Event Title

Exercise Increases Caspase-3 Expression in the Rat Hippocampus

Presenter Information

Nicole Lensmire
Eva Armour

Mentor 1

Rodney Swain

Location

Union Wisconsin Room

Start Date

27-4-2018 1:00 PM

Description

Previous research emphasizes brain plasticity due to aerobic exercise. In the hippocampus, exercise accelerates neurogenesis, the proliferation of new neurons in the dentate gyrus and changes astrocyte morphology. Identifying the cellular and molecular events that underlie exercise-induced increases in hippocampal volume are critical to understanding how exercise facilitates cognition and protects the brain from Alzheimer’s disease. Although markers for cell death differed across studies, all suggest elevated apoptosis following a single bout of exercise. Twenty, male rats were divided into two groups: inactive control (IC) and voluntary exercise (VX). VX animals had 24 hr access to a running wheel. Immunohistochemistry was used to label cleaved caspase-3, mature neurons, immature neurons, radial glia-like cells, and astrocytes. Our goal was initially to determine which of these cells were dying. Light and fluorescence microscopes were used for imaging. Unbiased stereology was used for quantification of labeling. Increased caspase-3 expression was found in VX animal’s hippocampi in astrocytes and radial glia-like cells. There was no significance for caspase-3 in neurons and it was not associated with apoptosis. Our results add to the small body of literature that suggests activated caspase-3 can serve as a non-apoptotic role, outside of major events like development or insult.

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Apr 27th, 1:00 PM

Exercise Increases Caspase-3 Expression in the Rat Hippocampus

Union Wisconsin Room

Previous research emphasizes brain plasticity due to aerobic exercise. In the hippocampus, exercise accelerates neurogenesis, the proliferation of new neurons in the dentate gyrus and changes astrocyte morphology. Identifying the cellular and molecular events that underlie exercise-induced increases in hippocampal volume are critical to understanding how exercise facilitates cognition and protects the brain from Alzheimer’s disease. Although markers for cell death differed across studies, all suggest elevated apoptosis following a single bout of exercise. Twenty, male rats were divided into two groups: inactive control (IC) and voluntary exercise (VX). VX animals had 24 hr access to a running wheel. Immunohistochemistry was used to label cleaved caspase-3, mature neurons, immature neurons, radial glia-like cells, and astrocytes. Our goal was initially to determine which of these cells were dying. Light and fluorescence microscopes were used for imaging. Unbiased stereology was used for quantification of labeling. Increased caspase-3 expression was found in VX animal’s hippocampi in astrocytes and radial glia-like cells. There was no significance for caspase-3 in neurons and it was not associated with apoptosis. Our results add to the small body of literature that suggests activated caspase-3 can serve as a non-apoptotic role, outside of major events like development or insult.