The effects of traumatic experience on the behavior, c-fos expression and functional connections in the mouse brain resting state networks

Toropova, K.A.; Ivashkina, O.I.; Ivanova, A.A.; Konovalova, E.V.; Anokhin, K.V.

Авторы: Toropova K.A., Ivashkina O.I., Ivanova Anna Andreevna, Konovalova E.V., Anokhin K.V.
Сборник: Conference proceedings 3rd International Conference Volga Neuroscience Meeting 2021
Год издания: 2021
Место издания: Lobachevsky State University of Nizhny Novgorod Nizhny Novgorod
Первая страница: 27
Последняя страница: 29
Аннотация: AimsIt is known that the brains of animals and humans is active at resting state. In this paper we investigate how past experience affects characteristics of such resting state networks in animals. To do this we subjected mice to single traumatic experience that induced posttraumatic stress disorder (PTSD) and then analyzed activity of their brain (including cortex; hippocampus; amygdala; basal ganglia; thalamus; hypothalamus and midbrain) by c-Fos cellular mapping during traumatic memory retrieval and at rest in comparison with non-stressed animals.Methods and ResultsPTSD development led to global changes in brain activity: number of c-Fos-active neurons was significantly increased in different brain areas during traumatic memory retrieval. Similarly PTSD induction strongly affects brain activity detected in resting state 7 days after: mice with prior traumatic experience had significantly increased number of c-Fos positive cells in comparison to naïve mice in cingulate cortex, retrosplenial cortex, parietal associative cortex, entorhinal cortex, basolateral and lateral amygdala, paraventricular thalamic nucleus and periaqueductal gray. Earlier these areas were shown to be involved in stress response and fear networks in humans and animals.Using correlational analysis and graph theory approach, we revealed structure connectivity in resting state networks of naïve and PTSD mice, developed functional resting state networks and determined their main clusters. In both groups of mice clusterization exceeded random level. At the same time, these clusters did not interact well with each other: global efficiency of experimental networks was at the level of random network. Resting state networks of PTSD and control mice differed (Fig. 1): PTSD network was less clustered and longer paths linked the clusters. Induction of PTSD led to global changes in the structure of resting state networks. In naive animals, cortical regions had the most connections, whereas in PTSD thalamus, striatum and amygdala had. PTSD destroyed virtually all functional connections present in naive mice; only fully connected cluster of auditory and visual cortices remained. In addition, if in naive animals the main hubs were cingulate and retrosplenial cortices in PTSD animals paraventricular thalamic nucleus became the hub. In contrast, amygdala functional connectivity was virtually zero in naive animals, whereas in PTSD significant number of connections between amygdala, associative cortices, and striatum were observed.In addition, we have shown that PTSD induction changes spontaneous behavior, causing elevated anxiety and decreased research activity in safe conditions of home cages. Behavior in conditioned fear, EPM and sensitization tests also changed, and these changes could be disrupted by protein synthesis inhibition during traumatic experience, which also returned brain activity and structure of resting networks to normal in PTSD animals.ConclusionsOur findings show that stressful experiences can alter spontaneous behavior, induced and spontaneous brain activity and patterns of functional connections in resting state neuronal networks long after traumatic episode. We assume that these changes reflect replay of neuronal ensembles of the animal's past subjective experience. This assumption was tested by disrupting the development of PTSD.
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