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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">mimmun</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинская иммунология</journal-title><trans-title-group xml:lang="en"><trans-title>Medical Immunology (Russia)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1563-0625</issn><issn pub-type="epub">2313-741X</issn><publisher><publisher-name>SPb RAACI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15789/1563-0625-EON-2329</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-2432</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>МАТЕРИАЛЫ ФОРУМА "ДНИ ИММУНОЛОГИИ В СПБ" 2021</subject></subj-group></article-categories><title-group><article-title>ЭМБРИОГЕНЕЗ НЕЙРОНАЛЬНЫХ ЭЛЕМЕНТОВ (ГЛИОБЛАСТОВ И ГАМКА-РЕЦЕПТОРОВ) НЕЙРОИММУННОЙ СИСТЕМЫ МОЗГА ЧЕЛОВЕКА ПРИ ПРЕНАТАЛЬНОМ ВЛИЯНИИ АЛКОГОЛЯ</article-title><trans-title-group xml:lang="en"><trans-title>EMBRIOGENESIS OF NEURONAL ELENENTS (GLIOBLASTS AND GABAA RECEPTORS) IN THE HUMAN BRAIN NEUROIMMUNE SYSTEM UNDER PRENATAL ALCOHOL EXPOSURE</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шушпанова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shushpanova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., ведущий научный сотрудник лаборатории клинической психонейроиммунологии инейробиологии, </p><p>634014, г. Томск, ул. Алеутская, 4</p></bio><bio xml:lang="en"><p>PhD (Medicine), Leading Research Associate, Laboratory of Clinical Psychoneuroimmunology and Neurobiology, </p><p>634014, Tomsk, Aleutskaya str., 4</p></bio><email xlink:type="simple">mental@tnimc.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Солонский</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Solonsky</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., ведущий научный сотрудник лаборатории клинической психонейроиммунологии и нейробиологии, </p><p>634014, г. Томск, ул. Алеутская, 4</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Leading Research Associate, Laboratory of Clinical Psychoneuroimmunology and Neurobiology, </p><p>634014, Tomsk, Aleutskaya str., 4</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шумилова</surname><given-names>С. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Shumilova</surname><given-names>S. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>лаборант-исследователь лаборатории клинической психонейроиммунологии и нейробиологии, </p><p>634014, г. Томск, ул. Алеутская, 4</p></bio><bio xml:lang="en"><p>Research Assistant, Laboratory of Clinical Psychoneuroimmunology and Neurobiology,</p><p>634014, Tomsk, Aleutskaya str., 4</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шушпанова</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shushpanova</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>научный сотрудник отдела по изучению проблем детской психиатрии,</p><p>г. Москва</p></bio><bio xml:lang="en"><p>Research Associate, Department for the Study of Problems of Child Psychiatry,</p><p>Moscow</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Бохан</surname><given-names>Н. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Bokhan</surname><given-names>N. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, академик РАН, заслуженный деятель науки РФ, заведующий отделением аддиктивных состояний, директор, 634014, г. Томск, ул. Алеутская, 4;</p><p>заведующий кафедрой психиатрии, наркологии и психотерапии, г. Томск</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Professor, Full Member, Russian Academy of Sciences, Honored Scientist of the Russian Federation; Head, Department of Addictive States, Director, 634014, Tomsk, Aleutskaya str., 4;</p><p>Head, Department of Psychiatry, Narcology and Psychotherapy, Tomsk</p></bio><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Научно-исследовательский институт психического здоровья ФГБНУ «Томский научный исследовательский медицинский центр Российской Академии наук»<country>Россия</country></aff><aff xml:lang="en">Research Institute of Mental Health, Tomsk National Research Medical Center of the Russian Academy of Sciences<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">ФГБНУ «Научный центр психического здоровья»<country>Россия</country></aff><aff xml:lang="en">Mental Health Research Center<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru">Научно-исследовательский институт психического здоровья ФГБНУ «Томский научный исследовательский медицинский центр Российской Академии наук»;&#13;
ФГБОУ ВО «Сибирский государственный медицинский университет»<country>Россия</country></aff><aff xml:lang="en">Research Institute of Mental Health, Tomsk National Research Medical Center of the Russian Academy of Sciences;&#13;
Siberian State Medical University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>19</day><month>10</month><year>2021</year></pub-date><volume>23</volume><issue>4</issue><fpage>871</fpage><lpage>880</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Шушпанова Т.В., Солонский А.В., Шумилова С.Н., Шушпанова О.В., Бохан Н.А., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Шушпанова Т.В., Солонский А.В., Шумилова С.Н., Шушпанова О.В., Бохан Н.А.</copyright-holder><copyright-holder xml:lang="en">Shushpanova T.V., Solonsky A.V., Shumilova S.N., Shushpanova O.V., Bokhan N.A.