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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) Fast axoplasmic transport in mammalian nerve in vitro was studied using an isotope labeling technique. The rate of outflow in cat sciatic nerve fibers of 410 mm/day in vitro was reduced at temperatures below 38 degrees C with a Q10 of 2.0 in the range 38-18 degrees C and a Q10 of 2.3 at 38-13 degrees C. 2) At a temperature of 11 degrees C a partial failure of transport occurred. At temperatures below 11 degrees C a complete block of fast axoplasmic transport occurred, a phenomenon termed "cold-block." No transport at all was seen over the temperature range of 10-0 degrees C for times lasting up to 48 hr. 3) Transport was resumed after a period of cold-block lasting up to 22 hr when the nerves were brought back to a temperature of 38 degrees C. Some deleterious effects due to cold-block were seen in the recovery phase as indicated by a reduction in crest amplitude, change in its form, and slowed rate. 4) The approximately P level (combined ATP and creatine phosphate) remained near control level in nerves kept at low or cold-block temperatures for times as long as 64 hr. The reduction in fast axoplasmic transport rate seen at low temperatures for times up to 22 hr was therefore considered due to a decrease in the utilization of ATP, a concept in accord with the "transport filament" model proposed to account for fast axoplasmic transport. 5) The sloping of the front of the crest over the temperature range of 18-13 degrees C suggests an additional factor at the lower temperatures. A disassembly of microtubules is discussed as a possible explanation of the cold-block phenomenon.
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PMID:Low temperature slowing and cold-block of fast axoplasmic transport in mammalian nerves in vitro. 5 88

Stop-flow techniques were used to determine how temperature affected the axonal transport of dopamine-beta-hydroxylase (DBH) activity in rabbit sciatic nerves in vitro. These nerves were cooled locally to 2 degrees C for 1.5 hr, which caused a sharp peak of DBH activity to accumulate above the cooled region. Accumulated DBH was then allowed to resume migration at various temperatures. From direct measurements of the rate of migration, we found that the axonal transport velocity of DBH was a simple exponential function of temperature between 13 degrees C and 42 degrees C. Over this range of temperatures, the results were well described by the equation: V=0.546(1.09)T, where V is velocity in mm/hr, and T is temperature in degrees centigrade. The Q10 between 13 degrees and 42 degrees C was 2.33, and an Arrhenius plot of the natural logarithm of velocity versus the reciprocal of absolute temperature yielded an apparent activation energy of 14.8 kcal. Transport virtually halted when temperature was raised to 47 degrees C, although only about half of the DBH activity disappeared during incubation at this temperature. Another transition occurred at 13 degrees C; below this temperature, velocity fell precipitously. This was not an artifact peculiar to the stop-flow system since the rate of accumulation of DBH activity proximal to a cold-block also decreased abruptly when the temperature above the block was reduced below 13 degrees C.
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PMID:Temperature-dependence of rapid axonal transport in sympathetic nerves of the rabbit. 6 Apr 64

The refractory period, the ability to transmit trains of impulses, and the effect of temperature on conduction, have been studied in the sciatic-tibial nerve trunks of Trembler mice, which suffer from a dominantly inherited hypertrophic neuropathy. Both the refractory period of transmission and the relative refractory period were increased in Trembler mice when compared with controls. The nerve trunks of Trembler mice were unable to conduct rapid trains of impulses, and conduction block occurred at rates of stimulation as low as 25 Hz. Cold block occurred at temperatures significantly higher in Trembler nerves than in controls. The conduction velocity increased in an approximately linear fashion in both Trembler and control nerves when the temperature was raised from 20 degrees C to 40 degrees C, and the slopes were not significantly different. The Q10 (27 degrees C-37 degrees C) was 1.5 and 1.6 for control and Trembler nerves respectively. Conduction block was regularly observed in Trembler nerves when the temperature was raised within the physiological range. The abnormalities are related to the pathological changes of chronic demyelination.
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PMID:Refractory period, conduction of trains of impulses, and effect of temperature on conduction in chronic hypertrophic neuropathy. 19 10

Incorporation of tritium from tritiated water into lipid fractions was measured in isolated hepatocytes from rainbow trout (Salmo gairdneri) acclimated to 5 degrees C and 20 degrees C. Hepatocytes from cold-acclimated trout exhibited significantly higher rates of tritium incorporation into both fatty acid and sterol fractions at assay temperatures of 15 degrees C and 20 degrees C than did hepatocytes from warm-acclimated trout. Tritium incorporation into the fatty acid fraction was nearly temperature independent in hepatocytes from warm-acclimated trout (Q10 = 1.39) but markedly temperature dependent (Q10 = 2.63) in hepatocytes from cold-acclimated trout; in contrast, rates of sterol synthesis were more temperature dependent in warm-acclimated trout. At 5 degrees C, fatty acid lipogenesis comprised a significantly greater percentage of the total tritium incorporation in hepatocytes from warm-acclimated trout and the percentage of total lipogenesis attributable to fatty acids decreased significantly in warm-acclimated trout as the assay temperature increased; the opposite trends were observed in cold-acclimated trout.
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PMID:Fatty acid and sterol synthesis by hepatocytes of thermally acclimated rainbow trout (Salmo gairdneri). 49 Jan 25

