Hibernation “trigger”: Opioid-like inhibitory action on brain function of the monkey

Oeltgen, Peter R.; Walsh, James; Hamann, Scott R.; Randall, David C.; Spurrier, Wilma A.; Myers, R.D.

doi:10.1016/0091-3057(82)90132-0

Cited by 70 publications

(15 citation statements)

References 11 publications

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“…Consistent with this characterization, DOPs induce a hypometabolic state of similar depth as the HIT, whereas mu-or kappa-opioid receptor agonists show no effect [97,98]. The involvement of opioid receptors is further substantiated by the inability of DOP to induce hypometabolism upon exposure to naloxon, a non-specific opioid receptor antagonist [99][100][101][102]. These findings raise the question whether DOPs make use of a direct Rx-Q relationship or act via the Rx-Ztn (Figure 6).…”

Section: Delta-opioidssupporting

confidence: 65%

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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Section: Delta-opioidssupporting

confidence: 65%

The physiology of artificial hibernation

Heger

2015

JCTRes

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“…The temperature and metabolic depressing effect of these opioid-like proteins (Oeltgen et al, 1982;Bruce et al, 1987), was to some extent consistent with the state-dependent effect of intracerebral opioids on temperature (Tanaka et al, 1985) Although a role for HIT in hibernation remains controversial these results demonstrate that some aspects of the hibernation physiology may involve opioid receptor stimulation (Horton et al, 1998) which may have practical applications in cardiology. Kondo and co-workers have demonstrated that synthesis of liver derived "hibernation specific protein complex (HSPC)", isolated from the blood of chipmunks (Citelus lateralis) but not non hibernators, was inhibited during hibernation consistent with an annual rhythm where the lowest levels coincided with the hibernation period (Kondo and Kondo, 1992).…”

Section: Molecular Prospective Of Hibernationmentioning

confidence: 67%

Arousal from hibernation and BAT thermogenesis against cold: central mechanism and molecular basis

Hashimoto

Gao

Kikuchi-Utsumi

et al. 2002

Journal of Thermal Biology

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“…Many parallels exist between SLP and hibernation: hibernation is triggered by ␦-opioid agonism, which can also induce hibernation in nonhibernating primates (Oeltgen et al, 1982(Oeltgen et al, , 1988; ␦-opioid triggered hibernation increases stress resistance (Bolling et al, 1997); hibernating and anoxiatolerant species harness PKA signaling (Storey, 1996;Holden and Storey, 1998); and repression of Akt suppresses energy-costly anabolic/growth processes to maintain cell viability over extended periods (Cai et al, 2004;Abnous et al, 2008). The SLP phenotype is induced by ␦-opioid agonism, involves PI3K-dependent signals and repression of Akt expression (Fig.…”

Section: Discussionmentioning

confidence: 99%

Sustained Ligand-Activated Preconditioning via δ-Opioid Receptors

Peart¹,

Hoe²,

Gross³

et al. 2010

J Pharmacol Exp Ther

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We have previously described novel cardioprotection in response to sustained morphine exposure, efficacious in young to aged myocardium and mechanistically distinct from conventional opioid or preconditioning (PC) responses. We further investigate opioid-dependent sustained ligand-activated preconditioning (SLP), assessing duration of protection, opioid receptor involvement, additivity with conventional responses, and signaling underlying preischemic induction of the phenotype. Male C57BL/6 mice were treated with morphine (75-mg subcutaneous pellet) for 5 days followed by morphine-free periods (0, 3, 5, or 7 days) before ex vivo assessment of myocardial tolerance to 25-min ischemia/45-min reperfusion. SLP substantially reduced infarction (by ϳ50%) and postischemic contractile dysfunction (eliminating contracture, doubling force development). Cardioprotection persisted for 5 to 7 days after treatment. SLP was induced specifically by ␦-receptor and not -or -opioid receptor agonism, was eliminated by ␦-receptor and nonselective antagonism, and was additive with adenosinergic but not acute morphine-or PC-triggered protection. Cotreatment during preischemic morphine exposure with the phosphoinositide-3 kinase (PI3K) inhibitor wortmannin, but not the protein kinase A (PKA) inhibitor myristoylated PKI-(14-22)-amide, prevented induction of SLP. This was consistent with shifts in total and phospho-Akt during the induction period. In summary, data reveal that SLP triggers sustained protection from ischemia for up to 7 days after stimulus, is ␦-opioid receptor mediated, is induced in a PI3K-dependent/PKA-independent manner, and augments adenosinergic protection. Mechanisms underlying SLP may be useful targets for manipulation of ischemic tolerance in young or aged myocardium.

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Hibernation “trigger”: Opioid-like inhibitory action on brain function of the monkey

Cited by 70 publications

References 11 publications

The physiology of artificial hibernation

The physiology of artificial hibernation

Arousal from hibernation and BAT thermogenesis against cold: central mechanism and molecular basis

Sustained Ligand-Activated Preconditioning via δ-Opioid Receptors

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