Effect of acute and repeated restraint stress on glucose oxidation to CO2 in hippocampal and cerebral cortex slices

Abstract

It has been suggested that glucocorticoids released during stress might impair neuronal function by decreasing glucose uptake by hippocampal neurons. Previous work has demonstrated that glucose uptake is reduced in hippocampal and cerebral cortex slices 24 h after exposure to acute stress, while no effect was observed after repeated stress. Here, we report the effect of acute and repeated restraint stress on glucose oxidation to CO 2 in hippocampal and cerebral cortex slices and on plasma glucose and corticosterone levels. Male adult Wistar rats were exposed to restraint 1 h/day for 50 days in the chronic model. In the acute model there was a single exposure. Immediately or 24 h after stress, the animals were sacrificed and the hippocampus and cerebral cortex were dissected, sliced, and incubated with Krebs buffer, pH 7.4, containing 5 mM glucose and 0.2 µCi D-[U-14 C] glucose. CO 2 production from glucose was estimated. Trunk blood was also collected, and both corticosterone and glucose were measured. The results showed that corticosterone levels after exposure to acute restraint were increased, but the increase was smaller when the animals were submitted to repeated stress. Blood glucose levels increased after both acute and repeated stress. However, glucose utilization, measured as CO 2 production in hippocampal and cerebral cortex slices, was the same in stressed and control groups under conditions of both acute and chronic stress. We conclude that, although stress may induce a decrease in glucose uptake, this effect is not sufficient to affect the energy metabolism of these cells. Correspondence

Interactions Between Chronic Stress and Chronic Consumption of Caffeine on the Enzymatic Antioxidant System

“…For example, after several exposures to restraint, we observed changes in the behavior of the animals, including less defecation. Measurements of corticosterone have also been made previously and, although the chronically restrained rats still release corticosterone after a new restraint session, the increase in this hormone levels in plasma is much smaller than that presented in the first days of stress [38].…”

Effect of Chronic Stress and L-Carnitine on Rat Stomach

“…**p < 0.01 vs. the value in control rats; # p < 0.05 vs. the value in stressed rats. [33]. Repeated exposure to stress leads to a process of adaptation to that stimulus.…”

Lipid peroxidation and total radical-trapping potential of the lungs of rats submitted to chronic and sub-chronic stress

“…It should be noted that in the chronic restraint stress model the increase in corticosterone levels after exposure to stress for 40 days is much lower than after the first stress session (32). In the present study, we chose to use variable chronic stress in order to reduce the predictability of treatment, which may occur with repeated exposure to the same stressor.…”

“…The increase in TRAP observed in the present study is probably enough to keep the steadystate ROS concentration under control, since no change in TBARS was observed during a short period of time (15 days). On the other hand, when exposed for longer periods of time (40 days of restraint), the animals possibly adapt to this stressor, as demonstrated by lower levels of corticosterone when compared to the initial days of treatment (32,35). The possible adaptation to a repeated stressor, with progressively smaller responses to it, may help to explain why variable chronic stress, but not repeated-restraint stress, induces lipoperoxidation after 40 days of treatment.…”