ReviewOxidative stress and redox regulation on hippocampal-dependent cognitive functions
Section snippets
Hippocampal-dependent learning and memory
Hippocampus is critical for the acquisition (learning), consolidation and retrieval of declarative memories (reviewed in [1]). It is also important for the formation of spatial memory [2], [3]. The hippocampus is located in the medial temporal lobe of the brain and is composed of two separate structures: the dentate gyrus (DG)
Redox potential and cell fate decision
Changes in intracellular redox potential and the extracellular microenvironment can impact cell fate decisions, including entering or exiting cell cycle, proliferation or differentiation, and survival or cell death. Redox couples, such as GSH/GSSG and NADPH/NADP+ are presence in high abundance in cells and the status of these redox couples can serve as important indicators for the reduction potential of intracellular environment, which then influence the activity of redox-sensitive proteins
Redox balance and hippocampal neurogenesis
Stem cells usually reside in an environment with low oxygen tension, and recent studies suggest that activation of hypoxia-inducible factor 1 alpha (HIF-1α) in low oxygen environment facilitates signaling pathways that favors self renewal and inhibits pathways that promote differentiation [67]. In addition to the external environment, intracellular ROS production increases as cells proceed through the differentiation process. Within the hippocampal redox environment that favors differentiation,
Redox balance and dendritic structure
Hippocampal-dependent learning is mainly mediated by excitatory neurons with granule cells in the dentate gyrus and pyramidal cells in the CA areas. Granule cells and pyramidal cells put out extensive dendrites that synapse with axons and dendrites from other neurons for proper control of synaptic transmissions. Dendritic spines are small protrusions on dendrites that receive input from synapses on axons. They constitute the post synaptic element of excitatory synapses and mediate the majority
Redox balance and hippocampal-dependent learning and memory
Several behavioral studies are designed based on the natural curiosity of rodents to explore novel objects and locations or their natural instincts to freeze when frightened to examine hippocampal-dependent and independent cognitive functions. In the novel object recognition paradigm, mice have the natural tendency to spend relatively more time exploring a novel object when it is presented with a familiar object at the same time. Such recognition memory depends on multiple brain areas, but most
Radiation, oxidative stress, and hippocampal functions
The brain is exposed to ionizing radiation in a number of clinical situations, predominantly in those involving cancer treatments. Radiation brain injury could involve macroscopic tissue destruction after relatively high doses of irradiation [81]. Less severe morphologic injury also occurs after radiotherapy and this injury can result in variable degrees of cognitive dysfunction [82], [83]. Such cognitive changes can occur in both pediatric and adult patients, and are often manifested as
Oxidative stress and age-related cognitive decline
Tissue levels of protein oxidation, lipid peroxidation, and DNA/RNA oxidation all go up with age [88], [89], [90], [91], and this is impart due to increased production of reactive oxygen species (ROS) and in part, due to decreased repair. Age-related increase of superoxide radicals in the brain can be visually illustrated by in vivo conversion of dihydroethidium (DHE) into its oxidized products, 2-hydroethidium and ethidium, which are DNA and RNA interchelating fluorescent dyes [92]. Whereas
Acknowledgments
This work was supported by VA Merit Review, Geriatric Research, Education, and clinical Center (GRECC), and the use of facility and resources at the VA Palo Alto Health Care System.
References (107)
Behav. Brain Res.
(2001)- et al.
Neuroscience
(1989) - et al.
Neuropsychologia
(2013) - et al.
Prog. Brain Res.
(1991) - et al.
Neurobiol. Aging
(2010) - et al.
Neurobiol. Learn. Mem.
(2004) - et al.
Free Radical Biol. Med.
(2001) - et al.
Semin. Cell Dev. Biol.
(2012) - et al.
J. Biol. Chem.
(2001) Arch. Biochem. Biophys.
(1997)
Free Radical Biol. Med.
J. Biol. Chem.
Free Radical Biol. Med.
Free Radical Biol. Med.
Free Radical Biol. Med.
J. Biol. Chem.
J. Biol. Chem.
J. Biol. Chem.
J. Biol. Chem.
Cell
Free Radical Biol. Med.
Free Radical Biol. Med.
Neurobiol. Aging
Int. J. Radiat. Oncol. Biol. Phys.
Int. J. Radiat. Oncol. Biol. Phys.
Int. J. Radiat. Oncol. Biol. Phys.
Neurosci. Lett.
Exp. Gerontol.
Biochim. Biophys. Acta
Neurobiol. Aging
Neurologist
Learn Mem.
Annu. Rev. Neurosci.
Prog. Brain Res.
Proc. Natl. Acad. Sci. U.S.A.
Development
Front. Behav. Neurosci.
Curr. Top. Behav. Neurosci.
Annu. Rev. Neurosci.
Nat. Med.
J. Neurosci.
J. Comp. Neurol.
J. Neurosci.
Proc. Natl. Acad. Sci. U.S.A.
Nat. Neurosci.
J. Neurosci.
Nature
J. Neurosci.
Curr. Biol.
J. Neurosci.
Cited by (111)
Transcriptomics of a cytoglobin knockout mouse: Insights from hepatic stellate cells and brain
2024, Journal of Inorganic BiochemistryAlterations in thiol redox state and lipid peroxidation in the brain areas of male mice during aging
2022, Advances in Redox Research