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However, the relationship between mitochondrial Zn2+ accumulation and their disruption has not been examined at the ultrastructural level in vivo. We employed a cardiac arrest model of transient global ischemia (TGI), combined with Timm\u2019s sulfide silver labeling, which inserts electron dense metallic silver granules at sites of labile Zn2+ accumulation, and used transmission electron microscopy (TEM) to examine subcellular loci of the Zn2+ accumulation. In line with prior studies, TGI-induced damage to CA1 was far greater than to CA3 pyramidal neurons, and was substantially progressive in the hours after reperfusion (being significantly greater after 4- than 1-hour recovery). Intriguingly, TEM examination of Timm\u2019s-stained sections revealed substantial Zn2+ accumulation in many postischemic CA1 mitochondria, which was strongly correlated with their swelling and disruption. Furthermore, paralleling the evolution of neuronal injury, both the number of mitochondria containing Zn2+ and the degree of their disruption were far greater at 4- than 1-hour recovery. These data provide the first direct characterization of Zn2+ accumulation in CA1 mitochondria after in vivo TGI, and support the idea that targeting these events could yield therapeutic benefits.<\/jats:p>","DOI":"10.1093\/jnen\/nlz042","type":"journal-article","created":{"date-parts":[[2019,5,31]],"date-time":"2019-05-31T09:10:27Z","timestamp":1559293827000},"page":"655-664","source":"Crossref","is-referenced-by-count":18,"title":["Rapid Intramitochondrial Zn2+ Accumulation in CA1 Hippocampal Pyramidal Neurons After Transient Global Ischemia: A Possible Contributor to Mitochondrial Disruption and Cell Death"],"prefix":"10.1093","volume":"78","author":[{"given":"Hong Z","family":"Yin","sequence":"first","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hwai-Lee","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung G","family":"Ji","sequence":"additional","affiliation":[{"name":"Department of Anatomy & Neurobiology, University of California, Irvine, Irvine, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuliya V","family":"Medvedeva","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guilian","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Afsheen K","family":"Bazrafkan","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niki Z","family":"Maki","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yama","family":"Akbari","sequence":"additional","affiliation":[{"name":"Department of Neurology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John H","family":"Weiss","sequence":"additional","affiliation":[{"name":"Department of Neurology"},{"name":"Department of Anatomy & Neurobiology, University of California, Irvine, Irvine, California"},{"name":"Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,5,9]]},"reference":[{"key":"2026041420164220700_nlz042-B1","doi-asserted-by":"crossref","first-page":"131","DOI":"10.2174\/1566524043479248","article-title":"The rise and fall of NMDA antagonists for ischemic stroke","volume":"4","author":"Hoyte","year":"2004","journal-title":"Curr Mol Med"},{"key":"2026041420164220700_nlz042-B2","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1016\/S1474-4422(02)00164-3","article-title":"Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?","volume":"1","author":"Ikonomidou","year":"2002","journal-title":"Lancet Neurol"},{"key":"2026041420164220700_nlz042-B3","doi-asserted-by":"crossref","first-page":"317","DOI":"10.1016\/0006-8993(89)90199-6","article-title":"Translocation of zinc may contribute to seizure-induced death of neurons","volume":"480","author":"Frederickson","year":"1989","journal-title":"Brain Res"},{"key":"2026041420164220700_nlz042-B4","doi-asserted-by":"crossref","first-page":"1013","DOI":"10.1126\/science.272.5264.1013","article-title":"The role of zinc in selective neuronal death after transient global cerebral ischemia","volume":"272","author":"Koh","year":"1996","journal-title":"Science"},{"key":"2026041420164220700_nlz042-B5","doi-asserted-by":"crossref","first-page":"247","DOI":"10.1016\/0304-3940(90)90002-Q","article-title":"Possible role of zinc in the selective degeneration of dentate hilar neurons after cerebral ischemia in the adult rat","volume":"109","author":"Tonder","year":"1990","journal-title":"Neurosci Lett"},{"key":"2026041420164220700_nlz042-B6","doi-asserted-by":"crossref","first-page":"9903","DOI":"10.1523\/JNEUROSCI.1713-04.2004","article-title":"Late calcium EDTA rescues hippocampal CA1 neurons from global ischemia-induced death","volume":"24","author":"Calderone","year":"2004","journal-title":"J Neurosci"},{"key":"2026041420164220700_nlz042-B7","doi-asserted-by":"crossref","first-page":"1273","DOI":"10.1523\/JNEUROSCI.22-04-01273.2002","article-title":"Blockade of Ca2+-permeable AMPA\/kainate channels decreases oxygen-glucose deprivation-induced Zn2+ accumulation and neuronal loss in hippocampal pyramidal neurons","volume":"22","author":"Yin","year":"2002","journal-title":"J Neurosci"},{"key":"2026041420164220700_nlz042-B8","doi-asserted-by":"crossref","first-page":"91","DOI":"10.1016\/0006-8993(85)91612-9","article-title":"Intravesicular localization of zinc in rat telencephalic boutons. 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