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Here, we explored the case of Huntington's disease (HD), where the striatum and, specifically, dopamine receptor 1 (D1R) and dopamine receptor 2 (D2R) medium\u2010sized spiny neurons (MSNs) exhibit differential susceptibility to the\n                    <jats:italic>HTT<\/jats:italic>\n                    CAG\u2010repeat expansion mutation, with D2R\u2010neurons being impacted earlier and more significantly. To unravel differences between D2R and D1R MSNs, we employed a multidimensional approach, integrating genomic, transcriptional, pattern distribution, and somatic instability analyses. Specifically, we used\n                    <jats:italic>Htt<\/jats:italic>\n                    CAG knock\u2010in mouse models harboring 18 (\n                    <jats:italic>Htt<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Q20<\/jats:italic>\n                    <\/jats:sup>\n                    : \u201ccontrol\u201d) or ~190 (\n                    <jats:italic>Htt<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Q175<\/jats:italic>\n                    <\/jats:sup>\n                    : \u201cHD\u201d) consecutive CAG repeats, expressing tdTomato and EGFP under the control of\n                    <jats:italic>Drd1<\/jats:italic>\n                    and\n                    <jats:italic>Drd2<\/jats:italic>\n                    promoters, respectively. First, comprehensive genomic and transcriptomic analyses following fluorescence\u2010activated cell sorting (FACS) of dissociated striatal neurons revealed distinct gene expression profiles with a significant upregulation of oxidative phosphorylation and translation pathways in D1R\u2010positive neurons already at the pre\u2010symptomatic stage. These transcriptional changes were not accompanied by major copy number variations, as shown by parallel genomic analysis. Secondly, histological analyses revealed a greater proportion of D1R\u2010positive neurons compared to D2R\u2010positive neurons in HD mice, particularly in the ventral\u2010medial neostriatum, with D2R\u2010positive neurons presenting an increased nuclear accumulation of mutant huntingtin aggregates. In summary, our integrative study suggests that the distinct vulnerability of MSNs in HD might result from a combination of an early transcriptional compensatory response of D1R neurons together with specific susceptibility of D2R neurons.\n                  <\/jats:p>","DOI":"10.1111\/bpa.70135","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T13:32:05Z","timestamp":1787751125000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Decoding neuronal vulnerability: Multidimensional analysis of\n                    <scp>D1R<\/scp>\n                    \u2010 and\n                    <scp>D2R<\/scp>\n                    \u2010 medium\u2010sized spiny neurons in Huntington's disease"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7439-4012","authenticated-orcid":false,"given":"Guendalina","family":"Bergonzoni","sequence":"first","affiliation":[{"name":"Laboratory of NeuroEpigenetics, Department of Cellular, Computational and Integrative Biology (CIBIO) University of Trento  Trento Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel","family":"Pellegrini","sequence":"additional","affiliation":[{"name":"Laboratory of NeuroEpigenetics, Department of Cellular, Computational and Integrative Biology (CIBIO) University of Trento  Trento Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aurora","family":"Savino","sequence":"additional","affiliation":[{"name":"Molecular Biotechnology Center, Department of Molecular Biotechnology and Health Sciences University of Turin  Turin 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