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PubMed1990

Effects of cold shock and phospholipase A2 on intact boar spermatozoa and sperm head plasma membranes.

Head plasma membranes (HPM) isolated from cryopreserved boar spermatozoa show an excessive fluidization, which might be involved in the loss of fertility. The current study assessed the ability of cold shock (5 degrees C) and phospholipase A2 (PA2) to duplicate these effects on membrane structure and to affect 45Ca2+ uptake and gross morphological characteristics of whole, fresh boar-sperm. The HPM from cold-shocked sperm showed a significantly greater rate of fluidization over time than did HPM from control sperm. Addition of PA2 (bee or snake venom, 0.1 or 10.0 ng/ml) to HPM from control sperm caused fluidization similar to cold shocking, but to a lesser degree (P less than 0.05). Cold-shocked intact sperm exhibited severe acrosomal disruption, loss of motility, and increased 45Ca2+ uptake relative to control sperm. Addition of PA2 (bee or snake venom, 0.1, 1.0., 10.0, and 1,000 ng/ml) to control sperm had no effect on gross morphology or motility while maintaining or increasing sperm extrusion of 45Ca2+. Therefore, although PA2 can, to some extent, duplicate the effects of cold shock on HPM molecular organization, its lipid hydrolytic action is insufficient to cause all the gross disruptions of severe thermal shock. Both PA2 and cold shock disrupted HPM structure, but only cold shock increased 45Ca2+ uptake, suggesting that cold shock may be increasing 45Ca2+ uptake in areas other than the head. Cold shock disrupts sperm on three levels; membrane molecular organization, intracellular Ca2+ regulation, and gross morphology/motility.

Animals↗
PubMed2007

Beyond the lipid hypothesis: mechanisms underlying phenotypic plasticity in inducible cold tolerance.

The physiological adjustment of organisms in response to temperature variation is a crucial part of coping with environmental stress. An important component of the cold response is the increase in membrane lipid unsaturation, and this has been linked to an enhanced resistance to the debilitating or lethal effects of cold. Underpinning the lipid response is the upregulation of fatty acid desaturases (des), particularly those introducing double bonds at the 9-10 position of saturated fatty acids. For plants and microbes there is good genetic evidence that regulation of des genes, and the consequent changes in lipid saturation, are causally linked to generation of a cold-tolerant phenotype. In animals, however, supporting evidence is almost entirely limited to correlations of saturation with cold conditions. We describe our recent attempts to provide a direct test of this relationship by genetic manipulation of the nematode Caenorhabditis elegans. We show that this species displays a strong cold tolerant phenotype induced by prior conditioning to cold, and that this is directly linked to upregulated des activity. However, whilst genetic disruption of des activity and lipid unsaturation significantly reduced cold tolerance, animals retained a substantial component of their stress tolerant phenotype produced by cold conditioning. This indicates that mechanisms other than lipid unsaturation play an important role in cold adaptation.

Acclimatization↗
PubMed1992

Segmental inhibition of laser-evoked brain potentials by ipsi- and contralaterally applied cold pressor pain.

An experiment was designed to quantify the inhibitory effect of cold pressor pain (ice water immersion) on brain potentials evoked by acute laser-induced pain. One hand (including the C7 dermatome) was immersed into ice water and simultaneously the laser-evoked brain potentials were elicited consecutively from the right and left lower forearms within the C7 dermatomes. The cold pressor pain was continuously rated on a visual analogue scale (VAS). The size of the averaged brain potentials evoked from the ipsi- and contralateral C7 dermatomes were reduced significantly during cold pressor pain. The largest decrease was obtained for the potentials evoked within the C7 dermatome ipsilateral to the cold pressor pain. The size (power) of the brain potentials to individual stimuli could be measured and was correlated to the intensity of the cold pressor pain (VAS score). During the onset phase of cold pressor pain, there was a decrease in power of the individual brain potentials evoked from the C7 dermatome contralateral to the cold pressor pain but the potentials, evoked from the C7 dermatome ipsilateral to cold pressor pain, were decreased more. The overall rating of the laser-induced pain intensity showed that the perceived intensity was lowest when evoked from the dermatome concurrently exposed to cold pressor pain.

