Differential Dopamine Regulation of Ca2+ Signaling and Its Timing Dependence in the Nucleus Accumbens

Publication date: Available online 7 April 2016
Source:Cell Reports
Author(s): Immani Swapna, Brian Bondy, Hitoshi Morikawa
Dopamine action in the nucleus accumbens (NAc) is thought to drive appetitive behavior and Pavlovian reward learning. However, it remains controversial how dopamine achieves these behavioral effects by regulating medium spiny projection neurons (MSNs) of the NAc, especially on a behaviorally relevant timescale. Metabotropic glutamate receptor (mGluR)-induced Ca²⁺ signaling dependent on the Ca²⁺- releasing messenger inositol 1,4,5-triphosphate (IP3) plays a critical role in controlling neuronal excitability and synaptic plasticity. Here, we show that transient dopamine application facilitates mGluR/IP3-induced Ca²⁺ signals within a time window of ∼2–10 s in a subpopulation of MSNs in the NAc core. Dopamine facilitation of IP3-induced Ca²⁺ signaling is mediated by D1 dopamine receptors. In dopamine-insensitive MSNs, activation of A2A adenosine receptors causes enhancement of IP3-evoked Ca²⁺ signals, which is reversed by D2 dopamine receptor activation. These results show that dopamine differentially regulates Ca²⁺ signaling on the order of seconds in two distinct MSN subpopulations.

Graphical abstract

Teaser

Swapna et al. demonstrate that transient dopamine (via D1 receptors) facilitates Ca²⁺ signaling on the order of seconds in a subpopulation of nucleus accumbens neurons. In a separate subpopulation, dopamine (via D2 receptors) does the opposite, reversing A2A adenosine receptor-mediated Ca²⁺ signal facilitation.


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