The Effect of Short-Term Feeding of a High-Coconut Oil or High-Fat Diet on Neuroinflammation and the Performance of an Object-Place Task in Rats.

The consumption of high-fat and high-sugar diets, in the form of junk food, and binge eating are now common. Increasing evidence suggests that a high-fat diet (HFD) can induce neuroinflammation and alter behavior. I aimed to study the effects of diets of differing fat content on neuroinflammation and spatial memory using an object-place (OP) task. Thirty-two adult male rats were allocated to four groups and fed a regular diet (Regular diet), a control diet (Control diet), an HFD (60% of calories from lard), or a high-coconut oil diet (HCOD; 60% of calories from coconut oil) for 3 days. Their water intake, food consumption, body mass, and metabolic variables were measured. HFD-fed rats showed significantly poorer performance on the OP task, as assessed using the discrimination index (- 0.208 ± 0.094), than the Regular (0.462 ± 0.078; P < 0.0001) and Control (0.379 ± 0.081; P = 0.0003) groups. However, no significant difference was observed in spatial memory between the HCOD and Regular groups. The concentrations of neuroinflammatory markers (interleukin [IL]-1ß, IL-6, tumor necrosis factor α, and nuclear factor κB) were also measured in the hippocampus and prefrontal cortex. HFD-fed rats showed significantly higher levels of neuroinflammatory markers than the Regular and Control diet-fed groups. HCOD feeding did not induce neuroinflammation in the hippocampus and prefrontal cortex compared with the Regular and Control groups.

New neurons restore structural and behavioral abnormalities in a rat model of PTSD.

Post-traumatic stress disorder (PTSD) has been associated with anxiety, memory impairments, enhanced fear, and hippocampal volume loss, although the relationship between these changes remain unknown. Single-prolonged stress (SPS) is a model for PTSD combining three forms of stress (restraint, swim, and anesthesia) in a single session that results in prolonged behavioral effects. Using pharmacogenetic ablation of adult neurogenesis in rats, we investigated the role of new neurons in the hippocampus in the long-lasting structural and behavioral effects of SPS. Two weeks after SPS, stressed rats displayed increased anxiety-like behavior and decreased preference for objects in novel locations regardless of the presence or absence of new neurons. Chronic stress produced by daily restraint for 2 or 6 hr produced similar behavioral effects that were also independent of ongoing neurogenesis. At a longer recovery time point, 1 month after SPS, rats with intact neurogenesis had normalized, showing control levels of anxiety-like behavior. However, GFAP-TK rats, which lacked new neurons, continued to show elevated anxiety-like behavior and enhanced serum corticosterone response to anxiogenic experience. Volume loss in ventral CA1 region of the hippocampus paralleled increases in anxiety-like behavior, occurring in all rats exposed to SPS at the early time point and only rats lacking adult neurogenesis at the later time point. In chronic stress experiments, volume loss occurred broadly throughout the dentate gyrus and CA1 after 6-hr daily stress but was not apparent in any hippocampal subregion after 2-hr daily stress. No effect of SPS was seen on cell proliferation in the dentate gyrus, but the survival of young neurons born a week after stress was decreased. Together, these data suggest that new neurons are important for recovery of normal behavior and hippocampal structure following a strong acute stress and point to the ventral CA1 region as a potential key mediator of stress-induced anxiety-like behavior.

Memory-related hippocampal brain-derived neurotrophic factor activation pathways from repetitive transcranial magnetic stimulation in the 3xTg-AD mouse line.

Alzheimer's disease is associated with a loss of plasticity and cognitive functioning. Previous research has shown that repetitive transcranial magnetic stimulation (rTMS) boosts cortical neurotrophic factors, potentially addressing this loss. The current study aimed to expand these findings by measuring brain-derived neurotrophic factor (BDNF), its downstream hippocampal signaling molecules, and behavioral effects of rTMS on the 3xTg-AD mouse line. 3xTg-AD (n = 24) and B6 wild-type controls (n = 26), aged 12 months, were given 14 days of consecutive rTMS at 10 Hz for 10 min. Following treatment, mice underwent a battery of behavioral tests and biochemical analysis of BDNF and its downstream cascades were evaluated via Western blot and ELISA. Results showed that brain stimulation did improve performance on the Object Place Task and increased hippocampal TrkB, ERK, and PLCγ in 3xTg-AD mice with minimal effects on wild-type mice. There was no significant difference in the levels of AKT and Truncated TrkB (TrkB.T1) between treatment and sham. Thus, rTMS has the potential to provide an efficacious non-invasive therapy for the treatment of Alzheimer's disease through activation of neurotrophic factor signaling.