{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T04:48:38Z","timestamp":1792212518206,"version":"4.4.0"},"reference-count":113,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cent Nerv Syst Dis"],"published-print":{"date-parts":[[2017,1,1]]},"abstract":"<jats:p>\n                    Dopamine D\n                    <jats:sub>3<\/jats:sub>\n                    receptors (D\n                    <jats:sub>3<\/jats:sub>\n                    R) modulate neuronal activity in several brain regions including cortex, striatum, cerebellum, and hippocampus. A growing body of evidence suggests that aberrant D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling contributes to multiple brain diseases, such as Parkinson\u2019s disease, essential tremor, schizophrenia, and addiction. In line with these findings, D\n                    <jats:sub>3<\/jats:sub>\n                    R has emerged as a potential target in the treatment of neurological disorders. However, the mechanisms underlying neuronal D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling are poorly understood, either in healthy or diseased brain. Here, I review the molecular mechanisms involved in D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling via monomeric D\n                    <jats:sub>3<\/jats:sub>\n                    R and heteromeric receptor complexes (e.g., D\n                    <jats:sub>3<\/jats:sub>\n                    R-D\n                    <jats:sub>1<\/jats:sub>\n                    R, D\n                    <jats:sub>3<\/jats:sub>\n                    R-D\n                    <jats:sub>2<\/jats:sub>\n                    R, D\n                    <jats:sub>3<\/jats:sub>\n                    R-A\n                    <jats:sub>2a<\/jats:sub>\n                    R, and D\n                    <jats:sub>3<\/jats:sub>\n                    R-D\n                    <jats:sub>3<\/jats:sub>\n                    nf). I focus on D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling pathways that, according to recent reports, contribute to pathological brain states. In particular, I describe evidence on both quantitative (e.g., increased number or affinity) and qualitative (e.g., switched signaling) changes in D\n                    <jats:sub>3<\/jats:sub>\n                    R that has been associated with brain dysfunction. I conclude with a description of basic mechanisms that modulate D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling such as desensitization, as disruption of these mechanisms may underlie pathological changes in D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling. Because several lines of evidence support the idea that imbalances in D\n                    <jats:sub>3<\/jats:sub>\n                    R signaling alter neural function, a better understanding of downstream D\n                    <jats:sub>3<\/jats:sub>\n                    R pathways is likely to reveal novel therapeutic strategies toward dopamine-related brain disorders.\n                  <\/jats:p>","DOI":"10.1177\/1179573517726335","type":"journal-article","created":{"date-parts":[[2017,8,16]],"date-time":"2017-08-16T07:24:07Z","timestamp":1502868247000},"page":"117957351772633","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":42,"title":["Abnormalities of Dopamine D\n                    <sub>3<\/sub>\n                    Receptor Signaling in the Diseased Brain"],"prefix":"10.1177","volume":"9","author":[{"given":"G Aleph","family":"Prieto","sequence":"first","affiliation":[{"name":"Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,8,16]]},"reference":[{"key":"bibr1-1179573517726335","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.61.5.641"},{"key":"bibr2-1179573517726335","doi-asserted-by":"crossref","unstructured":"Hornykiewicz O. Oleh Hornykiewicz. In: Squire LR, ed. The History of Neuroscience in Autobiography. Vol 4. 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