Enhanced responsiveness to central prostaglandin E or neuropeptide Y in cold-adapted rats

Uzsoki, Boglárka; Fekete, Anett; Pétervári, Erika; Balaskó, Márta; Székely, Miklós

doi:10.1016/s0306-4565(01)00067-5

Cited by 10 publications

(5 citation statements)

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“…About 10 days before the first thermoregulatory test a metal guide cannula was implanted into the right lateral cerebral ventricle (i.c.v.) of each rat under ketamine + xylazine anesthesia (78+13 mg kg -1 intraperitoneally) (12). On the morning of the tests the unanesthesized rats were semi-Acta Physiologica Hungarica 90, 2003 restrained in the usual cage and, together with the cage, they were placed into an opencircuit metabolic chamber at their thermoneutral temperatures (i.e.…”

Section: Methodsmentioning

confidence: 99%

“…Increased responsiveness of central thermoregulatory structures to various (thermal and non-thermal) stimuli has been concluded from experiments in which enhanced thermal responses to centrally applied prostaglandin E were found in CA rats as compared with NA animals (12). Greater feeding responses to central injections of neuropeptide Y were also observed.…”

Section: Acta Physiologica Hungarica 90 2003mentioning

confidence: 98%

“…Acta Physiologica Hungarica 90, 2003 exposure of comparable severity usually induces temperature fall. Apart from such acute cold exposures, central injections of prostaglandin E (PGE) also elicit exaggerated metabolic response and hyperthermia in CA rats as compared with their NA counterparts (7,12). Since CA animals are known to have enhanced thyroid function and the thermogenic capacity of their peripheral tissues is also high (1)(2)(3)(4), these enhanced reactions might possibly be explained by the high tissue thermogenesis, partly due to the enhanced thyroid function.…”

mentioning

confidence: 99%

“…Since CA animals are known to have enhanced thyroid function and the thermogenic capacity of their peripheral tissues is also high (1)(2)(3)(4), these enhanced reactions might possibly be explained by the high tissue thermogenesis, partly due to the enhanced thyroid function. Alternatively, not only the peripheral metabolic factors, but also the central regulation may be different in the CA status: in fact, CA rats exhibited enhanced central responses also to orexigenic stimuli (12).…”

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confidence: 99%

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Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Pétervári

Koncsecskó-Gáspár

Balaskó³

et al. 2003

Acta Physiologica Hungarica

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Cold-adapted (CA) rats, unlike non-adapted (NA) ones, give exaggerated metabolic response to acute cold exposure, with paradoxical "overshoot" core temperature (Tc) rise in the cold, and they also give enhanced hyperthermia to central injection of prostaglandin E1 (PGE1). The adaptation-dependent differences might be explained either by the high thermogenic capacity of peripheral tissues in CA rats or by differences in the central processing of regulatory signals. If high tissue metabolism sufficiently explains the extreme responses of CA animals, other hypermetabolic states (with high resting metabolic rate, RMR), e.g. hyperthyroidism, should also be accompanied by enhanced reactions. In the present study thermoregulatory responses to acute cold exposure or to PGE1 were compared in hypermetabolic CA, similarly hypermetabolic thyroxine-treated (T4) and control non-hypermetabolic NA rats (mean RMR = 8.12, 8.47 and 6.03 W kg(-1), respectively). Cold exposure was followed by paradoxical core temperature (Tc) rise of 0.5 to 0.7 degrees C only in CA rats, but by Tc fall (0.8 to 2.1 degrees C) in NA and T4 animals. Identical central stimuli (PGE1) induced larger elevations of Tc and metabolic rate in CA rats than in similarly hypermetabolic T4 or in non-hypermetabolic NA animals (mean Tc rise of 1.9 degrees C in CA vs. 0.9 degrees C in T4 and 1.0 degrees C in NA rats). Vasodilatation thresholds were also similar in NA and T4, but lowered in CA animals. A hypermetabolic status, per se, does not seem to explain the enhanced thermoregulatory responsiveness of CA animals, adaptation-induced central regulatory changes may be more important for the "overshoot" phenomenon.

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Section: Methodsmentioning

confidence: 99%

Section: Acta Physiologica Hungarica 90 2003mentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Pétervári

Koncsecskó-Gáspár

Balaskó³

et al. 2003

Acta Physiologica Hungarica

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“…Repeated microinjection of the GABAA agonist muscimol into the RPa, a key region for thermoregulatory cold defence, effectively mimicked a torpid state in rats kept at a T a of 15°C and under continuous darkness (Cerri et al ., 2013). Intracerebroventricular (ICV) injection of NPY led to a reduction of MR in mice (Walker & Romsos, 1993), and a mild but reliable T a ‐dependent hypothermic response in rat (Bouali et al ., 1995; Jolicoeur et al ., 1995; Uzsoki et al ., 2001). Additionally, inhibiting NST contributes to the reduction in T b .…”

Section: Induction Of Synthetic Torpor In Non‐hibernating Speciesmentioning

confidence: 99%

Human torpor: translating insights from nature into manned deep space expedition

et al. 2020

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During a long‐duration manned spaceflight mission, such as flying to Mars and beyond, all crew members will spend a long period in an independent spacecraft with closed‐loop bioregenerative life‐support systems. Saving resources and reducing medical risks, particularly in mental heath, are key technology gaps hampering human expedition into deep space. In the 1960s, several scientists proposed that an induced state of suppressed metabolism in humans, which mimics ‘hibernation’, could be an ideal solution to cope with many issues during spaceflight. In recent years, with the introduction of specific methods, it is becoming more feasible to induce an artificial hibernation‐like state (synthetic torpor) in non‐hibernating species. Natural torpor is a fascinating, yet enigmatic, physiological process in which metabolic rate (MR), body core temperature (Tb) and behavioural activity are reduced to save energy during harsh seasonal conditions. It employs a complex central neural network to orchestrate a homeostatic state of hypometabolism, hypothermia and hypoactivity in response to environmental challenges. The anatomical and functional connections within the central nervous system (CNS) lie at the heart of controlling synthetic torpor. Although progress has been made, the precise mechanisms underlying the active regulation of the torpor–arousal transition, and their profound influence on neural function and behaviour, which are critical concerns for safe and reversible human torpor, remain poorly understood. In this review, we place particular emphasis on elaborating the central nervous mechanism orchestrating the torpor–arousal transition in both non‐flying hibernating mammals and non‐hibernating species, and aim to provide translational insights into long‐duration manned spaceflight. In addition, identifying difficulties and challenges ahead will underscore important concerns in engineering synthetic torpor in humans. We believe that synthetic torpor may not be the only option for manned long‐duration spaceflight, but it is the most achievable solution in the foreseeable future. Translating the available knowledge from natural torpor research will not only benefit manned spaceflight, but also many clinical settings attempting to manipulate energy metabolism and neurobehavioural functions.

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Peptides and Temperature

Székely¹,

Balaskó²,

Pétervári³

2013

Handbook of Biologically Active Peptides

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Enhanced responsiveness to central prostaglandin E or neuropeptide Y in cold-adapted rats

Cited by 10 publications

References 20 publications

Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Human torpor: translating insights from nature into manned deep space expedition

Peptides and Temperature

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