</copyright-holder><license license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.mimmun.ru/mimmun/article/view/2432">https://www.mimmun.ru/mimmun/article/view/2432</self-uri><abstract><p>Воздействие алкоголя вызывает дисбаланс нейроиммунной функции и приводит к нарушению развития мозга. Алкоголь активирует сигнальные пути врожденного иммунитета в мозге. Нейроиммунные молекулы, экспрессируемые и секретируемые глиальными клетками головного мозга (микроглия, олигодендроглия), изменяют функцию нейронов и стимулируют в дальнейшем развитие алкогольного поведения. В передаче нейроиммунных сигналов участвуют различные сигнальные пути и клетки мозга. Глиальные клетки являются основными источниками иммунных медиаторов в головном мозге, которые отвечают на иммунные сигналы в центральной нервной системе и выделяют их. Целью настоящего исследования было изучение нейрональных элементов: морфометрических параметров глиобластов, синаптических структур и свойств синаптосомальных ГАМКА-бензодиазепиновых рецепторов нейроиммунной системы в эмбриогенезе мозга человека при перинатальном воздействии алкоголя. Выявлены изменения глиобластов в ткани мозга эмбрионов и плодов человека в условиях хронической пренатальной алкоголизации с увеличением срока беременности по сравнению с контрольными подгруппами: достоверное увеличение среднего количества глиобластов, длины периметров пресинаптических терминальных структур, постсинаптической плотности, пресинаптические терминальные области были значительно меньше (p &lt; 0,01) в исследуемой группе, чем в контрольной группе сравнения. Воздействие этанола приводит к снижению аффинности ГАМКАбензодиазепиновых рецепторов, что влияет на нейрональную пластичность, связанную с развитием и дифференцировкой клеток-предшественников (глиобластов и нейробластов) в период эмбриогенеза головного мозга человека и приводит к подавлению ГАМКергической функции в головном мозге. Это вызывает нарушение взаимосвязей эмбриональных клеток в головном мозге, приводит к чрезмерным явлениям апоптоза из-за активации глиальных клеток нервной ткани, нарушению нейроиммунной функции в развивающемся мозге, изменениям нейрональных цепей, а также к изменению баланса возбуждающих и тормозных эффектов, что оказывает влияние на функциональную активность в центральной нервной системе. Активация глии – это компенсаторная реакция, вызванная нейропластическими изменениями, направленная на адаптацию развивающегося мозга эмбриона и плода в условиях нейротоксичности и гипоксии под воздействием пренатальной алкоголизации материнского организма и влияния этанола на плод. Динамика изменений глиальных элементов и рецепторной активности в нервной ткани эмбрионов и плодов человека в условиях пренатального воздействия алкоголя свидетельствует о более выраженном влиянии алкоголя на самые ранние стадии развития эмбриона человека, что имеет большое практическое значение при планировании беременности и недопустимость алкоголизации матери во избежание негативных последствий у потомства. </p></abstract><trans-abstract xml:lang="en"><p>Exposure to alcohol causes imbalances in neuroimmune function and impaired brain development. Alcohol activates the innate immune signaling pathways in the brain. Neuroimmune molecules expressed and secreted by glial cells of the brain (microglia, oligodendroglia) alter the function of neurons and further stimulate the development of alcoholic behavior. Various signaling pathways and brain cells are involved in the transmission of neuroimmune signals. Glial cells are the main sources of immune mediators in the brain, which respond to and release immune signals in the central nervous system. The aim of this study was to study neuronal elements: morphometric parameters of glioblasts, synaptic structures and properties of synaptosomal GABAA-benzodiazepine receptors of the neuroimmune system in the embryogenesis of the human brain under perinatal exposure to alcohol. Changes in glioblasts in the brain tissue of human embryos and fetuses were revealed under conditions of chronic prenatal alcoholization with an increase in gestational age compared with control subgroups: a significant increase in the average number of glioblasts, the length of the perimeters of presynaptic terminal structures, postsynaptic density, presynaptic terminal regions were significantly less (p &lt; 0.01) in the study group than in the control comparison group. Exposure to ethanol leads to a decrease in the affinity of GABAA-benzodiazepine receptors, which affects neuronal plasticity associated with the development and differentiation of progenitor cells (glioblasts and neuroblasts) during embryogenesis of the human brain and leads to suppression of GABAergic function in the brain. This causes a disruption in the interconnection of embryonic cells in the brain, leads to excessive apoptosis due to the activation of glial cells of the nervous tissue, disruption of neuroimmune function in the developing brain, changes in neuronal circuits, as well as a change in the balance of excitatory and inhibitory effects, which affects the functional activity in the central nervous system. Glial activation is a compensatory reaction caused by neuroplastic changes aimed at adapting the developing brain of the embryo and fetus under conditions of neurotoxicity and hypoxia under the influence of prenatal alcoholization of the maternal organism and the effect of ethanol on the fetus. The dynamics of changes in glial elements and receptor activity in the nervous tissue of human embryos and fetuses under conditions of prenatal exposure to alcohol indicates a more pronounced effect of alcohol on the earliest stages of human embryo development, which is of great practical importance in planning pregnancy and the inadmissibility of alcoholization of the mother in order to avoid negative consequences in offspring. </p></trans-abstract><kwd-group xml:lang="ru"><kwd>эмбриогенез</kwd><kwd>нейроиммунная система</kwd><kwd>головной мозг</kwd><kwd>алкоголь</kwd><kwd>глиобласт</kwd><kwd>ГАМКА-рецептор</kwd><kwd>синапс</kwd></kwd-group><kwd-group xml:lang="en"><kwd>embryogenesis</kwd><kwd>neuroimmune system</kwd><kwd>brain</kwd><kwd>alcohol</kwd><kwd>glioblast</kwd><kwd>GABAA receptor</kwd><kwd>synapse</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Akiyoshi R., Wake H., Kato D., Horiuchi H., Ono R., Ikegami A., Haruwaka K., Omori T., Tachibana Y., Moorhouse A.J., Nabekura J. 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