Russian Journal of PhysiologyRussian Journal of PhysiologyРоссийский физиологический журнал им. И.М. Сеченова0869-81392658-655XThe Russian Academy of Sciences69825110.7868/S2658655X25110035EXPERIMENTAL ARTICLESЭКСПЕРИМЕНТАЛЬНЫЕ СТАТЬИResearch ArticleThe Features of Neural Mechanisms Underlying Visceral Pain Processing in the Basolateral Amygdala of Rats with Post-Inflammatory or Stress-Induced HyperalgesiaОСОБЕННОСТИ НЕЙРОНАЛЬНЫХ МЕХАНИЗМОВ ОБРАБОТКИ ВИСЦЕРАЛЬНЫХ БОЛЕВЫХ СИГНАЛОВ В БАЗОЛАТЕРАЛЬНОЙ АМИГДАЛЕ У КРЫС С КИШЕЧНОЙ ГИПЕРАЛГЕЗИЕЙ ВОСПАЛИТЕЛЬНОГО ИЛИ СТРЕССОРНОГО ГЕНЕЗАLyubashinaO. A.ЛюбашинаО. А.lyubashinaoa@infran.ruMehilyainenD. A.МехиляйненД. А.SivachenkoI. B.СиваченкоИ. Б.Pavlov Institute of Physiology of the Russian Academy of SciencesИнститут физиологии им. И.П. Павлова РАН1511202511111VOL 111, NO11 (2025)ТОМ 111, №11 (2025)1728174909122025Copyright ©; 2025, Russian Academy of SciencesCopyright ©; 2025, Российская академия наук2025Russian Academy of SciencesРоссийская академия наукhttps://journals.eco-vector.com/0869-8139/article/view/698251

Increased intestinal pain sensitivity (intestinal hyperalgesia) may be a consequence of intestinal inflammation or experienced stress. Both conditions are thought to be associated with a dysfunction of the basolateral amygdala (BLA), since they are accompanied by it’s neurochemical and molecular rearrangements. However, the accompanying changes in the neuronal mechanisms of BLA-executed control of visceral nociception and their possible specificity for post-inflammatory and stress-induced hyperalgesia remain unclear. The aim of the study was to compare the changes in the functional properties of visceral pain-responsive BLA neurons and their modulation by the infralimbic area of the medial prefrontal cortex (IL) that occur after intestinal inflammation or stress. The work was performed on male Wistar rats: 1) control, 2) subjected to experimental colitis and 3) subjected to prolonged emotional-painful stress. In animals from different groups, in awake state the intestinal hyperalgesia was assessed by recording the noxious colorectal distension (CRD)-induced visceromotor response, and under general anesthesia the microelectrode recording of the background impulse activity of BLA neurons and their responses to CRD before and after IL electrical stimulation was performed. It was found that rats from the postcolitis and stressed groups demonstrate intestinal hyperalgesia, which is more pronounced after stress. The postcolitis state is associated with a decrease, and the stressed state – with an increase in the background activity frequency of BLA neurons. It was shown for the first time that in both cases the BLA neurons that respond to CRD with excitation or inhibition increase their reactivity to the stimulating action of IL. The postcolitis period is characterized by an increase in the IL activating effect on the CRD-inhibited BLA neurons, whereas the poststress period is characterized by an increase in the IL-induced stimulation of excitated and inhibited nociceptive cells. The neuronal alterations revealed in the BLA may lead to the disturbances in the amygdala-executed control of the sensory and emotional components of visceral pain that are inherent to postinflammatory or stress-induced intestinal hyperalgesia, being thus a specific target for the treatment of such conditions in the clinic.

Усиление болевой чувствительности кишки (кишечная гипералгезия) может являться следствием кишечного воспаления или перенесенного стресса. Оба состояния связывают с дисфункцией базолатеральной амигдалы (БЛА), поскольку они сопровождаются нейрохимическими и молекулярными перестройками в ней. Однако сопутствующие изменения в нейрональных механизмах контроля БЛА висцеральной ноцицепции и их возможная специфика для поствоспалительной и постстрессорной гипералгезий остаются неясными. Целью исследования являлась сравнительная оценка изменений в функциональных свойствах реактивных к висцеральной боли нейронов БЛА и влияниях на них инфралимбической области медиальной префронтальной коры (ИК), которые возникают после кишечного воспаления или стресса. Работа выполнена на самцах крыс Вистар: 1) контрольных, 2) перенесших экспериментальный колит и 3) подвергнутых длительному эмоционально-болевому стрессу. У животных разных групп в бодрствующем состоянии оценивали кишечную гипералгезию посредством регистрации висцеромоторной реакции на болевое колоректальное растяжение (КРР), а под общей анестезией – производили микроэлектродную регистрацию фоновой импульсной активности нейронов БЛА и их реакций на КРР до и после электростимуляции ИК. Установлено, что крысы постколитной и стрессированной групп демонстрируют кишечную гипералгезию, которая больше выражена после стресса. Постколитное состояние ассоциировано со снижением, а постстрессорное – с повышением частоты фоновой активности нейронов БЛА. Впервые показано, что в обоих случаях усиливается реактивность нейронов БЛА, отвечающих на КРР возбуждением или торможением, к стимулирующим влияниям ИК. Для постколитного периода характерно усиление активирующего действия ИК на тормозящиеся при КРР нейроны БЛА, а для постстрессорного – на возбуждающиеся и тормозящиеся ноцицептивные клетки. Выявленные в БЛА нейрональные перестройки могут приводить к присущим поствоспалительной или постстрессорной кишечным гипералгезиям нарушениям в амигдалярном контроле сенсорного и эмоционального компонентов висцеральной боли и являться специфическими мишенями при лечении таких состояний в клинике.

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