{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T18:40:41Z","timestamp":1772822441027,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,3,21]],"date-time":"2014-03-21T00:00:00Z","timestamp":1395360000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Prenatal alcohol exposure has been linked to impairment in cerebellar structure and function, including eyeblink conditioning. The deep cerebellar nuclei, which play a critical role in cerebellar\u2010mediated learning, receive extensive inputs from brain stem and cerebellar cortex and provide the point of origin for most of the output fibers to other regions of the brain. We used in vivo<jats:sup>1<\/jats:sup>H magnetic resonance spectroscopy (<jats:styled-content style=\"fixed-case\">MRS<\/jats:styled-content>) to examine effects of prenatal alcohol exposure on neurochemistry in this important cerebellar region.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MRS data from the deep cerebellar nuclei were acquired from 37 children with heavy prenatal alcohol exposure and 17 non\u2010 or minimally exposed controls from the Cape Coloured (mixed ancestry) community in Cape Town, South Africa.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Increased maternal alcohol consumption around time of conception was associated with lower<jats:italic>N<\/jats:italic>\u2010Acetylaspartate (<jats:styled-content style=\"fixed-case\">NAA<\/jats:styled-content>) levels in the deep nuclei (<jats:italic>r\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>\u22120.33,<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05). Higher levels of alcohol consumption during pregnancy were related to lower levels of the choline\u2010containing metabolites (<jats:italic>r\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>\u22120.37,<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.01), glycerophosphocholine plus phosphocholine (Cho). Alcohol consumption levels both at conception (<jats:italic>r\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0.35,<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.01) and during pregnancy (<jats:italic>r\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0.38,<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.01) were related to higher levels of glutamate plus glutamine (Glx). All these effects continued to be significant after controlling for potential confounders.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The lower<jats:styled-content style=\"fixed-case\">NAA<\/jats:styled-content>levels seen in relation to prenatal alcohol exposure may reflect impaired neuronal integrity in the deep cerebellar nuclei. Our finding of lower Cho points to disrupted Cho metabolism of membrane phospholipids, reflecting altered neuropil development with potentially reduced content of dendrites and synapses. The alcohol\u2010related alterations in Glx may suggest a disruption of the glutamate\u2013glutamine cycling involved in glutamatergic excitatory neurotransmission.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12380","type":"journal-article","created":{"date-parts":[[2014,3,21]],"date-time":"2014-03-21T16:23:49Z","timestamp":1395419029000},"page":"1330-1338","source":"Crossref","is-referenced-by-count":36,"title":["An In Vivo<sup>1<\/sup>H Magnetic Resonance Spectroscopy Study of the Deep Cerebellar Nuclei in Children with Fetal Alcohol Spectrum Disorders"],"prefix":"10.1111","volume":"38","author":[{"given":"Lindie","family":"du Plessis","sequence":"first","affiliation":[{"name":"MRC\/UCT Medical Imaging Research Unit University of Cape Town Cape Town South Africa"},{"name":"Department of Human Biology University of Cape Town Cape Town South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph L.","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Department of Human Biology University of Cape Town Cape Town South Africa"},{"name":"Department of Psychiatry and Mental Health University of Cape Town Cape Town South Africa"},{"name":"Department of Psychiatry and Behavioral Neurosciences Wayne State University School of Medicine Detroit Michigan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra W.","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Department of Human Biology University of Cape Town Cape Town South Africa"},{"name":"Department of Psychiatry and Mental Health University of Cape Town Cape Town South Africa"},{"name":"Department of Psychiatry and Behavioral Neurosciences Wayne State University School of Medicine Detroit Michigan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aaron T.","family":"Hess","sequence":"additional","affiliation":[{"name":"MRC\/UCT Medical Imaging Research Unit University of Cape Town Cape Town South Africa"},{"name":"Department of Human Biology University of Cape Town Cape Town South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andre","family":"van der Kouwe","sequence":"additional","affiliation":[{"name":"Department of Radiology and Athinoula A. 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