Гипотетический нейронный механизм слепоты невнимания

Авторы

  • Изабелла Гершовна Силькис Институт высшей нервной деятельности и нейрофизиологии РАН https://orcid.org/0000-0002-7622-2684

DOI:

https://doi.org/10.33910/2687-1270-2022-3-1-23-40

Ключевые слова:

произвольное внимание, синаптическая пластичность, дофамин, неокортекс, таламус, базальные ганглии, гиппокамп, мозжечок

Аннотация

Одним из подходов к изучению сознания является исследование особенностей слепоты невнимания. Поскольку этот эффект возникает в отсутствие произвольного внимания, изучение механизмов последнего представляет значительный интерес. Нами предположено, что включение произвольного внимания в обработку сенсорной информации требует активации префронтальной коры и гиппокампа, а также выделения дофамина во входной структуре базальных ганглиев — стриатуме. Это способствует растормаживанию нейронов таламуса, а также субталамического и педункулопонтийного ядер, находящихся под тормозным влиянием со стороны базальных ганглиев. Если нейроны вентрального стриатума, на которых конвергируют входы из префронтальной и ретросплениальной областей коры, а также гиппокампа, активируются достаточно сильно, дофаминзависимая реорганизация активности в цепях «кора — базальные ганглии — таламус — кора» способствует формированию нейронных отображений сенсорных стимулов в соответствующих областях коры. Кроме того, облегчаются условия для циркуляции возбуждения в топографически организованных таламо-кортикальных цепях, в цепях, связывающих первичные и высшие области коры через таламические ядра высокого порядка, а также в цепях, связывающих кору и таламус с гиппокампом, мозжечком, субталамическим и педункулопонтийным ядрами. Принято считать, что повторное возбуждение высших областей коры лежит в основе осознанного восприятия. Тогда время, необходимое для осознания сенсорного стимула, должно зависеть от времени циркуляции активности в указанных цепях. Из предлагаемого механизма следует, что вызванное дефицитом дофамина усиление ингибирования таламуса, а также ослабление его возбуждения со стороны коры, мозжечка, субталамического и педункулопонтийного ядер должно приводить к увеличению интервала между двумя стимулами, необходимого для осознания второго. Это следствие согласуется с известными результатами исследований слепоты невнимания, показавшими, что этот интервал действительно увеличивается при болезни Паркинсона, а также при повреждении мозжечка или педункулопонтийного ядра.

Библиографические ссылки

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