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PubMed2002

Flash visual evoked potentials in the hypomyelinated mutant mouse shiverer.

Myelin basic protein (MBP) is an essential component of central nervous system (CNS) myelin, as demonstrated by shiverer mutant mice that have deletions of most of the Mbp structural gene. These mutants do not produce detectable MBP protein, and their CNS is hypomyelinated. Although the function of the visual pathway is presumed to be adversely affected by hypomyelination of the optic nerve, it has never been studied. We compared flash visual evoked potentials (FVEPs) of shiverer homozygotes with those of their wild-type littermates in order to characterize any dysfunction. There was a statistically significant delay in the implicit times of a negative component peaking at 85 ms and a large positive component peaking at 170 ms in the FVEPs of the shiverer mice. The amplitudes of the two components did not differ significantly in the shiverers and wild-type controls. Barring a retinal pathology, which cannot be excluded by these data, the delayed FVEP of the shiverer can likely be attributed to effects of hypomyelination of the optic nerve, optic tract and visual radiations on conduction time in the visual pathway and subsequent further post-synaptic delays.

Animals↗

PubMed1989

Restoration of myelin formation by a single type of myelin basic protein in transgenic shiverer mice.

A minigene containing mouse cDNA coding for the smallest type of myelin basic protein and including the native promoter was constructed and used to produce transgenic shiverer mice. The hypomyelinating mouse, the shiverer, has a deletion in its myelin basic protein gene, lacks all four types of myelin basic protein in its myelin, and shows abnormal behavior such as violent tremors. Five of twenty-one transgenic shiverer mice showed recovered protein synthesis, compact myelin formation, and normal behavior. These results suggest that a single type of myelin basic protein restores myelin formation and returns the shivering phenotype to normal in the transgenic shiverer mouse.

Animals↗

PubMed1994

Transplanted transgenically marked oligodendrocytes survive, migrate and myelinate in the normal mouse brain as they do in the shiverer mouse brain.

The dye Hoechst 33342 was combined with an immunodetectable transgene product (chloramphenicol acetyltransferase, CAT) expressed in differentiated oligodendrocytes to trace their fate after transplantation in the normal and the shiverer mouse brain. In the shiverer brain, the technique allowed us to visualize grafted cells inside myelin basic protein-positive myelin patches. Most of these cells were CAT-positive/Hoechst 33342-negative, reinforcing our hypothesis that cell division probably follows migration of grafted oligodendrocytes. Correlation of their morphology and distribution with their location in the host CNS suggested a local effect on the cell division and morphogenesis of the grafted material. When compared with transplantation of fragments of normal newborn donor tissue into the newborn shiverer brain, no difference could be seen between the behaviour of normal and transgenic oligodendrocytes. In the normal brain, transgenic oligodendrocytes survived at least 150 days and successfully myelinated the host axons. The timing of differentiation of grafted cells was similar in both types of recipient brains. Migration occurred rostrally and caudally. Although migrating cells could be observed along the meninges and the blood vessels, migration occurred preferentially along white matter tracts. The extent of migration was influenced by the site of implantation, and grafted cells could be found up to 6 mm from the grafting point. No differences in the timing of differentiation or the pattern or extent of migration could thus be demonstrated when transgenic oligodendrocytes were transplanted in the normal or the shiverer brain. This validates our previous studies using the newborn shiverer mouse as recipient.

Animals↗

PubMed1990

Chimeric and molecular genetic analysis of myelin-deficient (shiverer and mld) mutant mice.

The shiverer and myelin-deficient (mld) mutants are two allelic mutations. Both are characterized by hypomyelination in the CNS and deficient expression of the MBP gene. Chimeric analysis of the pathogenesis of shiverer showed that shiverer mutation acts intrinsic to the oligodendrocyte, which is the only cell type expressing the MBP gene in the CNS. Molecular genetic studies by several groups demonstrated that shiverer is a deletion mutation in the MBP gene. Consequently, no MBP is produced in the shiverer mutant. In mld, however, partial expression of the MBP gene was observed. Interestingly, MBP was expressed in a mosaic fashion in the CNS of mld mice. Molecular genetic studies revealed that the mld mutant has duplicated MBP genes in tandem on a distal part (E2-4) of chromosome 18q. The reduced expression was based on the level of mRNA. A large portion is inverted in the upstream copy, and an intact copy is located downstream. We showed in mld mutants that antisense RNA corresponding to the inverted segment is transcribed, and it forms RNA duplex, with the RNA transcribed from the normal gene located downstream.

