Fasting endurance and cold resistance without hypothermia in a small predatory bird: the metabolic strategy of Tengmalm's owl,Aegolius funereus

The energetic adaptations of non-breeding Tengmalm's owls (Aegolius funereus) to temperature and fasting were studied during the birds' autumnal irruptions in western Finland. Allometric analysis (including literature data and two larger owl species measured in this study) indicates that the basal metabolic rate of owls is below the mean level of non-passerine birds. However, the basal metabolic rate of the 130-g Tengmalm's owl (1.13 W) is higher than in other owls of similar size. This is probably related to its northern distribution and nomadic life history. Relative to its size, Tengmalm's owl has excellent cold resistance due to effective insulation (lower critical temperature +10°C, minimum conductance 0.19 mW·cm^-2·°C^-1). Radiotelemetric measurements of body temperature showed that the level of body temperature is lower than for birds in general (39.4°C at zero activity) and that the amplitude of the diurnal cycle is also low (0.2–0.6°C). In contrast to many other small birds, Tengmalm's owls do not enter hypothermia during a 5-day fast at thermoneutrality or in cold. Moreover, while the metabolic rate per bird shows the expected mass-dependent decrease, the mass-specific rate decreases only slightly during the fast. In line with this, there was no decrease in the plasma triiodothyronine concentration during the fast in the owl, whereas a dramtic drop was observed in the pigeon and Japanese quail that were used as a reference. Despite this, the owl has an excellent capacity for fasting because of its ability to accumulate extensive fat depots and its low overall metabolic rate. Fasting reduced evaporative water loss to 50% of that in the fed state. Calculations show that the oxygen consumption observed in fasting birds would involve a production of metabolic water barely sufficient to compensate for evaporative water loss. The threat of dehydration may thus set a limit to the decrease in metabolic rate in fasting owls (owls rely totally on water either ingested with food or produced metabolically). We conclude that the metabolic strategy in Tengmalm's owl is largely dictated by an evolutionary pressure for fasting endurance. With the restrictions set by small body size and water economy, this bird has apparently taken these adaptations to an extreme. The constraints that preclude hypothermia, which could increase the capacity for fasting even more, remain unknown.Abbreviations BM body mass - BMR basal metabolic rate - EWL vaporative water loss - MR metabolic rate - T₃ triiodothyronine - T _a ambient temperature - T _b body temperature - VO₂ oxygen consumption     

The effects of warming by active and passive means on the subsequent responses to cold water immersion

Two experiments were undertaken to investigate the effects of warming the body upon the responses during a subsequent cold water immersion (CWI). In both experiments the subjects, wearing swimming costumes, undertook two 45-min CWIs in water at 15° C. In experiment 1, 12 subjects exercised on a cycle ergometer until their rectal temperatures (T _re) rose by an average of 0.73°C. They were then immediately immersed in the cold water. Before their other CWI they rested seated on a cycle ergometer (control condition). In experiment 2, 16 different subjects were immersed in a hot bath (40° C) until their T _re rose by an average of 0.9° C; they were then immediately immersed in the cold water. Before their other CWI they were immersed in thermoneutral water (35° C; control condition). Heart rate in both experiments and respiratory frequency in experiment 1 were significantly (P < 0.05) higher during the first 30 s of CWI following active warming. In experiment 1, the rate of fall of T _re during the final 15 min of CWI was significantly (P < 0.01) faster when CWI followed active warming (2.46° C · h^–1) compared with the control condition (1.68°C · h^–1). However, this rate was observed when absolute T _re was still above that seen in the control CWIs. It is possible, therefore, that if longer CWIs had been undertaken, the two temperature curves may have converged and thereafter fallen at similar rates; this was the case with the aural temperature (T _au) seen in experiment 1 and the T _au and T _re in experiment 2. It is concluded that pre-warming is neither beneficial nor detrimental to survival prospects during a subsequent CWI.     

