A high fat diet does not exacerbate CA1 injury and cognitive deficits following global ischemia in rats.

A diet high in saturated fat and similar in composition to western diets (WD) has been shown to exacerbate injury following traumatic brain injury. Thus, we investigated the effects of a WD on cell death and functional outcome following global ischemia. First we assessed the effects of a 60-day WD regimen on temperature, activity and glucose levels in normal rats (Experiment 1). Second, we evaluated the influence of a 60-day WD regimen on hippocampal CA1 injury and learning and memory impairments following global ischemia in rats (Experiment 2). Male Sprague-Dawley rats, obtained at approximately 50 g, were randomly assigned to either the WD or the low-fat control diet (CD). Animals were fed for 30 days, then subjected to surgery (body temperature probe implantation in experiment 1; forebrain ischemia in experiment 2), and then they stayed on the same diet for another 30 days. Two and 4 weeks following surgery, learning and memory were assessed using the Morris Water Maze. At 60 days, rats were killed and viable hippocampal CA1 cells were quantified. Results from experiment 1 revealed no differences in glucose or temperature profiles between animals fed the WD and CD; however, WD animals were significantly less active than CD animals. Eight minutes of ischemia in experiment 2 induced severe hippocampal CA1 cell loss (approximately 90%) and learning and memory impairments relative to non-ischemic controls. However, the WD did not exacerbate CA1 injury or behavioural deficits. These findings suggest that a 60-day WD regimen does not significantly influence recovery following global ischemia.

Failure of estradiol to improve spontaneous or rehabilitation-facilitated recovery after hemorrhagic stroke in rats.

Estrogen influences not only the incidence of stroke, but also the amount of injury sustained from a stroke including intracerebral hemorrhage (ICH). In this study we tested whether delayed 17beta-estradiol (E2) treatment affects recovery following striatal ICH. Female rats were trained and tested on several behavioral tests to assess skilled reaching, spontaneous forelimb usage and walking ability. Two weeks following ovariectomy, rats were subjected to a moderate-sized ICH via infusion of collagenase into the striatum. One week later they were implanted with either an E2 pellet (0.36 mg; 60-day release) or they underwent a sham procedure. They were further divided into groups that received either environmental enrichment (EE) rehabilitation therapy (group housing in a complex cage with ramps, tunnels, etc.) or a control condition (group housing in a standard cage). Rats were then behaviorally evaluated out to 8 weeks post-ICH and then euthanized. Neither EE nor E2 affected lesion size, which averaged 62.8 mm(3) across all groups. The EE therapy improved recovery on some tests (e.g., traversing a horizontal ladder) whereas E2 treatment did not notably affect either spontaneous or EE-facilitated recovery. Thus, E2 fails to improve recovery or protect against brain injury when given after a 1-week delay in contrast to its clear neuroprotective effects when given before or soon after ICH.