Animals↗

PubMed2005

Functional changes in genetically dysmyelinated spinal cord axons of shiverer mice: role of juxtaparanodal Kv1 family K+ channels.

Axonal dysfunction after spinal cord injury (SCI) and other types of neurotrauma is associated with demyelination and exposure of juxtaparanodal K+ channels. In this study, sucrose gap electrophysiology using selective and nonselective K+ channel blockers, confocal immunohistochemistry, and Western blotting were used to study the role of Kv1.1 and Kv1.2 K+ channel subunits in dysmyelination-induced spinal cord axonal dysfunction in shiverer mice, which lack the gene encoding myelin basic protein (MBP) and exhibit incomplete myelin sheath formation on CNS axons. The shiverer spinal cord axons exhibited smaller amplitude of compound action potentials (CAPs), reduced conduction velocity, reduced excitability, and greater degree of high-frequency conduction failure. The "fast" K+ channel blocker 4-aminopyridine, the toxin DTX-I, which targets the Kv1.1 and Kv1.2, but not DTX- K, which has higher selectivity for Kv1.1, increased the amplitude and area of CAPs of shiverer mice spinal cord axons but had insignificant effects in wild-type mice. Confocal immunohistochemistry showed that, unlike wild-type mice, which have a precise juxtaparanodal localization of the Kv1.l and Kv1.2 K+ channel subunits, shiverer mouse axons displayed a dispersed distribution of these subunits along the internodes. In contrast, the Kv1.l and Kv1.2 subunits, Na+ channels remained highly localized to the nodal regions. Western blotting showed an increased expression of Kv 1.1 and 1.2 in the shiverer mouse spinal cord. These results provide evidence that the neurological deficits associated with myelin deficiency reflect the altered distribution and expression of the K+ channel subunits Kv1.l and Kv1.2 along the internodes of spinal cord axons associated with the biophysical consequences caused by alterations in the myelin sheaths.

Action Potentials↗

PubMed1999

Reduced levels of a specific myelin-associated oligodendrocytic basic protein isoform in shiverer myelin.

Myelin-associated oligodendrocytic basic protein (MOBP) and myelin basic protein (MBP) share many structural similarities. MOBP is synthesised by mature oligodendrocytes and localised at the major dense line (MDL), suggesting a role in the myelin compaction process. The shiverer mouse, a deletion mutant of the myelin basic protein (Mbp) gene, has poorly compacted myelin with essentially no MDL. In this study we compare the developmental expression of the Mobp gene in wild-type and shiverer mice. The significant finding is that one of the two abundant MOBP isoforms, the approximately 20-kD species, is poorly incorporated into shiverer myelin. The absence is specific to shiverer and is not a feature of dysmyelinating mutants with an abnormal intraperiod line. Our data suggest that incorporation of this MOBP isoform into shiverer myelin may be influenced by the presence of MBP or be a consequence of a disrupted MDL.

Aging↗

PubMed1991

Regulation of myelin basic protein gene transcription in normal and shiverer mutant mice.

We describe the measurement of myelin basic protein gene transcription rate, and of the accumulation of both mature mRNA and total transcripts from the myelin basic protein gene in brains from mice of wild-type and homozygous shiverer genotypes at several ages spanning postnatal development. In wild-type brains the accumulation of total transcripts as well as mature mRNA, and the transcription rate, all follow the same general pattern of rising sharply from a low level at birth to a peak at 20 days, and continuing at a somewhat reduced level into adulthood. Thus a major factor in the developmental regulation of myelin basic protein expression is the control of transcription rate. The shiverer mutation consists of a deletion of the 3' end of the myelin basic protein gene which completely prevents production of mature mRNA and protein, and results in severe dysmyelination and a trembling behavior. In shiverer brains, the transcription rates for the intact 5' end of the gene follow closely those seen in wild-type animals up to the age at which maximal myelination normally occurs. Total myelin basic protein transcripts follow a similar profile but at less than 5% the level seen in wild-type, and, as expected, no mature mRNA is detected. Thus the shiverer deletion does not remove information required for efficient, developmentally regulated transcription, and the low level of myelin basic protein gene transcripts in this mutant must be a result of their reduced stability. A higher than normal myelin basic protein gene transcription rate in older shiverer animals raises interesting questions regarding the regulatory mechanisms controlling myelinogenesis.

