Central neural substrates involved in temperature discrimination, thermal pain, thermal comfort, and thermoregulatory behavior

Craig, A. D.

doi:10.1016/b978-0-444-63912-7.00019-9

Cited by 22 publications

(10 citation statements)

References 206 publications

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“…However, it cannot be excluded that TRPA1 channels in other brain structures are the primary sites for the action of H 2 S and modulate the activity of thermoeffectors through their projections to neurons within the thermoregulation pathways. In support of that scenario, physiological function for TRPA1 was found in the somatosensory cortex [ 66 ], in the hippocampus [ 63 , 66 ], as well as in the supraoptic and solitary nuclei [ 67 , 68 ], which brain regions are also involved in the regulation of deep T b [ 47 , 69 , 70 ].…”

Section: Discussionmentioning

confidence: 93%

The Hypothermic Effect of Hydrogen Sulfide Is Mediated by the Transient Receptor Potential Ankyrin-1 Channel in Mice

et al. 2021

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Hydrogen sulfide (H2S) has been shown in previous studies to cause hypothermia and hypometabolism in mice, and its thermoregulatory effects were subsequently investigated. However, the molecular target through which H2S triggers its effects on deep body temperature has remained unknown. We investigated the thermoregulatory response to fast-(Na2S) and slow-releasing (GYY4137) H2S donors in C57BL/6 mice, and then tested whether their effects depend on the transient receptor potential ankyrin-1 (TRPA1) channel in Trpa1 knockout (Trpa1−/−) and wild-type (Trpa1+/+) mice. Intracerebroventricular administration of Na2S (0.5–1 mg/kg) caused hypothermia in C57BL/6 mice, which was mediated by cutaneous vasodilation and decreased thermogenesis. In contrast, intraperitoneal administration of Na2S (5 mg/kg) did not cause any thermoregulatory effect. