Orbitofrontal-striatal potentiation underlies cocaine-induced hyperactivity

Sebastiano Bariselli, Nanami L. Miyazaki, Meaghan C. Creed and Alexxai V. Kravitz ()
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Sebastiano Bariselli: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health
Nanami L. Miyazaki: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health
Meaghan C. Creed: Washington University Pain Center
Alexxai V. Kravitz: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract Psychomotor stimulants increase dopamine levels in the striatum and promote locomotion; however, their effects on striatal pathway function in vivo remain unclear. One model that has been proposed to account for these motor effects suggests that stimulants drive hyperactivity via activation and inhibition of direct and indirect pathway striatal neurons, respectively. Although this hypothesis is consistent with the cellular actions of dopamine receptors and received support from optogenetic and chemogenetic studies, it has been rarely tested with in vivo recordings. Here, we test this model and observe that cocaine increases the activity of both pathways in the striatum of awake mice. These changes are linked to a dopamine-dependent cocaine-induced strengthening of upstream orbitofrontal cortex (OFC) inputs to the dorsomedial striatum (DMS) in vivo. Finally, depressing OFC-DMS pathway with a high frequency stimulation protocol in awake mice over-powers the cocaine-induced potentiation of OFC-DMS pathway and attenuates the expression of locomotor sensitization, directly linking OFC-DMS potentiation to cocaine-induced hyperactivity.

Date: 2020
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DOI: 10.1038/s41467-020-17763-8

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