Behavioral, Electrophysiological, and Biochemical Consequences of Chronic Cytochrome Oxidase Inhibition in Rats

Bennett, Michael; Rose, Gregory M.

doi:10.1007/978-1-4757-9936-1_8

Cited by 2 publications

(2 citation statements)

References 62 publications

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“…Also, there were no group differences in motor activity and no overall differences in performance in day 1-5 training sessions that could account for the results. These studies were conducted with both normal rats and with rats having memory impairment caused by chronic cytochrome oxidase inhibition, a metabolic model of AD (Bennett et al, 1992; Bennett and Rose, 1998). Together these studies with low-dose MB given during the memory consolidation phase were the first to show MB’s enhancement of memory retention in both aversive (Martinez Jr. et al, 1978) and appetitive tasks in normal animals (Callaway et al, 2004), and to show restoration of memory in a model of AD (Callaway et al, 2002).…”

Section: Mb As a Memory-improving Drugmentioning

confidence: 99%

“…Chronic inhibition of cytochrome oxidase activity with systemic sodium azide in behaving rats has been used to model the memory deficits and cytochrome oxidase inhibition found in AD (Bennett et al, 1992; Bennett and Rose, 1998; Gonzalez-Lima and Cada, 1998; Gonzalez-Lima et al, 1998a; 1998b; Berndt et al, 2001). In a more direct test of the ability of MB to prevent deficits in cytochrome oxidase, Callaway et al (2002), administered MB in animals chronically treated with the specific cytochrome oxidase inhibitor sodium azide.…”

Section: Mb As a Memory-improving Drugmentioning

confidence: 99%

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Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue

Rojas

Bruchey

González-Lima

2012

Progress in Neurobiology

145

181

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This paper provides the first review of the memory-enhancing and neuroprotective metabolic mechanisms of action of methylene blue in vivo. These mechanisms have important implications as a new neurobiological approach to improve normal memory and to treat memory impairment and neurodegeneration associated with mitochondrial dysfunction. Methylene blue’s action is unique because its neurobiological effects are not determined by regular drug-receptor interactions or drug-response paradigms. Methylene blue shows a hormetic dose-response, with opposite effects at low and high doses. At low doses, methylene blue is an electron cycler in the mitochondrial electron transport chain, with unparalleled antioxidant and cell respiration-enhancing properties that affect the function of the nervous system in a versatile manner. A major role of the respiratory enzyme cytochrome oxidase on the memory-enhancing effects of methylene blue is supported by available data. The memory-enhancing effects have been associated with improvement of memory consolidation in a network-specific and use-dependent fashion. In addition, low doses of methylene blue have also been used for neuroprotection against mitochondrial dysfunction in humans and experimental models of disease. The unique auto-oxidizing property of methylene blue and its pleiotropic effects on a number of tissue oxidases explain its potent neuroprotective effects at low doses. The evidence reviewed supports a mechanistic role of low-dose methylene blue as a promising and safe intervention for improving memory and for the treatment of acute and chronic conditions characterized by increased oxidative stress, neurodegeneration and memory impairment.

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Section: Mb As a Memory-improving Drugmentioning

confidence: 99%

Section: Mb As a Memory-improving Drugmentioning

confidence: 99%

Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue

Rojas

Bruchey

González-Lima

2012

Progress in Neurobiology

145

181

View full text Add to dashboard Cite

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Effects of Chronic Sodium Azide on Brain and Muscle Cytochrome Oxidase Activity: A Potential Model to Investigate Environmental Contributions to Neurodegenerative Diseases

Berndt¹,

Callaway²,

González-Lima³

2001

Journal of Toxicology and Environmental Health, Part A

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Deficits in oxidative phosphorylation have been implicated in many neurodegenerative diseases. In this study, cytochrome oxidase activity was inhibited following a 28-d systemic administration of nonlethal sodium azide via subcutaneous osmotic pumps. Quantitative enzyme histochemistry was performed on tissue sections from brain, skeletal muscle, and heart to localize cytochrome oxidase activity both globally and in regions within each tissue. Significant decreases of cytochrome oxidase activity were found in the brain and skeletal muscle but not heart. In addition, regions within each tissue were also analyzed, such as cortex and striatum in the brain and red and white fibers in skeletal muscle. The tissue specific inhibition of cytochrome oxidase by sodium azide could serve as a positive control for studies of other mitochondrial toxins in aerobically compromised cells. Therefore, chronic nonlethal sodium azide administration may provide a potential rat model for the study of mitochondrial dysfunction and the role of environmental pollutants in brain and muscle tissues affected in certain neurodegenerative diseases.

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Behavioral, Electrophysiological, and Biochemical Consequences of Chronic Cytochrome Oxidase Inhibition in Rats

Cited by 2 publications

References 62 publications

Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue

Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue

Effects of Chronic Sodium Azide on Brain and Muscle Cytochrome Oxidase Activity: A Potential Model to Investigate Environmental Contributions to Neurodegenerative Diseases

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