Adult↗
PubMed2000

Cold stress induces switchover of respiratory pathway to lactate glycolysis in psychrotrophic Rhizobium strains.

Two psychrotrophic strains of Rhizobium, DDSS69, a non-cold acclimated strain, and ATR1, a cold acclimated strain, were subjected to cold stress. A 4-fold increase in the specific activity of lactate dehydrogenase (LDH) was characteristic for cold stressed cells of DDSS69, whereas ATR1 showed a higher LDH activity in general, which increased 1.5-fold under cold stress. Cold sensitive mutants of DDSS69 which could not grow below 15 degrees C, in contrast to the wild type which could grow at 5 degrees C, were isolated using Tn5-tagged mutagenesis. These mutants showed a 40% lower LDH activity than the wild type grown at 5 degrees C that was comparable to the wild type grown at 15 degrees C. High specific activity of succinic dehydrogenase (SDH) at 28 degrees C in both strains and mutants indicated that aerobic respiration via the citrate cycle is the normal mode of saccharide utilization. Shifts to lower temperatures decreased the specific activity of SDH. However, alcohol dehydrogenase (ADH) activity remained very low in both the strains and the mutants at low temperatures indicating that a shift from aerobic saccharide metabolism to anaerobic one under cold stress involves lactate glycolysis rather than alcohol fermentation. There was an increase in membrane-bound ATPase activity under cold stress which is correlated to higher LDH activity. These data show that, in psychrotrophic Rhizobium strains, cold stress induces a switchover of respiratory metabolism from aerobic to anaerobic pathway, especially lactate glycolysis.

Adenosine Triphosphatases↗
PubMed2001

Interpretation of the finger skin temperature response to cold provocation.

OBJECTIVES: To compare alternative methods of interpreting the response of finger skin temperature (FST) to cold provocation for the detection of the abnormal cold response observed in vibration-induced white finger (VWF). METHOD: The FST response to cold provocation was measured in 36 male subjects: 12 office workers, 12 manual workers and 12 manual workers with symptoms of VWF. The FSTs were monitored continuously on the distal phalanges of all five fingers of a test hand for 2 min before, for 5 min during, and for 10 min following, immersion of the test hand in water at 15 degrees C. Of the fingers investigated, 147 were reported not to exhibit blanching and 33 were reported to exhibit blanching. Twenty-one alternative methods of interpreting the response of FSTs to cold provocation were assessed. These were grouped as: (1) areas above the response profile (i.e. the area above the curve showing the FSTs as a function of time during cooling and recovery), (2) areas below the response profile, (3) absolute temperatures during and following cold provocation, (4) percentage differences in FSTs, (5) the times taken for FSTs to rise by specified amounts and (6) rates of change of FSTs. Differences in the response to cooling between those fingers reported to blanch and the fingers not reported to blanch were tested, and receiver operating characteristics (ROCs) were used to compare the sensitivity and specificity of the various measures to symptoms of VWF. RESULTS: The areas above the response profile, areas below the response profile, percentage FSTs, absolute FSTs and rates of change of FSTs tended to discriminate between healthy and unhealthy subjects on a group basis. However, some of these methods of interpreting the FST response to cold provocation did not show a high sensitivity or specificity to vascular dysfunction on individual fingers. The area above the response profile, the percentage of initial temperature at the fifth minute of recovery and the maximum temperature during the 10-min recovery period, were found to show the highest sensitivity and specificity to symptoms of vascular dysfunction. CONCLUSIONS: The method chosen to interpret the FST response to cold provocation affects the ability of the test to detect an abnormal cold response. The area above the response profile, the percentage of initial temperature at the fifth minute of recovery and the maximum temperature achieved during a 10-min recovery period appear to be the most suitable measures for monitoring vascular function in workers exposed to hand-transmitted vibration. It is suggested that the FST response to cold provocation should be interpreted with respect to the state of initial blood flow.

