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<p>Using real-time PCR, changes in the gene expression of TNFα and its receptor TNFRSF1A, factors involved in the regulation of inflammatory processes and synaptic plasticity, were examined in the hippocampus, frontal cortex, and cerebellum of adult male Wistar rats following either the formation of long-term spatial memory in the Morris water maze or forced swimming stress using a comparable time protocol. An increase in <i>Tnfa</i> gene expression was observed in all three brain regions. In contrast, elevated <i>Tnfrsf1a</i> expression was detected only in the hippocampus and frontal cortex but not in the cerebellum of both trained and stressed rats in comparison with the intact controls. Notably, <i>Tnfa</i> expression in the hippocampus of trained animals was significantly lower than that in untrained stressed rats. Furthermore, <i>Tnfrsf1a</i> expression showed a negative correlation with the success rate of long-term memory formation. These findings suggest the existence of adaptive mechanisms associated with long-term memory formation that act to suppress proinflammatory signaling pathways in the brain.</p>

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Expression Levels of the Immunomodulatory Cytokine TNFα and Its Receptor TNFRSF1A in Rat Brain Structures during Long-Term Spatial Memory Formation and Forced Swim Stress

  • 期刊论文

  • 发表日期：

    2025年11月1日

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  • A. M. Ratmirov,
  • M. A. Gruden,
  • Z. I. Storozheva

摘要

Using real-time PCR, changes in the gene expression of TNFα and its receptor TNFRSF1A, factors involved in the regulation of inflammatory processes and synaptic plasticity, were examined in the hippocampus, frontal cortex, and cerebellum of adult male Wistar rats following either the formation of long-term spatial memory in the Morris water maze or forced swimming stress using a comparable time protocol. An increase in Tnfa gene expression was observed in all three brain regions. In contrast, elevated Tnfrsf1a expression was detected only in the hippocampus and frontal cortex but not in the cerebellum of both trained and stressed rats in comparison with the intact controls. Notably, Tnfa expression in the hippocampus of trained animals was significantly lower than that in untrained stressed rats. Furthermore, Tnfrsf1a expression showed a negative correlation with the success rate of long-term memory formation. These findings suggest the existence of adaptive mechanisms associated with long-term memory formation that act to suppress proinflammatory signaling pathways in the brain.