AMP does not induce torpor

Swoap, Steven J.; Rathvon, Meaghan Kelly; Gutilla, Margaret J.

doi:10.1152/ajpregu.00888.2006

Cited by 75 publications

(74 citation statements)

References 43 publications

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“…adenosine monophosphate (Swoap et al 2006), H 2 S (Blackstone et al 2005) and 2-deoxy-D-glucose (Freinkel et al 1972)). Whether these responses are functionally similar to natural torpor has remained unclear (Swoap et al 2006), in part because manipulations such as fasting entail a non-trivial risk of death (Hudson & Scott 1979).…”

Section: Introductionmentioning

confidence: 99%

Daily torpor in mice: high foraging costs trigger energy-saving hypothermia

et al. 2009

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Many animal species employ natural hypothermia in seasonal (hibernation) and daily (torpor) strategies to save energy. Facultative daily torpor is a typical response to fluctuations in food availability, but the relationship between environmental quality, foraging behaviour and torpor responses is poorly understood. We studied body temperature responses of outbred ICR (CD-1) mice exposed to different food reward schedules, simulating variation in habitat quality. Our main comparison was between female mice exposed to low foragingcost environments and high-cost environments. As controls, we pair-fed a group of inactive animals (no-cost treatment) the same amount of pellets as high-cost animals. Mice faced with high foraging costs were more likely to employ torpor than mice exposed to low foraging costs, or no-cost controls (100% versus 40% and 33% of animals, respectively). While resting-phase temperature showed a non-significant decrease in high-cost animals, torpor was not associated with depressions in active-phase body temperature. These results demonstrate (i) that mice show daily torpor in response to poor foraging conditions; (ii) that torpor incidence is not attributable to food restriction alone; and (iii) that high levels of nocturnal activity do not preclude the use of daily torpor as an energy-saving strategy. The finding that daily torpor is not restricted to conditions of severe starvation puts torpor in mice in a more fundamental ecological context.

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Section: Introductionmentioning

confidence: 99%

Daily torpor in mice: high foraging costs trigger energy-saving hypothermia

et al. 2009

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“…Intraperitoneal injections of 5'-AMP have been shown to induce an artificial hypometabolic state in mice and rats as evidenced by a profound drop in Tb (Figure 8) [61,[76][77][78]. The putative contention is that intraperitoneal administration of high 5'-AMP concentrations (e.g., 500 mg/kg) lead to extensive 5'-AMP uptake by erythrocytes [79], after which the high intracellular levels of 5'-AMP drive the adenylate equilibrium (ATP + AMP  2 ADP) towards production of ADP, thereby depleting erythrocyte ATP levels [76,77].…”

Section: Adenosine Monophosphatementioning

confidence: 99%

“…As a result, erythrocyte 2,3-disphosphoglycerate is upregulated, limiting the binding of oxygen to hemoglobin's oxygen binding sites (referred to as oxygen affinity hypoxia) [76]. In addition to the already impaired oxygen transport, the severe cardiovascular depression following 5'-AMP administration has the potential to further exacerbate this hypoxic state (referred to as circulatory hypoxia) [78]. Although there is no conclusive evidence that these types of hypoxia have the ability to induce an anapyrexic state, the generally pervasive hypoxic state likely uses the S-Ztn-Tb(-Ta)-Q relationship ( Figure 6A) to induce hypometabolism through CB signaling.…”

Section: Adenosine Monophosphatementioning

confidence: 99%

The physiology of artificial hibernation

Heger

2015

JCTRes

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Incomplete understanding of the mechanisms responsible for induction of hibernation prevent translation of natural hibernation to its artificial counterpart. To facilitate this translation, a model was developed that identifies the necessary physiological changes for induction of artificial hibernation. This model encompasses six essential components: metabolism (anabolism and catabolism), body temperature, thermoneutral zone, substrate, ambient temperature, and hibernation-inducing agents. The individual components are interrelated and collectively govern the induction and sustenance of a hypometabolic state. To illustrate the potential validity of this model, various pharmacological agents (hibernation induction trigger, delta-opioid, hydrogen sulfide, 5'-adenosine monophosphate, thyronamine, 2-deoxyglucose, magnesium) are described in terms of their influence on specific components of the model and corollary effects on metabolism. Relevance for patients: The ultimate purpose of this model is to help expand the paradigm regarding the mechanisms of hibernation from a physiological perspective and to assist in translating this natural phenomenon to the clinical setting.

