Hippocampal Corticosterone Levels Research Articles

Effects of different dark chocolate diets on memory functions and brain corticosterone levels in rats under chronic stress

Introduction: Stress influences cognitive behavior adversely, whereas dark chocolate exhibits positive effects on memory processes. This study investigated the effects of different dark chocolate diets on various aspects of brain functions in rats under chronic stress Methods: Thirty-five rats were randomly allocated into five groups: control, stress, stress with different (compulsory, optional and restricted) dark chocolate diets. Latency, dark stay (DS) time and the number of entrance to the dark compartment were respectively evaluated as memory, memory consolidation and locomotor activity by passive avoidance test. Results: There were significant differences between initial latency and latency after 1 day in all groups. In the stress-compulsory and restricted dark chocolate diet groups, latency after 1 day increased significantly. Moreover, the DS time was not significantly higher in the stressed group than the control group. The DS time and number of entrance to dark compartment decreased significantly in the stress-compulsory dark chocolate diet group compared to the stressed group. Furthermore, the number of entrance to dark compartment was significantly higher for the stress- optional dark chocolate diet compared to those with the compulsory diet. Additionally, serum and hippocampal corticosterone levels, except in the frontal cortex, were significantly lower only in the stress-compulsory dark chocolate diet group compared to the stressed group. Conclusion: Different dark chocolate diets had various effects on brain functions under chronic stress. Respectively, the compulsory and optional dark chocolate diets had the best and least effects on brain function improvement. Only the compulsory dark chocolate diet could improve brain functions such as memory, memory consolidation and locomotor activity.

The Effect of Preventive, Therapeutic and Protective Exercises on Hippocampal Memory Mediators in Stressed Rats.

Exercise plays a significant role in learning and memory. The present study focuses on the hippocampal corticosterone (CORT), interleukin-1 beta (IL-1β), glucose, and brain-derived neurotrophic factor (BDNF) levels in preventive, therapeutic, and protective exercises in stressful conditions. Forty male rats were randomly divided into four groups: the control group and the preventive, therapeutic, and protective exercise groups. The treadmill running was applied at a speed of 20-21m/min and a chronic stress of 6 hours/day for 21 days. Subsequently, the variables were measured in the hippocampus. The findings revealed that the hippocampal CORT levels in the preventive exercise group had a significant enhancement compared to the control group. In the protective and particularly the therapeutic exercise groups, the hippocampal CORT levels declined. Furthermore, the hippocampal BDNF levels in the preventive and the therapeutic exercise groups indicated significantly decreased and increased, respectively, in comparison with the control group. In the preventive exercise group, however, the hippocampal glucose level turned out to be substantially higher than that in the control group. It appears that the therapeutic exercise group had the best exercise protocols for improving the hippocampal memory mediators in the stress conditions. By contrast, the preventive exercise group could not improve these mediators that had been altered by stress. It is suggested that exercise time, compared to stress, can be considered as a crucial factor in the responsiveness of memory mediators.

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats.

Evidence suggests that there are positive effects of exercise on learning and memory. Moreover, some studies have demonstrated that forced exercise plays the role of a stressor. This study was aimed at investigating the effects of different timing of exercise and exercise withdrawal on memory, and serum and hippocampal corticosterone (CORT) levels. Wistar rats were randomly divided into five groups: control, sham, exercise-rest (exercise withdrawal), rest-exercise (exercised group), and exercise-exercise (continuous exercise). Rats were forced to run on a treadmill for 1 h/day at a speed 20-21-m/min. Memory function was evaluated by the passive avoidance test in different intervals (1, 7 and 21 days) after foot shock. Findings showed that after the exercise withdrawal, short-term and mid-term memories, had significant enhancement compared to the control group, while the long-term memory did not present this result. In addition, the serum and hippocampal CORT levels were at the basal levels after the rest period in the exercise-rest group. In the rest-exercise group, exercise improved mid- and long-term memories, whereas continuous exercise improved all types short-, mid- and long-term memories, particularly the mid-term memory. Twenty-one and forty-two days of exercise significantly decreased the serum and hippocampal CORT levels. It seems that exercise for at least 21 days with no rest could affect biochemical factors in the brain. Also, regular continuous exercise plays an important role in memory function. Hence, the duration and withdraw of exercise are important factors for the neurobiological aspects of the memory responses.

