Dopamine is at the heart of basal ganglia circuits controlling self-paced motor actions, where it is believed to act by differentially modulating direct- and indirect-pathway striatal projection neurons (dSPNs and iSPNs)
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To date, this has largely been understood in the context of mean firing rate, with dopamine increasing the discharge of dSPNs while depressing that of iSPNs
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Here, we use two-photon microscopy to monitor intracellular Ca2+ signals in dSPNs and iSPNs simultaneously and find that the overall number of dSPNs and iSPNs encoding motor actions is not fixed, but is rather dynamically modulated by dopamine
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Specifically, we show that iSPN ensembles are inversely related to extracellular dopamine levels, in general agreement with current notions of dopamine action
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By contrast, dSPNs follow an “inverted-U” shaped response, where too little or too much dopamine negatively impacts ensemble size
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Surprisingly, dopamine does not strongly or differentially modulate the frequency of calcium transients in either pathway
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In addition, we show that dSPN and iSPN ensembles do not adapt similarly to chronic loss of dopamine in a model of Parkinson’s disease and respond differently to subsequent dopamine replacement therapy
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Our results indicate that DA regulates striatal output by dynamically reconfiguring its sparse ensemble code and suggest that DA modulates how many target neurons are eligible for synaptic plasticity
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Our work also provides novel insights into the pathophysiology of Parkinson’s disease and a possible explanation for why long-term levodopa treatment eventually induces uncontrolled involuntary movements
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Big Congrats to postdoc Marta Maltese with help from Jeff March and Zander Bashaw
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