Adult↗
PubMed2001

Poly-beta-hydroxybutyrate metabolism is affected by changes in respiratory enzymatic activities due to cold stress in two psychrotrophic strains of Rhizobium.

Cold stress resulted in a decrease in the poly-beta-hydroxybutyrate (PHB) content of non-cold-acclimated Rhizobium DDSS69 cultures. Analysis of the specific activity of beta-ketothiolase and beta-hydroxybutyrate dehydrogenase revealed that decrease in PHB levels was a result of the inhibition of synthesis of PHB rather than an increase in its breakdown. Rhizobium ATR1, a cold-acclimated strain, revealed the presence of a stable PHB metabolism that did not show any significant differences either in PHB levels or in the activity of enzymes of the PHB metabolism under cold stress, suggesting that PHB is not involved in cold tolerance. Analysis of specific activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase of the pentose phosphate pathway showed the upward regulation of alternate pathways of carbohydrate metabolism under cold stress to rapidly generate energy to overcome the stress. There is diversity in the switching mechanisms of carbon metabolism among cold-acclimated and non-cold-acclimated Rhizobium isolates. Upward regulation of malate dehydrogenase in both isolates suggests that it is a critical input for cold tolerance.

Carbohydrate Metabolism↗
PubMed2000

Does cold acclimation induce nonshivering thermogenesis in juvenile birds? Experiments with Pekin ducklings and Japanese quail chicks.

The capability to produce heat in cold by nonshivering thermogenesis (NST) was studied in Pekin ducklings and Japanese quail chicks acclimated to cold for 3 weeks using indirect calorimetry (oxygen consumption) and electromyography from breast (M. pectoralis) and leg muscles (quails: M. gastrocnemius; ducklings: M. gastrocnemius, M. iliofibularis). Respiration of muscles in vitro was studied by measuring cytochrome c oxidase activity. In both species, cold acclimation induced clear morphometric and physiological changes, but no clear evidence of nonshivering thermogenesis. This was evident because increased shivering at least in one muscle coincided with increased oxygen consumption. In ducklings, however, amplitudes of shivering EMGs were low (<30 microV) in all muscles studied in both the control and cold-acclimated groups. Ducklings reacted to cold mainly by means of increasing body weight (1796 g in control, 2095 g in cold-acclimated) and circulatory changes. Acclimation did not change oxygen consumption either in vivo or in vitro. In quails, in addition to increased body weight (78.1 g control, 89.9 g cold-acclimated), improved insulation and metabolic adaptation to cold (increased respiration in vivo and in M. pectoralis in vitro) was also utilized. In Japanese quail chicks, 3 weeks of cold acclimation does not seem to induce NST, while in Pekin ducklings the existence of NST could not be totally excluded because of weak overall shivering activity.

Acclimatization↗
PubMed2001

Cold acclimation increases basal heart rate but decreases its thermal tolerance in rainbow trout (Oncorhynchus mykiss).

Rainbow trout (Oncorhynchus mykiss, Walbaum) were acclimated to 4 degrees C and 17 degrees C for more than 4 weeks and heart rate was determined in the absence and presence of adrenaline to see how thermal adaptation influences basal heart rate and its beta-adrenergic control in a eurythermal fish species. The basal heart rate in vitro was higher in cold-acclimated than warm-acclimated rainbow trout at temperatures below 17 degrees C. On the other hand, adaptation to cold decreased thermal tolerance of heart rate so that the maximal heart rates were achieved at 17 degrees C (75 +/- 4 bpm) and 24 degrees C (88 +/- 2 bpm) in cold-acclimated and warm-acclimated trout, respectively. Beta-adrenergic response of the heart was enhanced by cold-adaptation, since adrenaline (100 nmol l(-1)) caused stronger stimulation of heart rate in cold-acclimated (29 +/- 14%) than in warm-acclimated fish (10 +/- 1%; P = 0.03). Furthermore, adrenaline strongly opposed the temperature-dependent deterioration of force production in cold-acclimated trout but not in warm-acclimated trout. The results indicate that adaptation to cold increases basal heart rate but decreases its thermal tolerance in rainbow trout. Cold acclimation up-regulates the beta-adrenergic system, and beta-adrenoceptor activation seems to provide cardioprotection against high temperatures in the cold-adapted rainbow trout.