Diurnal and stress‐induced intra‐hippocampal corticosterone rise attenuated in 11β‐HSD1‐deficient mice: a microdialysis study in young and aged mice

11β‐Hydroxysteroid dehydrogenase type 1 (11β‐HSD1) locally regenerates active glucocorticoids from their inert forms thereby amplifying intracellular levels within target tissues including the brain. We previously showed greater increases in intra‐hippocampal corticosterone (CORT) levels upon Y‐maze testing in aged wild‐type than in 11β‐HSD1−/− mice coinciding with impaired and intact spatial memory, respectively. Here we examined whether ageing influences 11β‐HSD1 regulation of CORT in the dorsal hippocampus under basal conditions during the diurnal cycle and following stress. Intra‐hippocampal CORT levels measured by in vivo microdialysis in freely behaving wild‐type mice displayed a diurnal variation with peak levels in the evening that were significantly elevated with ageing. In contrast, the diurnal rise in intra‐hippocampal CORT levels was greatly diminished in 11β‐HSD1−/− mice and there was no rise with ageing; basal intra‐hippocampal CORT levels were similar to wild‐type controls. Furthermore, a short (3 min) swim stress induced a longer lasting increase in intra‐hippocampal CORT levels in wild‐type mice than in 11β‐HSD1−/− mice despite no genotypic differences in elevation of plasma CORT. These data indicate that 11β‐HSD1 activity contributes substantially to diurnal and stress‐induced increases in hippocampal CORT levels. This contribution is even greater with ageing. Thus, 11β‐HSD1 inhibition may be an attractive target for treating cognitive impairments associated with stress or ageing.

Vitamin A status regulates glucocorticoid availability in Wistar rats: consequences on cognitive functions and hippocampal neurogenesis?

A disruption of the vitamin A signaling pathway has been involved in age-related memory decline and hippocampal plasticity alterations. Using vitamin A deficiency (VAD), a nutritional model leading to a hyposignaling of the retinoid pathway, we have recently demonstrated that retinoic acid (RA), the active metabolite of vitamin A, is efficient to reverse VAD-induced spatial memory deficits and adult hippocampal neurogenesis alterations. Besides, excess of glucocorticoids (GCs) occurring with aging is known to strongly inhibit hippocampal plasticity and functions and few studies report on the counteracting effects of RA signaling pathway on GCs action. Here, we have addressed whether the modulation of brain GCs availability could be one of the biological mechanisms involved in the effects of vitamin A status on hippocampal plasticity and functions. Thus, we have studied the effects of a vitamin A-free diet for 14 weeks and a 4-week vitamin A supplementation on plasma and hippocampal corticosterone (CORT) levels in Wistar rats. We have also investigated corticosteroid binding globulin (CBG) binding capacity and 11beta-Hydrosteroid Dehydrogenase type 1 (11β-HSD1) activity, both important modulators of CORT availability at the peripheral and hippocampal levels respectively. Interestingly, we show that the vitamin A status regulates levels of free plasma CORT and hippocampal CORT levels, by acting through a regulation of CBG binding capacity and 11β-HSD1 activity. Moreover, our results suggest that increased CORT levels in VAD rats could have some deleterious consequences on spatial memory, anxiety-like behavior and adult hippocampal neurogenesis whereas these effects could be corrected by a vitamin A supplementation. Thus, the modulation of GCs availability by vitamin A status is an important biological mechanism that should be taken into account in order to prevent age-related cognitive decline and hippocampal plasticity alterations.

218. Elevated hippocampal corticosterone levels may be responsible for sensitizing microglia of healthy aged rats

218. Elevated hippocampal corticosterone levels may be responsible for sensitizing microglia of healthy aged rats