere Scientifico Ospedale Santa Lucia, Rome, Italy, and 3 Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York 10021
A complex chain of intracellular signaling events, critically important in motor control, is activated by the stimulation of D1-like dopamine (DA) receptors in striatal neurons. At corticostriatal synapses on medium spiny neurons, we provide evidence that the D1-like receptor-dependent activation of DA and cyclic adenosine 3',5' monophosphate-regulated phosphoprotein 32 kDa is a crucial step for the induction of both long-term depression (LTD) and long-term potentiation (LTP), two opposing forms of synaptic plasticity. In addition, formation of LTD and LTP requires the activation of protein kinase G and protein kinase A, respectively, in striatal projection neurons. These kinases appear to be stimulated by the activation of D1-like receptors in distinct neuronal populations.
Key words: basal ganglia; brain slices; dopamine; intracellular recordings; nitric oxide synthase-positive interneurons; phosphatases; protein kinase C; protein kinase G
Copyright © 2000 Society for Neuroscience 0270-6474/00/20228443-09$05.00/0
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