Brain ECF antioxidant interactions in hamsters during arousal from hibernation

Osborne, Peter G.; Hashimoto, Masaaki

doi:10.1016/j.bbr.2006.12.006

Cited by 6 publications

(10 citation statements)

References 46 publications

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“…ECF levels of all amino acids, including amino acid neurotransmitters, increased as the hamster aroused from torpor along a similar profile to body temperature rather than metabolic rate. The only exception was urate which reflected the profile of metabolic rate and has been demonstrated to be xanthine oxidoreductase dependently synthesized during arousal (Osborne and Hashimoto 2007).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the brain contains a plethora of substrates and compounds at non‐cenothermic levels (Lust et al. 1989; Osborne and Hashimoto 2007), yet the torpid hamster retains the ability to respond to tactile stimulation (Osborne et al. 2005), hypercapnic gas (Lyman 1951; Osborne et al.…”

mentioning

confidence: 99%

“…Cortical blood flow is enormously reduced (Osborne and Hashimoto 2003), the EEG is essentially isoelectric (Chatfield et al 1951;Chatfield and Lyman 1954;Gabriel et al 1998) while intrahippocampal synaptic connectivity is greatly reduced (Magarinos et al 2006). In addition, the brain contains a plethora of substrates and compounds at non-cenothermic levels (Lust et al 1989;Osborne and Hashimoto 2007), yet the torpid hamster retains the ability to respond to tactile stimulation (Osborne et al 2005), hypercapnic gas (Lyman 1951;Osborne et al 2005) and can appropriately monitor the internal milieu of the body and coordinate spontaneous arousal, the stimulus for which remains a mystery.…”

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confidence: 99%

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Mammalian cerebral metabolism and amino acid neurotransmission during hibernation

Osborne¹,

Hashimoto

2008

Journal of Neurochemistry

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This report demonstrates that during the torpor phase of hibernation, hamsters utilize 14C and 13C glucose in torpor‐specific brain metabolic pathways. Microdialysis of 14C glucose into the striatum rapidly induced a steady state labeling of extracellular fluid (ECF) lactate and labeling of tissue GABA, glutamate, glutamine, and alanine in ipsilateral and contralateral striata. The same tissue metabolites were labeled in cortex, hypothalamus, and brainstem after microdialysis of 14C lactate into the lateral ventricle. Serine, aspartate, glycine, taurine, tyrosine, and methionine were not synthesized from glucose or lactate during torpor. ECF levels of amino and organic acids were low and unchanging during torpor and increased late during arousal to cenothermia. Labeled intracellular 14C GABA and glutamate were not communicated to the striatal ECF or ventricular space during torpor. 13C NMR demonstrated rapid formation of lactate and functional tricarboxylic acid cycles in GABAergic and glutamatergic neurons, and enrichment of glutamine and alanine after i.v. 13C glucose. Large changes in tissue levels of amino acids occur prior to or during entrance into torpor but not during torpor. It is proposed that cerebral intracellular dehydration, the enlargement of ECF and the biochemistries associated with brain water homeostasis may have a role in regulating hibernation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Mammalian cerebral metabolism and amino acid neurotransmission during hibernation

Osborne¹,

Hashimoto

2008

Journal of Neurochemistry

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“…Interestingly, studies in both the arctic ground squirrel (Ma et al 2004; Toien et al 2001) and the Syrian hamster (Okamoto et al 2006) have reported a three- to four-fold increase in serum uric acid following induced arousal from the hibernating state. Another study, however, did not report a change in uric acid in the Syrian hamster with induced arousal (Osborne and Hashimoto 2007); however, in none of these studies was the arousal linked with the state of fat stores in the body, and absolute uric acid levels are low in these animals since these mammals express uricase. In contrast, studies of hibernating snakes have occasionally documented extremely high uric acid levels posthibernation, with levels reaching as high as 70 mg/dl (4.1 mM) and which can be associated with visceral gout and death (Dutton and Taylor 2003).…”

Section: Lessons From the Emperor Penguin: The Foraging Hypothesismentioning

confidence: 95%

Lessons from comparative physiology: could uric acid represent a physiologic alarm signal gone awry in western society?

et al. 2008

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Uric acid has historically been viewed as a purine metabolic waste product excreted by the kidney and gut that is relatively unimportant other than its penchant to crystallize in joints to cause the disease gout. In recent years, however, there has been the realization that uric acid is not biologically inert but may have a wide range of actions, including being both a pro- and anti-oxidant, a neurostimulant, and an inducer of inflammation and activator of the innate immune response. In this paper, we present the hypothesis that uric acid has a key role in the foraging response associated with starvation and fasting. We further suggest that there is a complex interplay between fructose, uric acid and vitamin C, with fructose and uric acid stimulating the foraging response and vitamin C countering this response. Finally, we suggest that the mutations in ascorbate synthesis and uricase that characterized early primate evolution were likely in response to the need to stimulate the foraging “survival” response and might have inadvertently had a role in accelerating the development of bipedal locomotion and intellectual development. Unfortunately, due to marked changes in the diet, resulting in dramatic increases in fructose- and purine-rich foods, these identical genotypic changes may be largely responsible for the epidemic of obesity, diabetes and cardiovascular disease in today’s society.

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“…tion including modulation of immune response, thrombolysis and cold tolerance (20,40). Despite the proposed roles of hibernation as neuroprotective, the neurochemical mechanisms that control thermoregulation and regulated metabolic suppression during entrance, maintenance and arousal from hibernation is yet to be fully explored.…”

Section: Intrauterine Hypoxiamentioning

confidence: 99%

Brain-Regulated Metabolic Suppression during Hibernation: A Neuroprotective Mechanism for Perinatal Hypoxia–Ischemia

Nathaniel

2008

International Journal of Stroke

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Hypoxic-ischemic brain injury in the perinatal period is a major cause of chronic disability and acute mortality in newborns. Despite numerous therapeutic strategies that reduce hypoxia-ischemia-induced damage in different experimental animal models, most of them have failed to translate to clinical therapies. This challenge calls for an urgent need to explore novel approaches to develop effective therapies for the clinical management of perinatal hypoxia-ischemia brain injury. This review focuses on studies that investigate neuroprotective related events during mammalian hibernation, characterized by dramatic reductions in several parameters including body temperature, oxygen consumption and heart rate, such that it is difficult to tell if the hibernating animal is dead or alive. The first part of this article reviews the mechanisms of metabolic suppression related events during hibernation. In the second part, hypoxic-ischemic events in the perinatal brain are discussed, and in turn, contrasted with brains experiencing metabolic suppression during mammalian hibernation. In the last part of this article, the diverse neuroprotective adaptations of hibernators and the mechanisms that might be involved in mammalian hibernation, and how they could in turn, contribute to neurprotection during perinatal hypoxia-ischemia related injuries are discussed. This article appraises the novel idea that knowledge of the central mechanisms involved in the regulatory metabolic suppression, during which; hibernators switch themselves off without dissolving their brains could represent brain neuroprotective strategy for the clinical management of perinatal hypoxia-ischemia brain injuries in newborns.

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Brain ECF antioxidant interactions in hamsters during arousal from hibernation

Cited by 6 publications

References 46 publications

Mammalian cerebral metabolism and amino acid neurotransmission during hibernation

Mammalian cerebral metabolism and amino acid neurotransmission during hibernation

Lessons from comparative physiology: could uric acid represent a physiologic alarm signal gone awry in western society?

Brain-Regulated Metabolic Suppression during Hibernation: A Neuroprotective Mechanism for Perinatal Hypoxia–Ischemia

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