Acclimatization↗
PubMed2005

ThermoTRP channels and cold sensing: what are they really up to?

Cooling is sensed by peripheral thermoreceptors, the main transduction mechanism of which is probably a cold- and menthol-activated ion channel, transient receptor potential (melastatin)-8 (TRPM8). Stronger cooling also activates another TRP channel, TRP (ankyrin-like)-1, (TRPA1), which has been suggested to underlie cold nociception. This review examines the roles of these two channels and other mechanisms in thermal transduction. TRPM8 is activated directly by gentle cooling and depolarises sensory neurones; its threshold temperature (normally approximately 26-31 degrees C in native neurones) is very flexible and it can adapt to long-term variations in baseline temperature to sensitively detect small temperature changes. This modulation is enabled by TRPM8's low intrinsic thermal sensitivity: it is sensitised to varying degrees by its cellular context. TRPM8 is not the only thermosensitive element in cold receptors and interacts with other ionic currents to shape cold receptor activity. Cold can also cause pain: the transduction mechanism is uncertain, possibly involving TRPM8 in some neurones, but another candidate is TRPA1 which is activated in expression systems by strong cooling. However, native neurones that appear to express TRPA1 respond very slowly to cold, and TRPA1 alone cannot account readily for cold nociceptor activity or cold pain in humans. Other, as yet unknown, mechanisms of cold nociception are likely.

Adaptation, Physiological↗
PubMed1999

Differential down-regulation of beta3-adrenergic receptor mRNA and signal transduction by cold exposure in brown adipose tissue of young and senescent rats.

Diminished beta3 adrenergic-stimulated thermogenesis in brown adipose tissue (BAT) in senescent rats is restored by a short period of cold exposure. To investigate if the mechanism of this restoration involves preferential up-regulation of beta3-adrenergic signal transduction in senescent compared with young rats, we examined the steady state levels of beta3-adrenergic receptor messenger ribonucleic acid (beta3AR mRNA) and the dose/response relationship for the activation of adenylyl cyclase by the selective beta3-adrenergic agonist, BRL 37344 in BAT membranes from young and senescent rats with or without 2 days cold exposure at 8 degrees C. beta3AR mRNA declined by 30% with age and by 60% with cold exposure in young rats. In contrast, cold exposure did not down-regulate beta3AR mRNA in senescent rats. BRL 37344-stimulated adenylyl cyclase activity was 38% less in senescent rats and was desensitized by cold exposure decreasing maximum stimulation by 78% and increasing, the dissociation constant 2.5-fold. Cold exposure decreased BRL 37344-stimulated adenylyl cyclase activity to a lesser extent in senescent rats (50%), such that the activity was similar in cold-exposed young and old rats. These data indicate that although cold exposure did not, as we hypothesized, up-regulate beta3-adrenergic signal transduction in the senescent rats, cold exposure preferentially down-regulated beta3AR mRNA and beta3AR-mediated adenylyl cyclase in the young compared with senescent rats.

Adenylyl Cyclases↗
PubMed2006

Osmotin induces cold protection in olive trees by affecting programmed cell death and cytoskeleton organization.