Cyclo(Leu-Gly) has opposite effects on D-2 dopamine receptors in different brain areas

Cyclo(Leu-Gly) (cLG), a diketopiperazine analog of Pro-Leu-Gly-NH2 (MIF), affects a number of physiological and behavioral responses to the endogenous neurotransmitter, dopamine (DA). In the present series of experiments, the effect of in vivo administration of cLG (8 mg/kg) was investigated five days following subcutaneous administration. It was found that cLG administration of cLG (8 mg/kg) was investigated five days following subcutaneous administration. It was found that cLG administration caused a supersensitive behavioral response, measured by increased stereotypic sniffing, to the DA agonist, apomorphine (APO). At the same time, an increase was found in the affinity for dopamine (DA), as measured by dopamine inhibition of 3H-spiroperidol binding to D-2 DA receptors in striatum (nigro-striatal DA tract). In contrast, the same peptide treatment caused a subsensitive physiological response to APO-induced hypothermia, concomitant with a decrease in affinity for dopamine, as measured by DA inhibition of 3H-spiroperidol binding to D-2 DA receptors in hypothalamus (incerto-hypothalamic DA tract). These results suggest that a single neuromodulatory agent, the peptide cLG, can elicit diametrically opposite effects on D-2 DA receptors and on the corresponding physiological endpoints in two different brain areas.     

Bone Marrow Depletion as a Coincidental Finding to Hypothermia in Macaca mulatta

Three of 16 juvenile rhesus monkeys (Macaca mulatta) and 1 rhesus of 79 adult rhesus and cynomolgus monkeys (Macaca fascicularis) were found comatose in a state of profound hypothermia after a heating failure occurred in the room in which they were housed. One juvenile monkey died shortly thereafter. The three other monkeys were revived with gradual warming and supportive therapy but later experienced separate acute clinical crises manifesting shock and died at 19, 31, and 51 days after the initial episode. Histopathologic findings of severe bone marrow depletion were observed in each of the three monkeys that died after the initial episode.     

D-amphetamine-induced hypothermia and hypermotility in rats: Changes after systemic administration of beta-endorphin

Systemically administered beta-endorphin was tested in rats for its ability to modify the hypothermia and hypermotility induced by d-amphetamine. Colonic temperature and motor activity were measured in a cold (4°C) ambient temperature in animals given IP injections of beta-endorphin (0.1, 1.0, or 3.0 mg/kg), naloxone (10 mg/kg), or morphine (30 mg/kg). The same measurements were taken in animals given beta-endorphin (1.0 mg/kg) in combination with naloxone or saline pretreatment and d-amphetamine (15 mg/kg) or saline post-treatment. Morphine alone had a biphasic effect on thermoregulation, but did not affect d-amphetamine-induced hypothermia. Activity scores were decreased by morphine, in both d-amphetamine and saline treated animals. The thermal response of rats to beta-endorphin alone was variable, depending on dosage, but all 3 dosages partially blocked the hypothermic effect of d-amphetamine. Naloxone blocked the thermal effects of both beta-endorphin and d-amphetamine. Motor activity tended to be decreased by naloxone, regardless of amphetamine treatment, but beta-endorphin tended to increase activity in amphetamine-treated animals and reduce it in saline-treated controls. In their actions on both thermoregulation and activity, naloxone and beta-endorphin appeared to interact independently with d-amphetamine, often producing effects in the same direction, but in combination, they tended to be mutually inhibitory.     

In vivo release of dopamine during perfusion of neurotensin in substantia nigra of the unrestrained rat

The functional effect of neurotensin on the kinetics of dopamine (DA) release in the substantia nigra of the freely moving rat was investigated. After guide tubes for push-pull perfusion were implanted stereotaxically just above the substantia nigra, endogenous stores of DA in this structure were labelled by micro-injection of 0.02–0.05 μCi of [¹⁴C]-DA. Then an artificial cerebrospinal fluid (CSF) was perfused within the site at a rate of 20 μl/min at successive 5 min intervals. Neurotensin added to the CSF perfusate in concentrations of 0.05–0.1 μg/μl evoked an immediate, Ca⁺⁺ dependent release of DA from sites directly within the substantia nigra or a delayed efflux when the peptide was perfused at the edge of this structure. Neurotensin failed to affect the pattern of release of this monoamine at sites which were not within the substantia nigra. Further, the body temperature of the rat also was not altered by neurotensin at any of the sites of perfusions. A relatively inactive analogue of the peptide, [D-Arg]⁹ neurotensin, was essentially without effect on DA activity. In double isotope experiments in which the substantia nigra of the rat was labelled with both [³H]-5-HT and [¹⁴C]-DA, the perfusion with neurotensin failed to affect 5-HT efflux while the release of DA was enhanced. Chromatographic analysis of the metabolites of DA in samples of push-pull perfusates revealed that neurotensin enhanced significantly the level of DOPAC and HVA. Overall, these results demonstrate that in the unrestrained rat neurotensin acts selectively within the substantia nigra to alter the presynaptic, Ca⁺⁺ dependent release of DA. It is suggested that the mechanism by which the tri-decapeptide functions within this brainstem structure is through its modulation of nigral dopaminergic neurons.