Temperature Deactivation of the Depolarizing TRP Current as a Mechanism of Hypothermia-Related Inhibition of Neuronal Activity: a Model Study

Коrogod, S. М.; Demianenko, L. E.

doi:10.1007/s11062-017-9605-2

Cited by 5 publications

(7 citation statements)

References 31 publications

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“…The Trpm5 model was a modification of our earlier model 66 . The latter described the channel voltage and temperature gating by the equations derived from a two-state kinetic scheme (Eqs.…”

Section: Methodsmentioning

confidence: 99%

Trpm5 channels encode bistability of spinal motoneurons and ensure motor control of hindlimbs in mice

et al. 2021

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Bistable motoneurons of the spinal cord exhibit warmth-activated plateau potential driven by Na+ and triggered by a brief excitation. The thermoregulating molecular mechanisms of bistability and their role in motor functions remain unknown. Here, we identify thermosensitive Na+-permeable Trpm5 channels as the main molecular players for bistability in mouse motoneurons. Pharmacological, genetic or computational inhibition of Trpm5 occlude bistable-related properties (slow afterdepolarization, windup, plateau potentials) and reduce spinal locomotor outputs while central pattern generators for locomotion operate normally. At cellular level, Trpm5 is activated by a ryanodine-mediated Ca2+ release and turned off by Ca2+ reuptake through the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump. Mice in which Trpm5 is genetically silenced in most lumbar motoneurons develop hindlimb paresis and show difficulties in executing high-demanding locomotor tasks. Overall, by encoding bistability in motoneurons, Trpm5 appears indispensable for producing a postural tone in hindlimbs and amplifying the locomotor output.

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“…The Trpm5 model was a modification of our earlier model 66 . The latter described the channel voltage and temperature gating by the equations derived from a two-state kinetic scheme (Eqs.…”

Section: Methodsmentioning

confidence: 99%

Trpm5 channels encode bistability of spinal motoneurons and ensure motor control of hindlimbs in mice

et al. 2021

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“…One possible reason for this delay is that cooling slows molecular processes. The slowing down of these processes can result in delays in signal conduction and synaptic transmission (Asztely et al, 1997;Cais et al, 2008;De Koninck and Mody, 1994;Esmann and Skou, 1988;Hartmann and Nothwang, 2011;Iversen and Neal, 1968;Jenkins et al, 1999;Koike and Nagata, 1979;Korogod and Demianenko, 2017;Owen et al, 2019;Postlethwaite et al, 2007;Pyott and Rosenmund, 2002;Sabatini and Regehr, 1996). In addition to delays in signal transduction, another possible reason may be the inactivation of GABAergic inhibition.…”

Section: Discussionmentioning

confidence: 99%

Effects of focal cortical cooling on somatosensory evoked potentials in rats

Gotoh,

Dezawa,

Takashima

et al. 2023

Preprint

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Although the focal brain cooling technique is widely used to examine brain function, the effects of variations in cortical temperature on sensory information processing and neural mechanisms remain underexplored. To elucidate the mechanisms of temperature modulation in somatosensory processing, this study aimed to examine how P1 and N1 deflections of somatosensory evoked potentials (SEPs) depend on cortical temperature and how excitatory and inhibitory inputs contribute to this temperature dependency. SEPs were generated through electrical stimulation of the contralateral forepaw in anesthetized rats. The SEPs were recorded while cortical temperatures were altered between 18–37°C: without any antagonists; with gamma-aminobutyric acid type A (GABAA) receptor antagonist, gabazine; with aminomethylphosphonic acid (AMPA) receptor antagonist (NBQX), orN-Methyl-D-aspartic acid (NMDA) receptor antagonist ([R]-CPP). The effects of different gabazine concentrations (0, 1, and 10 µM) were examined in the 35–38°C range. The P1/N1 amplitudes and their peak- to-peak differences plotted against cortical temperature showed an inverted U relationship with their maximum at approximately 27.5°C when no antagonists were administered. The negative correlation between these amplitudes and temperatures ≥27.5°C plateaued after gabazine administration, which occurred progressively as the gabazine concentration increased. In contrast, the correlation remained negative after the administration of NBQX and (R)-CPP. GABAergic inhibitory inputs contribute to the negative correlation between SEP amplitude and cortical temperature around the physiological cortical temperature by suppressing SEPs to a greater extent at higher temperatures.

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“…Temperature dependence is inherent in practically all types of ion currents as corresponding current-conducting channels change their biophysical properties with temperature [ 40 ]. Hodgkin and Huxley showed, >60 years ago, that temperature could profoundly influence membrane excitability [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Temperature sensitivity was also described in the K2P channels, specifically in the TREK-1, TREK-2 and TRAAK channels [ 40 , 49 , 52 ]. Of note, TREK-1 and TRAAK have been cloned from human skeletal muscle [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Serum potassium changes during hypothermia and rewarming: a case series and hypothesis on the mechanism

Boubes

Batlle

Tang

et al. 2022

Clinical Kidney Journal

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Introduction Hypokalemia is known to occur in association with therapeutically induced hypothermia and is usually managed by the administration of potassium (K+). Methods We reviewed data from 74 patients who underwent therapeutic hypothermia protocol at our medical institution. Results In 4 patients in whom close data on serum K+ and temperature was available, a strong positive correlation between serum K+ and body temperature was found during the rewarming phase when serum K+ increased. Based on the close positive relationship between serum K+ and total body temperature, we hypothesize that serum K+ falls during hypothermia owing to decreased activity of temperature dependent K+ exit channels that under normal conditions are sufficiently active to match cellular K+ intake via Na+/K+/ATPase. Upon rewarming, reactivation of these channels results in a rapid increase in serum K+ as a result of K+ exit down its concentration gradient. Conclusion Administration of K+ during hypothermia should be done cautiously and avoided during rewarming to avoid potentially life threatening hyperkalemia. K+ exit via temperature dependent K+ channels provides a logical explanation for the rebound hyperkalemia. K+ exit channels may play a bigger role than previously appreciated in the regulation of serum K+ during normal and pathophysiological conditions.

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Temperature Deactivation of the Depolarizing TRP Current as a Mechanism of Hypothermia-Related Inhibition of Neuronal Activity: a Model Study

Cited by 5 publications

References 31 publications

Trpm5 channels encode bistability of spinal motoneurons and ensure motor control of hindlimbs in mice

Trpm5 channels encode bistability of spinal motoneurons and ensure motor control of hindlimbs in mice

Effects of focal cortical cooling on somatosensory evoked potentials in rats

Serum potassium changes during hypothermia and rewarming: a case series and hypothesis on the mechanism

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