Osmotin is a pathogenesis-related protein exhibiting cryoprotective functions. Our aim was to understand whether it is involved in the cold acclimation of the olive tree (Olea europaea L.), a frost-sensitive species lacking dormancy. We exposed olive trees expressing tobacco osmotin gene under the 35S promoter (35S:osm) [in the same manner as wild type (wt) plants] to cold shocks in the presence/absence of cold acclimation, and monitored changes in programmed cell death (PCD), cytoskeleton, and calcium ([Ca2+]c) signalling. In the wt, osmotin was immunolocalized only in cold-acclimated plants, and in the tissues showing PCD. In the 35S:osm clones, the protein was detected also in the non-acclimated plants, and always in the tissues exhibiting PCD. In the non-acclimated wt protoplasts exposed to cold shock, a transient decrease in phallotoxin signal suggests a temporary disassembly of F-actin, a transient increase occurred instead in 35S:osm protoplasts exposed to the same shock. Transient increases in [Ca2+]c were observed only in the wt protoplasts. However, when F-actin was depolymerized by cytochalasin or latrunculin, and microtubules by colchicine, increase in [Ca2+]c also occurred in the 35S:osm protoplasts. Successive cold shocks caused transient rises in [Ca2+]c and transient decreases in the phallotoxin signal in wt protoplasts. No change occurred in [Ca2+]c occurred in the 35S:osm protoplasts. The phallotoxin signal transiently increased at the first shock, but did not change after the subsequent shocks, and an overall signal reduction occurred with shock repetition. Following acclimation, no cold shock-induced change in [Ca2+]c levels and F-actin signal occurred either in wt or 35S:osm protoplasts. The results show that osmotin is positively involved in the acclimation-related PCD, in blocking the cold-induced calcium signalling, and in affecting cytoskeleton in response to cold stimuli.

Acclimatization↗
PubMed1997

Role of Escherichia coli cspA promoter sequences and adaptation of translational apparatus in the cold shock response.

A shift in growth temperature from 37 degrees C to 15 degrees C leads to a dramatic increase in the level of CspA, the major cold shock protein of Escherichia coli. To investigate the molecular basis of this induction, we considered the relevance of transcriptional and posttranscriptional controls by analyzing the steady-state levels of transcripts and the expression of reporter genes in cells carrying a set of cspA promoter fragments of variable length fused to lacZ or cat genes. We demonstrate that: (i) the core cspA promoter (from -40 to +16) responds to cold shock and a mutation at -36 increases the relative activity of the promoter at low temperature by threefold; (ii) the sequences upstream of -40 have a positive effect on expression at 37 degrees C, but no effect on the cold shock response; (iii) by virtue of their influence on mRNA stability, the downstream sequences (from +81 to +165) reduce expression at 37 degrees C and increase the intensity of the cold shock response; (iv) mutations in the GCACATCA and CCAAT motifs, present at +1/-4 and between the -10 and -35 elements, respectively, do not affect the cold shock response of the cspA promoter; (v) following cold shock, a modification of the protein synthetic machinery takes place that allows preferential translation of cspA mRNA relative to the non-cold shock cat and lacZ mRNAs. The quantitatively modest transcriptional activation shown by the core promoter of cspA following cold shock suggests that transcriptional activation can significantly contribute to cold shock induction only when coupled to posttranscriptional controls, such as alterations in mRNA stability and the translational apparatus.

Adaptation, Physiological↗
PubMed2004

Cold-stress-induced modulation of antioxidant defence: role of stressed conditions in tissue injury followed by protein oxidation and lipid peroxidation.

