QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

Help viewing high resolution images Return to article

Fig. 1. Anoxia or severe hypoxia typically lead to energy deficit (1), subsequent disruption of ion homeostasis and neuronal depolarization (2, 3). Release of neurotransmitters, including the excitotoxin glutamate, and activation of NMDA and AMPA receptors contribute to the flood of Ca²⁺ from extra- and intracellular stores, which leads to calcium overload (4). Activated microglia release inflammatory cytokines and nitric oxide and contribute to oxidative stress and neuronal cell death (5). Increased reactive oxygen species (ROS) production leads to oxidative modification of cellular components, which contributes to cell death (6). During hibernation, multiple adaptations, in addition to hypothermia, are hypothesized to act in concert to produce pronounced neuroprotection. Decreased demand for oxygen, as well as downregulation of Ca²⁺ channels, maintains energy balance, ion homeostasis and minimizes Ca²⁺ overload. Evidence suggests that immune modulation attenuates inflammatory response, and upregulation of antioxidant defense systems maintains redox balance, thus minimizing the neurodegenerative cascade (Sidky et al., 1972; Spurrier and Dawe, 1973; Drew et al., 1999; Zhou et al., 2001b; Toien et al., 2001). IL-1ß, interleukin-1ß; NO, nitric oxide; ROS, reactive oxygen species; ER, endoplasmic reticulum; NMDA, N-methyl-D-aspartate; Glu, glutamate; OGD, oxygen glucose deprivation.

Return to article