Heat Response (heat + response)

Distribution by Scientific Domains


Selected Abstracts


Noxious heat-induced CGRP release from rat sciatic nerve axons in vitro

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2001
S. K. Sauer
Abstract Noxious heat may act as an endogenous activator of the ionotropic capsaicin receptor (VR1) and of its recently found homologue VRL1, expressed in rat dorsal root ganglion cells and present along their nerve fibres. We have previously reported that capsaicin induces receptor-mediated and Ca++ -dependent calcitonin gene-related peptide (CGRP) release from axons of the isolated rat sciatic nerve. Here we extended the investigation to noxious heat stimulation and the transduction mechanisms involved. Heat stimulation augmented the CGRP release from desheathed sciatic nerves in a log,linear manner with a Q10 of ,,15 and a threshold between 40 and 42 °C. The increases were 1.75-fold at 42 °C, 3.8-fold at 45 °C and 29.1-fold at 52 °C; in Ca++ -free solution these heat responses were abolished or reduced by 71 and 92%, respectively. Capsazepine (10 µm) and Ruthenium Red (1 µm) used as capsaicin receptor/channel antagonists did not significantly inhibit the heat-induced release. Pretreatment of the nerves with capsaicin (100 µm for 30 min) caused complete desensitization to 1 µm capsaicin, but a significant heat response remained, indicating that heat sensitivity is not restricted to capsaicin-sensitive fibres. The sciatic nerve axons responded to heat, potassium and capsaicin stimulation with a Ca++ -dependent CGRP release. Blockade of the capsaicin receptor/channels had little effect on the heat-induced neuropeptide release. We conclude therefore that other heat-activated ion channels than VR1 and VRL1 in capsaicin-sensitive and -insensitive nerve fibres may cause excitation, axonal Ca++ influx and subsequent CGRP release. [source]


Low-threshold heat response antagonized by capsazepine in chick sensory neurons, which are capsaicin-insensitive

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2000
Antonia Marín-Burgin
Abstract The heat-transducing receptor VR1 cloned from rat sensory neurons can be activated by both noxious heat and capsaicin. As the response of sensory neurons to capsaicin is species dependent, it is conceivable that the responses to noxious heat and to capsaicin are transduced by distinct receptors across different species. Therefore, we investigated responses to noxious heat from a capsaicin-insensitive (chick) and a capsaicin-sensitive (rat) species. In chick, whole-cell patch-clamp experiments in isolated dorsal root ganglion neurons revealed two populations of neurons with different thresholds to noxious heat, activated at ,,43 °C and ,,53 °C. In cobalt uptake experiments, the proportion of neurons showing a heat-induced response increased with increasing heat stimuli. Application of capsaicin (1,10 ,m) did not result in inward currents or cobalt uptake. Rat neurons yielded comparable results in heat experiments, but were capsaicin-sensitive. Although chick neurons are insensitive to capsaicin, the competitive capsaicin antagonist capsazepine (1,10 ,m) was effective in blocking heat-induced responses, verified by patch-clamp and cobalt uptake methods. The noncompetitive capsaicin antagonist ruthenium red (10 ,m) reduced to almost nil the proportion of heat-responsive neurons identified with the cobalt uptake method. These findings suggest that chick DRG neurons express a low-threshold heat-transducing receptor with a pharmacological profile distinct from the low-threshold heat receptor VR1 cloned from rat DRG neurons. The data support the idea that there might be heat receptor subtypes with differences in the capsaicin binding site. [source]


Quantifying the heterogeneous heat response of Escherichia coli under dynamic temperatures