1. Single unit activities were recorded from the neurones in the preoptic area and anterior hypothalamus of developing new-born rats (aged 1-24 days old) during thermal stimulation of the brain. During the first 2 weeks of life, about 80% of these neurones had low spontaneous firing rates between 0.1 and 5 impulses/sec at 38 degrees C hypothalamic temperature (Thyp). 2. Out of 640 units studied, 118 units increased the firing rate upon elevation of Thyp (warm-units) and fourteen showed the opposite type of response to temperature changes (cold-units). Warm-units were found in the rats of all the age span studied and cold-units were recorded in the rats more than 8 days old. 3. Thermal coefficients of warm-units and cold-units varied between +0.11 and +2.47 and between -0.10 and -0.49 impulses/sec, degrees C, respectively. Number of warm-units with higher rates of firing and greater thermal coefficients, comparable to those of warm-units in the adult, gradually increased with growth. The thermal responsiveness of warm-units, when expressed by Q10, are already high even in the immediate neonatal period. Their Q10 values were in the range between 2 and 38.5 (mean 6.4). 4. Units responding to extrahypothalamic temperatures were only found in the rats more than 14 days old. 5. All the six warm-units tested increased the firing rates following subcutaneous injections of capsaicin, while the majority of thermo-unresponsive units were not affected by this drug. 6. It is suggested that thermo-responsive neurones in the preoptic area and anterior hypothalamus in the new-born rat have attained some degree of electrophysiological maturity, despite their slowly firing characteristics.
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PMID:Hypothalamic thermo-responsive neurones in the new-born rat. 51 57

1. The efflux of radioactive sodium was measured from squid axons during simultaneous voltage clamp experiments such that it was possible to determine the efflux of sodium associated with a measured voltage clamp current. 2. The extra efflux of sodium associated with voltage clamp pulses increased linearly with the magnitude of the depolarization above 40 mV. A 100 mV pulse of sufficient duration to produce all of the sodium current increased the rate constant of efflux by about 10(-6). 3. Application of 100 nM tetrodotoxin eliminated the sodium current and the extra efflux of radioactive sodium. 4. Cooling the axon increased the extra efflux/voltage clamp pulse slightly with a Q10 of 1/1-1. On the same axons cooling increased the integral of the sodium current with a Q10 of 1/1-4. 5. Replacing external sodium with Tris, dextrose or Mg-mannitol reduced the extra efflux of sodium by about 50%. The inward sodium current was replaced with an outward current as expected. 6. Replacing external sodium with lithium also reduced the extra efflux by about 50% but the currents seen in lithium were slightly larger than those in sodium. 7. The effect of replacing external sodium was not voltage dependent. Cooling reduced the effect so that there was less reduction of efflux on switching to Tris ASW in the cold than in the warm. 8. The extra efflux of sodium into sodium-free ASW is approximately the same as the integral of the sodium current. Adding external sodium produces a deviation from the independence principle such that there is more exchange of sodium than predicted. Such a deviation from prediction was noted by Hodgkin & Huxley (1952c). 9. Using the equations of Hodgkin & Huxley (1952c) modified to include the deviation from independence reported in this paper and its temperature dependence, one can predict the temperature dependence of the sodium efflux associated with action potentials and obtain much better agreement than is possibly without these phenomena. 10. This deviation from independence in the sodium fluxes is the type expected from some kind of mixing and binding of sodium within the membrane phase.
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PMID:Sodium efflux from voltage clamped squid giant axons. 85 99

