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In this study, we examined the possibility that ultrastructural changes of nigrostriatal dopamine terminals could contribute to this neurochemical imbalance using a serial block face\/scanning electron microscope (SBF\/SEM) and three\u2010dimensional reconstruction to analyse striatal tyrosine hydroxylase\u2010immunoreactive (TH\u2010IR) terminals and their synapses in a DYT1(\u0394E) knockin (DYT1\u2010KI) mouse model of DYT1 dystonia. Furthermore, to study possible changes in vesicle packaging capacity of dopamine, we used transmission electron microscopy to assess the synaptic vesicle size in striatal dopamine terminals. Quantitative comparative analysis of 80 fully reconstructed TH\u2010IR terminals in the WT and DYT1\u2010KI mice indicate (1) no significant difference in the volume of TH\u2010IR terminals; (2) no major change in the proportion of axo\u2010spinous versus axo\u2010dendritic synapses; (3) no significant change in the post\u2010synaptic density (PSD) area of axo\u2010dendritic synapses, while the PSDs of axo\u2010spinous synapses were significantly smaller in DYT1\u2010KI mice; (4) no significant change in the contact area between TH\u2010IR terminals and dendritic shafts or spines, while the ratio of PSD area\/contact area decreased significantly for both axo\u2010dendritic and axo\u2010spinous synapses in DYT1\u2010KI mice; (5) no significant difference in the mitochondria volume; and (6) no significant difference in the synaptic vesicle area between the two groups. Altogether, these findings suggest that abnormal morphometric changes of nigrostriatal dopamine terminals and their post\u2010synaptic targets are unlikely to be a major source of reduced striatal dopamine release in DYT1 dystonia.<\/jats:p>","DOI":"10.1111\/ejn.16197","type":"journal-article","created":{"date-parts":[[2023,12,20]],"date-time":"2023-12-20T22:45:18Z","timestamp":1703112318000},"page":"1407-1427","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Ultrastructural analysis of nigrostriatal dopaminergic terminals in a knockin mouse model of DYT1 dystonia"],"prefix":"10.1111","volume":"59","author":[{"given":"Ke","family":"Pan","sequence":"first","affiliation":[{"name":"Emory National Primate Research Center Emory University  Atlanta Georgia USA"},{"name":"Department of Physical Therapy &amp; Human Movement Sciences Northwestern University  Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyder A.","family":"Jinnah","sequence":"additional","affiliation":[{"name":"Department of Neurology Emory University  Atlanta Georgia USA"},{"name":"Department of Human Genetics and Pediatrics Emory University  Atlanta Georgia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen J.","family":"Hess","sequence":"additional","affiliation":[{"name":"Department of Neurology Emory University  Atlanta Georgia USA"},{"name":"Department of Pharmacology and Chemical Biology Emory University  Atlanta Georgia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoland","family":"Smith","sequence":"additional","affiliation":[{"name":"Emory National Primate Research Center Emory University  Atlanta Georgia USA"},{"name":"Department of Neurology Emory University  Atlanta Georgia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rosa M.","family":"Villalba","sequence":"additional","affiliation":[{"name":"Emory National Primate Research Center Emory University  Atlanta Georgia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,12,20]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1975.sp010974"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0361-9230(84)90128-X"},{"key":"e_1_2_11_4_1","first-page":"53","article-title":"Dopamine transmission in DYT1 dystonia","volume":"94","author":"Augood S. 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