Animals↗

PubMed1982

Chimeric analysis of the pathogenesis of dysmyelination of shiverer mutant mice. Presence of patches of MBP-positive and negative sites in white matter indicating the absence of humoral factors for dysmyelination.

Shiverer is an autosomal recessive mutant mouse characterized by abnormal and poor myelin formation of the central nervous system. Chimera mice were produced from wild-type control (C57BL/6N) and the shiverer mutant mice (BALB/C) by the aggregation technique in order to analyze the pathogenesis of the shiverer mutation. The coat color was a mosaic of both strains. Immunohistochemically we have examined sections of cerebellar white matter of the chimera using antiserum against myelin basic protein (MBP), since MBP is absent in the myelin of the shiverer. Patches of MBP-negative and positive sites were observed in cerebellar white matter. The myelin sheaths, both positive and negative to MBP staining, were well mixed in the white matter but each stained myelin sheath was clearly visible, even in the mixed part. The possibility that humoral factors caused dysmyelination could be eliminated, and it is suggested that the shiverer mutation occurs intrinsic to the cells themselves.

Animals↗

PubMed1997

Clonidine decreases vasoconstriction and shivering thresholds, without affecting the sweating threshold.

PURPOSE: This study was conducted to test the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold and dose-dependent decreases in vasoconstriction and shivering thresholds. METHODS: Six healthy subjects (two female) were studied on four days after taking clonidine in oral doses of either 0 (control), 3, 6 or 9 micrograms.kg-1. The order followed a balanced design in a double-blind fashion. Oesophageal temperature and mean skin temperature (from 12 sites) were measured. Subjects were seated in 37 degrees C water which was gradually warmed until sweating occurred (sweat rate increased above 50 g.m-2.h-1). The water was then cooled gradually until thresholds for vasoconstriction (onset of sustained decrease in fingertip blood flow) and shivering (sustained elevation in metabolism) were determined. Thresholds were then referred to as the core temperature, adjusted to a designated mean skin temperature of 33 degrees C. RESULTS: High dose clonidine similarly decreased the adjusted core temperature thresholds for vasoconstriction by 1.16 +/- 0.30 degrees C and for shivering by 1.63 +/- 0.23 degrees C (P < 0.01). The dose response effects were linear for both cold responses with vasoconstriction and shivering thresholds decreasing by 0.13 +/- 0.05 and 0.19 +/- 0.09 degree C.microgram-1 respectively (P < 0.0001). The sweating threshold was unaffected by clonidine, however the interthreshold range between sweating and vasoconstriction thresholds increased from control (0.19 +/- 0.48 degree C) to high dose clonidine (1.31 +/- 0.54 degrees C). CONCLUSION: The decreases in core temperature thresholds for cold responses and increased interthreshold range are consistent with the effects of several anaesthetic agents and opioids and is indicative of central thermoregulatory inhibition.

Adrenergic alpha-Agonists↗

PubMed2026

Acute mild cold exposure with shivering reduces 24 h glucose levels in individuals with type 2 diabetes but not prediabetes.