Ascending neuronal activity in the lateral funiculus of the spinal cord of pigeons (spinalized at about C4, recordings at about C6) has been studied with regard to effects of temperature changes with a thermode in the vertebral canal between Th4 and C8. 2. Both warm-sensitive (35) and cold-sensitive (14) neurons were found. According to the change in impulse frequency during steplike thermal stimuli, different reaction types could be distinguished. Twenty-four warm-sensitive and seven cold-sensitive units showed a proportional frequency change without any dynamic reaction. Three other warm-sensitive neurons had an additional dynamic reaction (excitatory overshoot during warming, inhibition during cooling). Five warm-sensitive and three cold-sensitive units showed no static sensitivity but responded with outstanding dynamic frequency changes during rising or falling temperature. The activity of some neurons stopped suddenly above (4) or below (3) a critical temperature, which was always near the normal spinal temperature (about 41 degrees C). Altogether the reaction to rapid temperature changes was consistently greatest near the normal body temperature. 3. The mean static sensitivity of 17 warm-sensitive units was + 4.2 plus or minus 1.3 imp./sec. degrees C (mean value and s. d.) and that of three cold-sensitive ones minus 2.3 plus or minus 0.3 imp./sec. degrees C in the range 35 degrees minus 45 degrees C (vertebral canal temperature). The temperature coefficient (Q10) which was calculated for the same neurons showed great variations with mean values of about 5 for both warm- and cold-sensitive units.
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PMID:Temperature-sensitive ascending neurons in the spinal cord of pigeons. 116 39

Impulse propagation velocity as a function of temperature in the range 5--20degreesC was obtained by external recording from the giant axon of Loligo pealei. The stellar nerve was set into a chamber allowing continuous superfusion, temperature control, and double recording of the impulse. Velocity was calculated from the interval between the spike peaks. The Q10 of velocity was about 1.8. At all temperatures, the velocity increased with time so that only data obtained during the 1st h or 2 could be generally considered to be comparable. Impulse block occurred below --3.4degreesC, in contrast to the giant axon of L. vulgaris, which blocks at about 0degreeC, but at the higher range of temperatures, the velocity in the L. pealei axons was not as well sustained as in those of L. vulgaris. The expected impulse velocity was calculated from Huxley's stability function f(beta) by approximating that function to a fourth-order polynominal and by substituting into it suitable ratios of available Q10 values relating to membrane conductance, ionic current, capacitance, and axoplasmic resistance. The calculation provided an improved fit to published experimental data on L. vulgaris. The difference in slope of the log velocity versus temperature plots, between the presumably warm acclimatized L. vulgaris and the cold-acclimatized L. pealei, was present in both experimental and calculated curves.
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PMID:Temperature and impulse velocity in giant axon of squid Loligo pealei. 120 Jan 43

The effects of muscle temperature on the development of muscular power are discussed. Temperature influences power (both metabolic and mechanical) by means of its effects on the rate of ATP hydrolysis and/or resynthesis. One would therefore expect reduced power outputs at cold muscle temperatures in humans. However, this is not the case during submaximal aerobic exercise. In fact, no changes in metabolic power output at any given submaximal work load were found at cold muscle temperatures, despite the reduced rate of ATP resynthesis and/or splitting. To explain this, it has been postulated that the fraction of active muscle mass at any given time instant could increase in the cold, thus compensating for the reduced ATP splitting rate. This means that the aerobic ATP resynthesis in the cold may be carried out at a slower rate by a greater activated muscle mass. This compensation cannot be operational when maximal power is attained, for in this case the instantaneously activated muscle mass is constant and limited. In fact the maximal aerobic power and the maximal instantaneous anaerobic power decrease with decreasing muscle temperature, as indicated by an average Q10 of 1.4 in the physiological muscle temperature range. The reduction in maximal aerobic power in the cold may be the consequence particularly of a decrease in O2 supply associated with reduced maximal cardiac output and muscle blood flow. On the other hand, the Q10 of the maximal anaerobic power should strictly depend on the reduced rate of ATP hydrolysis. The Q10 of the latter, however, according to Arrhenius law, should be 2 to 3 instead of 1.4.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cold and muscle performance. 148 70

The maximal instantaneous muscle power (wi,max) probably reflects the maximal rate of adenosine 5'-triphosphate (ATP) hydrolysis (ATPmax), a temperature-dependent variable, which gives rise to the hypothesis that temperature, by affecting ATPmax, may also influence wi,max. This hypothesis was tested on six subjects, whose vastus lateralis muscle temperature (Tmuscle) was monitored by a thermocouple inserted approximately 3 cm below the skin surface. The Wi,max was determined during a series of high jumps off both feet on a force platform before and after immersion up to the abdomen for 90 min in a temperature controlled (T = 20 +/- 0.1 degrees C) water bath. Control Tmuscle was 35.8 +/- 0.7 degrees C, with control Wi,max being 51.6 (SD 8.7) W.kg-1. After cold exposure, Tmuscle decreased by about 8 degrees C, whereas wi,max 27% lower. The temperature dependence of Wi,max was found to be less (Q10 less than 1.5, where Q10 is the temperature coefficient as calculated in other studies) than reported in the literature for ATPmax. Such a low Q10 may reflect an increase in the mechanical equivalent of ATP splitting, as a consequence of the reduced velocity of muscle contraction occurring at low Tmuscle.
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PMID:Effects of temperature on the maximal instantaneous muscle power of humans. 155 56


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