The aim of this study was to determine the effects of cold stress on antioxidant enzyme activities and examine protein oxidation and lipid peroxidation in various tissues (brain, liver, kidney, heart and stomach). Twenty male Wistar rats (3 months old) weighing 220 +/- 20 g were used. The rats were randomly divided into two groups of ten: the control group and the cold stress group. Cold stress was applied to the animals by maintaining them in a cold room (5 degrees C) for 15 min/day for 15 days. Blood samples were taken for measuring plasma corticosterone levels. Tissues were obtained from each rat for measuring the antioxidant enzyme activities, protein oxidation and lipid peroxidation. Corticosterone levels were increased in the cold stress group. Copper, zinc superoxide dismutase activities were increased in the brains, livers and kidneys, whereas they decreased in the hearts and stomachs of rats in the cold stress group. Catalase activities were increased in the brains, livers, kidneys and hearts, whereas they decreased in the stomachs of rats in the cold stress group. Selenium-dependent glutathione peroxidase activities were increased in the brain, liver, heart and stomach. Reduced glutathione levels were decreased, while levels of protein carbonyl, conjugated diene and thiobarbituric-acid-reactive substances were increased in all tissues of the cold stress group. These results lead us to conclude that cold stress can disrupt the balance in an oxidant/antioxidant system and cause oxidative damage to several tissues by altering the enzymatic and non-enzymatic antioxidant status, protein oxidation and lipid peroxidation.

Adaptation, Physiological↗
PubMed1988

Allergic responses and subsequent development of airway hyperreactivity to cold provocation in the rat trachea: pharmacological modulation.

An in vitro model of airway hyperreactivity to cold provocation was developed. Cold provocation (10 degrees C) alone was not sufficient to cause contraction of rat isolated tracheal smooth muscle preparations. However, following recovery from antigen-induced responses in sensitized rat tracheal segments, cold provocation resulted in marked contractile responses. L-652,731 (a Paf-acether antagonist) and atropine significantly attenuated antigen-induced responses and subsequent development of airway hyperreactivity to cold provocation. Indomethacin augmented allergic responses and subsequent development of airway hyperreactivity to cold challenge. Nordihydroguaiaretic acid, FPL 55712 and theophylline did not exert any effect. The data obtained in this study showed that (i) Paf-acether and acetylcholine may play an important role in the mediation of allergic responses and subsequent development of airway hyperreactivity to cold provocation; (ii) the significant attenuation of antigen-induced airway hyperreactivity to cold provocation by Ca2+ channel blockers (nifedipine, bepridil and TMB-8) suggests an increase in Ca2+ influx/permeability following antigen challenge which appears to be responsible for the development of airway hyperreactivity to cold provocation; and (iii) 5-HT, prostaglandins or thromboxanes and leukotrienes play little or no role in the mediation of allergic responses and subsequent development of airway hyperreactivity to cold exposure in rat trachea.

Acetylcholine↗
PubMedDate not supplied

Interactions of iron deficiency, anemia, and thyroid hormone levels in response of rats to cold exposure.

We have earlier shown that iron-deficient rats have increased urinary norepinephrine (NE) excretion. They also have an exaggerated rise in urinary NE when placed in the cold, a stimulus known to cause increased NE excretion in normal rats. Nonetheless, they fall to maintain body temperature. We have now examined the thyroidal response to cold in iron-deficient rats. As others have shown, control rats had a rise in plasma levels of thyroxine (T4) and triiodothyronine (T3) soon after entering the cold environment (4 degree C); they also maintained a rectal temperature above 36 degree C. In the iron-deficient rats, basal levels of T3 and T4 were normal, but there was little or no increase after 6 hr in the cold, and, as before, body temperatures fell. Injections of T3, 10 microgram/kg, 15 min before cold exposure improved the ability of iron-deficient rats to maintain body temperature, but they still did not do as well as the controls. We conclude that the inability of iron-deficient rats to increase T3 levels after cold exposure is one factor in their poor resistance to cold. The defect could involve inability to augment thyroid secretion, imparied ability to convert T4 to T3 in peripheral tissues, or both. Preliminary data suggest that anemia is an important and perhaps critical factor in the cold sensitivity of iron deficiency. Transfusing iron-deficient rats from their usual hematocrit of 15-20 to one of 30 restores cold resistance to normal. Transfusion also allows a more normal thyroid response, with a rise in T3 and T4 levels, so thyroid hormones may be a factor in the improvement produced by transfusion.

