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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">vavilov</journal-id><journal-title-group><journal-title xml:lang="ru">Вавиловский журнал генетики и селекции</journal-title><trans-title-group xml:lang="en"><trans-title>Vavilov Journal of Genetics and Breeding</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">2500-3259</issn><publisher><publisher-name>Institute of Cytology and Genetics of Siberian Branch of the RAS</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18699/VJ17.261</article-id><article-id custom-type="elpub" pub-id-type="custom">vavilov-1019</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>ГЕНЕТИКА ПОВЕДЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>BEHAVIORAL GENETICS</subject></subj-group></article-categories><title-group><article-title>Генетическая линия крыс Крушинского – Молодкиной как уникальная экспериментальная модель судорожных состояний</article-title><trans-title-group xml:lang="en"><trans-title>The Krushinsky – Molodkina genetic rat strain as a unique experimental model of seizure states</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>Полетаева</surname><given-names>И. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Poletaeva</surname><given-names>I. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>биологический факультет</p></bio><bio xml:lang="en"><p>Department of Biology</p></bio><email xlink:type="simple">ingapoletaeva@mail.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>Костына</surname><given-names>З. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kostyna</surname><given-names>Z. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>биологический факультет</p></bio><bio xml:lang="en"><p>Department of Biology</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>Сурина</surname><given-names>Н. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Surina</surname><given-names>N. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>биологический факультет</p></bio><bio xml:lang="en"><p>Department of Biology</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>Федотова</surname><given-names>И. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Fedotova</surname><given-names>I. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>биологический факультет</p></bio><bio xml:lang="en"><p>Department of Biology</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>Зорина</surname><given-names>З. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Zorina</surname><given-names>Z. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>биологический факультет</p></bio><bio xml:lang="en"><p>Department of Biology</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Московский государственный университет им. М.В. Ломоносова<country>Россия</country></aff><aff xml:lang="en">Lomonosov Moscow State University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>24</day><month>07</month><year>2017</year></pub-date><volume>21</volume><issue>4</issue><fpage>427</fpage><lpage>434</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Полетаева И.И., Костына З.А., Сурина Н.М., Федотова И.Б., Зорина З.А., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Полетаева И.И., Костына З.А., Сурина Н.М., Федотова И.Б., Зорина З.А.</copyright-holder><copyright-holder xml:lang="en">Poletaeva I.I., Kostyna Z.A., Surina N.M., Fedotova I.B., Zorina Z.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://vavilov.elpub.ru/jour/article/view/1019">https://vavilov.elpub.ru/jour/article/view/1019</self-uri><abstract><p>Исследование генетических механизмов, лежащих в основе нормальных и патологических признаков поведения животных, важно не только для общего понимания работы центральной нервной системы (ЦНС) позвоночных, но и для благополучия человека, в частности в борьбе с заболеваниями мозга. Накопление знаний о функциях генов, экспрессирующихся в ЦНС и связанных со специфическими функциями мозга, которые сегодня определяются успехами молекулярной генетики, не делает менее актуальным исследование фенотипического проявления генетически детерминированных признаков, в особенности патологических. Эпилепсия как одно из заболеваний ЦНС занимает важное место в таких работах. Несмотря на большое количество новых противосудорожных средств, значительная доля случаев этой болезни по-прежнему не поддается лечению. В связи с этим исследование механизмов эпилептогенеза на моделях востребовано, поскольку может способствовать выявлению тех особенностей развития повышенной судорожной готовности, которые пока остаются мало изученными. Одним из четких, но непростых для генетического исследования признаков является аудиогенная эпилепсия (судороги в ответ на сильный звук), которая рассматривается в этой статье. Важное свойство аудиогенной эпилепсии как модели – возможность анализа интенсивных тонических судорог в условиях хронического эксперимента (т. е. с повторной провокацией этого состояния у одного и того же животного, что невозможно в случае фармакологических или «электрошоковых» судорог). В статье дается краткая характеристика инбредной линии крыс Крушинского – Молодкиной, первой из линий, селектированных на этот признак. Характерный «рисунок» судорожного припадка, наиболее частое проявление его у грызунов, постиктальные аномальные состояния (в частности, каталепсия) и ряд других патологических признаков делают этот феномен важным не только как модель патологии, но и как явление общебиологической значимости. Влияние генетического фона (продемонстрированное для случаев коморбидности этих судорог с депрессией и тревожностью) может оказаться решающим фактором в определении механизмов других аномалий ЦНС. Развитие аудиогенных судорог как физиологического феномена, сопровождающего другие патологические состояния, было также предметом исследований коллег Д.К. Беляева в Институте цитологии и генетики.</p></abstract><trans-abstract xml:lang="en"><p>The study of genetic mechanisms, which underlie normal and abnormal behavioral traits, are important not only for fundamental knowledge of CNS function, but also for human well-being, as well as in the aspect of treatment of brain diseases. Accumulation of knowledge concerning the functions of genes, which are expressed in the CNS and are involved in the specific brain functions determined now by the success of molecular genetics, but it could not overshadow the importance of phenotype expression investigation of genetically determined traits, especially pathological ones. Epilepsy, as one of CNS diseases, occupies an important place in the row of these studies. In spite of numerous anticonvulsant drugs a significant proportion of epilepsy cases are still resistant to drug treatments. It means that the study of various aspects of epileptogenesis using animal models should be welcomed as it will help to elucidate those aspects of increased seizure proneness that are now out of scope of research attention. The distinct trait of this domain, which is not easy to analyze genetically, is audiogenic epilepsy (the seizure attack in response to loud sound). The important feature of audiogenic epilepsy is that the intense tonic seizures could be induced and analyzed repeatedly which makes it possible to induce the seizures repeatedly in the course of chronical experiments with the same animal, which is not possible in the cases of pharmacologically or electrically induced seizures. The Krushinsky – Molodkina (KM) inbred rat strain, which was the first among strains selected for audiogenic epilepsy, is briefly characterized. The specific seizure pattern, the rodent proneness for audiogenic epilepsy, as well as abnormal postictal states (catalepsy, in particular) illustrate the importance of this phenomenon not only as a model of certain brain pathology, but also as a matter of general biological importance. The importance of genetic background factor (demonstrated in the case of study of comorbidity (audiogenic epilepsy, anxiety and depression)) could be crucial in the studies of other CNS anomalies. The audiogenic seizures as a physiological phenomenon which often accompanies several brain pathologies had been in the scope of research interests for D.K. Belyaev and his colleagues in his Institute.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>генетика поведения</kwd><kwd>аудиогенная эпилепсия</kwd><kwd>крысы линии Крушинского – Молодкиной</kwd></kwd-group><kwd-group xml:lang="en"><kwd>behavior genetics</kwd><kwd>audiogenic epilepsy</kwd><kwd>Krushinsky – Molodkina rat strain</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">Akbar М.T., Rattray M., Williams R.J., Chong N.W., Meldrum B.S. Reduction of GABA and glutamate transporter messenger RNA in the severe seizure genetically epilepsy-prone rat. Neuroscience. 1998; 85:1235-1251.</mixed-citation><mixed-citation xml:lang="en">Akbar М.T., Rattray M., Williams R.J., Chong N.W., Meldrum B.S. Reduction of GABA and glutamate transporter messenger RNA in the severe seizure genetically epilepsy-prone rat. 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