AIMS/HYPOTHESIS: Repeated cold exposure with shivering has been proposed as a potential strategy to enhance glucose metabolism by increasing energy expenditure and substrate utilisation. However, acute effects/benefits of cold-induced shivering on glucose homeostasis in metabolically compromised individuals are unknown. Here, we aimed to determine whether cold exposure at two different intensities improves 24 h glucose homeostasis in individuals with prediabetes and type 2 diabetes. METHODS: In a randomised crossover trial conducted in the South Limburg/Maastricht region of the Netherlands, men and postmenopausal women with prediabetes (n=12) and stable type 2 diabetes (n=12), aged 40-75 years, body mass index ≥27 and ≤35 kg/m2, non-smoking and sedentary, underwent two whole-body cold exposure sessions using a water-perfused suit. Session order was randomised using an online randomisation tool (randomizer.org); participants were masked to the cold exposure intensity received, but investigators were not. Sessions were designed to elicit ~1.5-fold (mild, 15°C) and ~2.5-fold (moderate, 4°C) increases in resting metabolic rate (RMR). Continuous glucose monitoring assessed interstitial glucose concentrations over 24 h periods before and after each intervention, with controlled diet and activity. Shivering was confirmed via indirect calorimetry and electromyography. RESULTS: In both study groups and periods, RMR increased significantly vs baseline (p<0.001 for all). In prediabetes, the increase in the final 1 h of cold was 1.53 × RMR in mild and 1.94 × RMR in moderate cold. In type 2 diabetes, the increase was 1.57 × RMR and 2.09 × RMR in the final 1 h of mild and moderate cold, respectively. In prediabetes, neither mild nor moderate cold exposure altered mean 24 h glucose levels. In contrast, after mild cold exposure the type 2 diabetes group exhibited a significant reduction in mean 24 h glucose levels (-0.6 ± 0.5 mmol/l, p=0.003) and fasting glucose (-0.6 ± 0.8 mmol/l, p=0.019), as well as an increase in time in normal range (+8.8 ± 10.3%, p=0.013) and reduced time in hyperglycaemia (-10.9 ± 12.9%, p=0.014). Moderate cold did not significantly affect any of the glucose outcomes in type 2 diabetes. Baseline fasting glucose, age and ALT levels were predictors of the glucose-lowering response, suggesting greater benefits in individuals who have higher baseline glucose levels, are younger and/or have more optimal liver health, i.e. lower ALT. CONCLUSIONS/INTERPRETATION: Acute mild cold exposure with shivering reduced 24 h glucose levels in individuals with type 2 diabetes. No changes were observed in prediabetes. The observed effects appear to depend on baseline metabolic status rather than acute substrate utilisation during cold exposure. These findings support the potential of cold exposure as an adjunct non-pharmacological therapy for type 2 diabetes, although further mechanistic studies and validation in larger cohorts are warranted. TRIAL REGISTRATION: ClinicalTrials.gov NCT05576025 FUNDING: Dutch Organisation for Knowledge and Innovation in Health, Healthcare and Well-being (ZonMw): 09120012010062.

Humans↗

PubMedDate not supplied

Measurement and prediction of peak shivering intensity in humans.

Prediction equations of shivering metabolism are critical to the development of models of thermoregulation during cold exposure. Although the intensity of maximal shivering has not yet been predicted, a peak shivering metabolic rate (Shivpeak) of five times the resting metabolic rate has been reported. A group of 15 subjects (including 4 women) [mean age 24.7 (SD 6) years, mean body mass 72.1 (SD 12) kg, mean height 1.76 (SD 0.1) m, mean body fat 22.3 (SD 7)% and mean maximal oxygen uptake (VO2max) 53.2 (SD 9) ml O2.kg-1.min-1] participated in the present study to measure and predict Shivpeak. The subjects were initially immersed in water at 8 degrees C for up to 70 min. Water temperature was then gradually increased at 0.8 degree C.min-1 to a value of 20 degrees C, which it was expected would increase shivering heat production based on the knowledge that peripheral cold receptors fire maximally at approximately this temperature. This, in combination with the relatively low core temperature at the time this water temperature was reached, was hypothesized would stimulate Shivpeak. Prior to warming the water from 8 to 20 degrees C, the oxygen consumption was 15.1 (SD 5.5) ml.kg-1.min-1 at core temperatures of approximately 35 degrees C. After the water temperature had risen to 20 degrees C, the observed Shivpeak was 22.1 (SD 4.2) ml O2.kg-1.min-1 at core and mean skin temperatures of 35.2 (SD 0.9) and 22.1 (SD 2.2) degrees C, respectively. The Shivpeak corresponded to 4.9 (SD 0.8) times the resting metabolism and 41.7 (SD 5.1)% of VO2max. The best fit equation predicting Shivpeak was Shivpeak (ml O2.kg-1.min-1) = 30.5 + 0.348 x VO2max (ml O2.kg-1.min-1) - 0.909 x body mass index (kg.m-2) - 0.233 x age (years); (P = 0.0001; r2 = 0.872).

