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. 2021 Nov 26;15:785703. doi: 10.3389/fncel.2021.785703

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Copyright © 2021 Komatsu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A model illustrating of GPR52 inhibition for the treatment of Huntington’s disease. In the striatum, GPR52 is expressed in the striatopallidal MSNs in which dopamine D2 receptor (D2R) is expressed. GPR52 inhibition or the antagonists leads to proteasomal degradation of the mutant huntingtin protein (mHTT). Oppositely, GPR52 activation via intracellular cAMP rise transports mHTT to the endoplasmic reticulum and protects against its degradation. Meanwhile, GPR52 is not expressed in the striatonigral MSNs where dopamine D1 receptor (D1R) is expressed. Second generation antipsychotics (SGA), such as quetiapine, blocks D2R-mediated signaling.