Anemia, Hypochromic↗
PubMed1990

Behavior and body weight changes under intermittent exposure to cold in C57BL/6J mice.

This experiment examined effects of the intermittent exposure to cold. C57BL/6J mice were exposed to cold (4-5 degrees C) for six hours in light (L-cold group) or dark (D-cold group) period and their wheel-running and drinking activities, daily amounts of food and water intake, and body weight were analyzed. Wheel running and drinking decreased during cold exposure, while they increased in postcold period. These behavioral changes were more clearly found in the D-cold group. Body weight of the D-cold group was kept constant for all days of cold exposure, while that of the L-cold group tended to increase. These results are discussed from the view points of adaptive significance of postcold behaviors and the relationship between behavioral and physiological adaptations.

Animals↗
PubMed1991

Changes in blood pressure and dipsogenic responsiveness to angiotensin II during chronic exposure of rats to cold.

Hypertension accompanies chronic exposure of rats to cold (5-6 degrees C). Systolic, diastolic, and mean blood pressures become elevated, and hypertrophy of the heart occurs. A previous study from this laboratory suggested that the renin-angiotensin system may play a role. The present study was carried out to assess this further. Thus, in addition to measurement of systolic blood pressure at intervals during exposure to cold, plasma renin activity and the dipsogenic responsiveness to acute administration of angiotensin II were also measured to assess the functional status of the renin-angiotensin system. The results showed a significant (p less than 0.05) increase in systolic blood pressure during the third week of exposure to cold. In contrast, plasma renin activity (PRA) increased within the first week of exposure to cold, and declined thereafter to reach the level of the control by the third week of exposure to cold. By the fourth week, PRA decreased to a level significantly (p less than 0.05) below that of the control group. The responsiveness to acute administration of angiotensin II (AII), as assessed by the drinking response, increased significantly (p less than 0.05) by the third week of exposure to cold and remained significantly elevated during the fourth week. There was a significant (p less than 0.01) direct relationship between dipsogenic responsiveness to AII and blood pressure in the cold-treated (r = .57), but not the control group (r = .12). There was also a significant (r = -.91) indirect linear relationship between PRA and dipsogenic responsiveness to AII. Cold-treated rats had significant increases in urinary norepinephrine output and weights of heart, kidneys, adrenals, and brown adipose tissue characteristic of rats acclimated to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1991

Behavioral changes in cold-stressed mice related to a central calcium-dependent-catecholamine synthesizing system.

An investigation was carried out regarding the mechanism of behavioral changes in mice elicited by cold stress. Cold stress was induced in adult male mice by restraining them from free action for 2 h at 4 degrees C. As the control test, mice were restrained from free action for 2 h at room temperature. The locomotor counts in cold-stressed mice were found to be lower than in controls. The counts in cold-stressed mice were increased by IP pretreatment with EDTA or alpha-methyltyrosine (tyrosine hydroxylase inhibitor), and were further decreased by IP pretreatment with CaCl2. On the other hand, serum calcium and brain calcium levels in cold-stressed mice were increased 15-30 min and 30 min, respectively, after restraint under cold temperatures, and returned to original levels 1 h after restraint. Also, the biochemical and immunohistochemical brain dopamine levels in cold-stressed mice were higher than in control mice. The increment of brain dopamine levels in the control mice was also observed by the administration of CaCl2. Furthermore, the ability of cold stress to enhance the dopamine level in mice brains was attenuated by IP pretreatment with alpha-methyltyrosine. In light of previous reports that central calcium activates catecholamine-synthesizing enzymes via a calmodulin-dependent system, it is suggested that cold stress enhances the brain calcium level, and then increased calcium enhances dopamine synthesis in the brain through a central calcium-dependent catecholamine synthesizing system. Subsequently, increased dopamine induces behavioral changes.

Animals↗