Adult↗

PubMed1996

Metabolic changes associated with sustained 48-hr shivering thermogenesis in the newborn pig.

Metabolic changes associated with sustained 48-hr shivering thermogenesis were studied in piglets maintained at 34 (thermoneutrality) or 25 degrees C (cold) between 6 and 54 hr of life. Despite their high shivering activity and elevated heat production, cold-exposed piglets exhibited a slightly lower rectal temperature than thermoneutral animals (-1.1 degrees C; P < 0.01) at the end of the treatment. The enhancement of heat production and shivering activity were associated with a decrease in muscle glycogen (-47%; P < 0.05) and total lipid content (-23%; P < 0.05), a reduction of blood lactate levels (P < 0.05) and an enhancement of muscle cytochrome oxidase activity (+20%; P < 0.05) which suggests that muscle oxidative potential was increased by cold exposure. Potential for capturing lipids (lipoprotein lipase activity) was also higher in the red rhomboideus muscle (+71%; P < 0.01) and lower in adipose tissue (-58%; P < 0.01) of the cold-exposed piglets. Measurements performed at the mitochondrial level show no changes in rhomboideus muscle, but respiratory capacities (state IV and FCCP-stimulated respiration) and intermyofibrillar mitochondria oxidative and phosphorylative (creatine kinase activity) capacities were enhanced in longissimus dorsi muscle (P < 0.05). These changes may contribute to provide muscles with nonlimiting amount of readily oxidable substrates and ATP necessary for shivering thermogenesis. A rise in plasma norepinephrine levels was also observed during the second day of cold exposure (P < 0.05).

Animals↗

PubMedDate not supplied

Comparison of ondansetron and meperidine for prevention of shivering in patients undergoing spinal anesthesia.

BACKGROUND AND OBJECTIVES: Perioperative hypothermia is a common problem in anesthesia practice. Regional anesthesia, like general anesthesia, influences the thermoregulatory process. The aim of our study was to compare the efficacy of ondansetron and meperidine in the prevention of shivering during and after spinal anesthesia. METHODS: In this double-blind study, 75 patients were randomized into 3 groups. Group O and Group M were given ondansetron 8 mg and meperidine 0.4 mg/kg intravenously immediately before spinal anesthesia, respectively. Group C received saline at identical times. The core temperatures and the incidence of shivering were recorded. Association between maximum block height and mean rectal temperatures of the patients were also evaluated. RESULTS: The core temperature was preserved in both ondansetron and meperidine groups with respect to the control group. Shivering was observed in 8% of patients in groups O and M and 36% in group C. The correlation between maximum block height and mean rectal temperatures was lost in the ondansetron and meperidine groups. CONCLUSION: Ondansetron and meperidine have similar anti-shivering effects. In addition, both ondansetron and meperidine altered the correlation between the core temperature and block level during spinal anesthesia.

Adult↗

PubMed1987

Suppression of shivering decreases oxygen consumption and improves hemodynamic stability during postoperative rewarming.

Thirty-three patients undergoing elective myocardial revascularization were prospectively randomized into two study groups (Group S and Group P) to permit evaluation of the effects of shivering on oxygen consumption per minute (VO2), carbon dioxide production per minute (VCO2), and hemodynamic performance. Group S was allowed to shiver during the postoperative rewarming period, and Group P received hourly injections of pancuronium bromide and Metubine (metocurine) sulfate with sedation to block the shivering response. Group S demonstrated significantly higher increases in VO2 and VCO2, lower systolic blood pressure and mixed venous oxygen saturation, and a greater use of inotropic support than the patients in Group P. Suppression of the shivering response minimized increases in VO2 and VCO2, improved hemodynamic stability, and resulted in a decreased need for inotropic support.

Body Temperature↗

PubMed1998

The effect of exercise training in cold on shivering and nonshivering thermogenesis in adult and aged C57BL/6J mice.

