Acute restraint stress and epinephrine administration disrupt cognitive and emotional functions in male rats via modulation of proinflammatory cytokines, MCT-2, and neurogranin.

Stress triggers neuroendocrine and physiological changes, often resulting in cognitive impairments and heightened anxiety. This study aims to investigate the effects of acute stress and epinephrine administration on learning, memory, and anxiety-like behavior, as well as their impact on proinflammatory cytokines, neurogranin expression, and brain energy metabolism. In this study, three experimental groups were established, each comprising eight rats: control, acute stress, and acute stress combined with epinephrine. The acute stress model consisted of 60 min of restraint stress. Epinephrine was administered following the stress procedure. Memory performance was evaluated using the Morris water maze (MWM), while anxiety-like behavior was assessed through the open field test (OFT). Levels of proinflammatory cytokines, neurogranin, MCT2, glycogen, and corticosterone levels were measured. In the probe test, the acute stress group exhibited significantly poorer performance compared to the control group. Epinephrine administration induced anxiogenic effects in stressed animals. Neurogranin and glycogen levels in the hippocampus and prefrontal cortex were significantly reduced in rats exposed to stress + epinephrine compared to controls. MCT2 expression was also significantly lower in the stress + epinephrine group. IL-1β level was elevated in the prefrontal cortex of the stress + epinephrine group compared to the control group, while, TNF-α levels were found to be elevated in the hippocampus. Epinephrine administration in conjunction with acute stress has been shown to reduce hippocampal levels of neurogranin, MCT-2, and glycogen, while simultaneously increasing proinflammatory cytokine levels. These molecular alterations appear to contribute to both impaired hippocampal-dependent learning and heightened anxiety-like behavior.