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“…Through one or more steps of dephosphorylation, ATP can be sequentially degraded to adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine. It has long been observed that adenosine induces hypothermia in a dose-dependent manner in mice [118][119][120]. Furthermore, the adenosine A1 receptor may play a key role because A1 receptor agonists other than adenosine also induce hypothermia [120,121].…”

Section: Adenosine and Adenine Nucleotidesmentioning

confidence: 99%

“…Some side effects of hypothermic drugs are quite common, such as reduction in mobility, cardiovascular function and decreased metabolism, as they are part of the hypothermic mechanisms [15,55,84,119,126]. In extreme cases, however, the side effects are so severe that their detrimental effects on ischemia outweigh the protective effects of the hypothermia [126], precluding their use against stroke.…”

Section: Summary and Considerationsmentioning

confidence: 99%

Drug-Induced Hypothermia in Stroke Models: Does it Always Protect?

Zhang¹,

Wang²,

Zhao³

et al. 2013

CNSNDDT

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Ischemic stroke is a common neurological disorder lacking a cure. Recent studies show that therapeutic hypothermia is a promising neuroprotective strategy against ischemic brain injury. Several methods to induce therapeutic hypothermia have been established; however, most of them are not clinically feasible for stroke patients. Therefore, pharmacological cooling is drawing increasing attention as a neuroprotective alternative worthy of further clinical development. We begin this review with a brief introduction to the commonly used methods for inducing hypothermia; we then focus on the hypothermic effects of eight classes of hypothermia-inducing drugs: the cannabinoids, opioid receptor activators, transient receptor potential vanilloid, neurotensins, thyroxine derivatives, dopamine receptor activators, hypothermia-inducing gases, adenosine, and adenine nucleotides. Their neuroprotective effects as well as the complications associated with their use are both considered. This article provides guidance for future clinical trials and animal studies on pharmacological cooling in the setting of acute stroke. KeywordsBrain ischemia; Hypothermic; Neuroprotection; Pharmacological cooling Send correspondence to: Dr. Feng Zhang, Department of Neurology, University of Pittsburgh School of Medicine, 3500 Terrace Street, Pittsburgh, PA, 15213, USA, Telephone: 412-383-7604, Fax: 412-648-1239, zhanfx2@upmc.edu NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 1. Hypothermia and strokes IntroductionTherapeutic hypothermia is defined as a 2-6°C reduction of core body temperature [1][2][3] and is a promising neuroprotective approach against brain injury induced by strokes. In hemorrhagic stroke, hypothermia reduces brain edema [4,5] and improves neurologic function [4][5][6][7]. In ischemic stroke, hypothermia is also protective, which has been proven in randomized clinical trials in human cardiac arrest and in animal studies of focal and global ischemia [8,9]. However, the impact of hypothermia on patients with acute ischemic stroke still needs to be explored [10]. During the past decades, studies on hypothermia and ischemic stroke have suggested that the required amplitude of protective hypothermia depends on its time of initiation relative to stroke onset, duration, and depth of hypothermia [1,9,11]. Optimal protection is typically gained when hypothermia is induced as early as possible after stroke onset, with a mild-to-moderate hypothermia of 32 to 35°C that lasts at least one to two hours [1, 2, 12-14]. Protective mechanism of hypothermia in ischemic strokeAlthough hypothermia is effective in protecting against experimental models of ischemic stroke, the precise protective mechanisms are not yet fully understood. It has been suggested that the protective mechanisms are multifold, including reductions in metabolic rate, cerebral blood flow, blood-brain barrier damage, as well as decreases in excitotoxicity, apoptosis, inflammation and free radical production [15]. On average, hypothermia red...

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AMP does not induce torpor

Cited by 75 publications

References 43 publications

Daily torpor in mice: high foraging costs trigger energy-saving hypothermia

Daily torpor in mice: high foraging costs trigger energy-saving hypothermia

The physiology of artificial hibernation

Drug-Induced Hypothermia in Stroke Models: Does it Always Protect?

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