To understand the mechanisms of improvement of cold-induced heat production in aged mice following exercise training, the relative contributions of shivering and nonshivering thermogenesis to cold-induced metabolic responses were assessed in adult and aged C57BL/6J male mice, which inhabited sedentarily at room temperature, or were subjected either to a regimen of moderate intensity exercise training at 6 degrees C, or to sedentary repeated exposures to the same temperature. The main findings were that (1) aged mice had greater cold-induced nonshivering thermogenesis, but lower shivering than adult mice; (2) exercise training in a cold environment enhanced cold-induced nonshivering thermogenesis in adult mice, but suppressed it in aged animals; (3) exercise training in a cold environment increased shivering thermogenesis in both age groups, but this increase was much greater in aged mice; (4) the increase of cold-induced shivering thermogenesis was mainly responsible for increased cold tolerance in aged mice after exercise training in a cold environment.

Aging↗

PubMed2006

Dexmedetomidine and meperidine prevent postanaesthetic shivering.

BACKGROUND AND OBJECTIVE: This placebo-controlled study was performed to evaluate the efficacy of dexmedetomidine compared with meperidine and placebo in preventing postanaesthetic shivering. METHODS: We studied 120 patients (ASA I-II) scheduled for elective abdominal or orthopaedic surgery of about 1-3 h duration. Forty patients in each group randomly received 1 microg kg(-1) of dexmedetomidine, 0.5 mg kg(-1) of meperidine or saline 0.9% as placebo, intravenously (i.v.). Mean arterial pressure, heart rate, oxygen saturation and central body temperature were measured. Extubation, awakening and orientation times, shivering, pain, recovery and sedation scores were recorded. RESULTS: Postanaesthetic shivering was seen in 22 patients in the placebo group, four patients in the meperidine group and six patients in the dexmedetomidine group. Sedation scores were significantly higher in the dexmedetomidine group compared with meperidine and placebo groups. Both dexmedetomidine and meperidine caused a significantly prolonged extubation and awakening time compared with placebo. Also, dexmedetomidine caused a significantly prolonged orientation time compared with other two groups. CONCLUSION: Intraoperative intravenously administration of dexmedetomidine 1 microg kg(-1) reduces postanaesthetic shivering as does meperidine 0.5 mg kg(-1) in patients after major surgery.

Adolescent↗

PubMed1999

Nefopam and clonidine in the prevention of postanaesthetic shivering.

Postanaesthetic shivering affects up to 70% of patients after general anaesthesia, and may be very distressing. Various drugs have been used to treat or prevent postanaesthetic shivering, but the ideal one has not yet been found. Sixty patients undergoing elective abdominal or orthopaedic surgery under general anaesthesia were included in a randomised, double-blind study. Patients received clonidine (3 microgram.kg-1), nefopam (0.15 mg.kg-1) or saline 0.9% as a placebo at the end of surgery, prior to extubation. Nefopam and clonidine significantly reduced the incidence and severity of shivering in comparison with the placebo. The recovery time, between the end of anaesthesia and extubation, was significantly longer in the clonidine-treated patients [13.6 (5.2) min] than in either the nefopam [9.6 (2.8) min] or the placebo [10.0 (5.4) min] groups. Mean arterial blood pressure and heart rate were significantly lower in the clonidine group compared with both other groups. Our results suggest that nefopam and clonidine are effective in the prevention of postanaesthetic shivering. However, following clonidine administration the recovery time was prolonged and hypotension was significantly greater than after nefopam.

Adult↗

PubMed2001

Effects of shivering prevention on haemodynamic and metabolic demands in hypothermic postoperative neurosurgical patients.

We evaluated the haemodynamic and metabolic effects of prevention of shivering after prophylactic nefopam administration in neurosurgical patients undergoing craniotomy and mild systemic hypothermia (33-35 degrees C). Forty patients were enrolled in a randomised, double-blind study. Before extubation, patients received intravenously either nefopam 0.12 mg.kg-1 or an equal volume of saline 0.9%. Left ventricular systolic work index, oxygen consumption index and systemic lactate concentration were recorded before, immediately after and every 20 min for 2 h after extubation. Shivering appeared in two patients treated with nefopam and in all control patients (p < 0.001). Both left ventricular systolic work index and oxygen consumption index were similar in the two groups before extubation, increased after extubation, and further increased in control patients showing a statistical difference compared to patients treated with nefopam. Our results suggest that nefopam is effective in preventing postoperative shivering in patients undergoing neurosurgery and mild hypothermia and attenuates the haemodynamic effects of shivering during rewarming.

Adult↗