JOURNAL OF APPLIED MICROBIOLOGY, Issue 4 2010
E. Van Derlinden
Abstract Aims:, Non-sigmoid growth curves of Escherichia coli obtained at constant temperatures near the maximum growth temperature (Tmax) were previously explained by the coexistence of two subpopulations, i.e. a stress-sensitive and a stress-resistant subpopulation. Mathematical simulations with a heterogeneous model support this hypothesis for static experiments at 45°C. In this article, the behaviour of E. coli, when subjected to a linearly increasing temperature crossing Tmax, is studied. Methods and Results:, Subpopulation dynamics are studied by culturing E. coli K12 MG1655 in brain heart infusion broth in a bioreactor. The slowly increasing temperature (°C h,1) starting from 42°C results in growth up to 60°C, a temperature significantly higher than the known Tmax. Given some additional presumptions, mathematical simulations with the heterogeneous model can describe the dynamic experiments rather well. Conclusions:, This study further confirms the existence of a stress-resistant subpopulation and reveals the unexpected growth of E. coli at temperatures significantly higher than Tmax. Significance and Impact of the Study:, The growth of the small stress-resistant subpopulation at unexpectedly high temperatures asks for a revision of currently applied models in food safety and food quality strategies. [source]


Response surfaces for the combined effects of heat shock and smoke on germination of 16 species forming soil seed banks in south-east Australia

AUSTRAL ECOLOGY, Issue 6 2007
PAUL B. THOMAS
Abstract There is limited understanding of how fire-related cues such as heat shock and smoke can combine to affect the germination response of seeds from fire-prone vegetation because combinations of multiple levels of both cues have rarely been investigated. Germination response surfaces were determined for the combination of heat shock and smoke by applying factorial combinations of temperature (up to 100°C) and aerosol smoke (0,20 min) to 16 species that form soil seed banks in the Sydney region of south-eastern Australia. Duplicate populations of three species were also examined to assess the constancy of a species response surface. Of the 19 populations examined, 16 showed a germination response to both the fire cues, which combined interactively in 14 populations, and independently in two. No population responded only to a single cue; however, seeds of 11 populations responded to heat in the absence of smoke, and nine responded to smoke in the absence of heat. Heat applied in the absence of smoke negatively affected germination in seven populations, either progressively as temperature increased, or above a set temperature. Negative germination responses over part of the temperature range were fully reversed at higher temperatures for unsmoked seeds of four populations (curvilinear heat response). Smoke effects were most frequently positive over all or part of the range of durations used, and when combined with heat frequently fully or partially reversed negative heat effects. Three populations required the obligatory combination of smoke and heat. A novel response to the cues was observed for three species, with smoke reversing negative heat effects at 75°C, being supplanted by a positive heat response of unsmoked seed at 100°C. The response surface for duplicate populations of two of the three species examined was variable. Heat shock and smoke frequently combined to affect germination, in both positive and negative ways. Consequently, to gain an accurate assessment of the response of seeds to fires, an experimental design that samples within the potential response zones of germination cues is essential. [source]


Noxious heat-induced CGRP release from rat sciatic nerve axons in vitro

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2001
S. K. Sauer
Abstract Noxious heat may act as an endogenous activator of the ionotropic capsaicin receptor (VR1) and of its recently found homologue VRL1, expressed in rat dorsal root ganglion cells and present along their nerve fibres. We have previously reported that capsaicin induces receptor-mediated and Ca++ -dependent calcitonin gene-related peptide (CGRP) release from axons of the isolated rat sciatic nerve. Here we extended the investigation to noxious heat stimulation and the transduction mechanisms involved. Heat stimulation augmented the CGRP release from desheathed sciatic nerves in a log,linear manner with a Q10 of ,,15 and a threshold between 40 and 42 °C. The increases were 1.75-fold at 42 °C, 3.8-fold at 45 °C and 29.1-fold at 52 °C; in Ca++ -free solution these heat responses were abolished or reduced by 71 and 92%, respectively. Capsazepine (10 µm) and Ruthenium Red (1 µm) used as capsaicin receptor/channel antagonists did not significantly inhibit the heat-induced release. Pretreatment of the nerves with capsaicin (100 µm for 30 min) caused complete desensitization to 1 µm capsaicin, but a significant heat response remained, indicating that heat sensitivity is not restricted to capsaicin-sensitive fibres. The sciatic nerve axons responded to heat, potassium and capsaicin stimulation with a Ca++ -dependent CGRP release. Blockade of the capsaicin receptor/channels had little effect on the heat-induced neuropeptide release. We conclude therefore that other heat-activated ion channels than VR1 and VRL1 in capsaicin-sensitive and -insensitive nerve fibres may cause excitation, axonal Ca++ influx and subsequent CGRP release. [source]