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Dopamine and cAMP-Regulated Phosphoprotein 32 kDa Controls Both Striatal Long-Term Depression and Long-Term Potentiation, Opposing Forms of Synaptic Plasticity

2000/11/15 by Paolo Calabresi, Paolo Gubellini, Diego Centonze +6
Biochemistry, Genetics and Molecular Biology · Neuroscience · #Ion channel regulation and function #Neuroscience and Neuropharmacology Research #Receptor Mechanisms and Signaling

paper · pdf · doi:10.1523/jneurosci.20-22-08443.2000

openalex publication_date 2000/11/15 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01

Abstract

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.

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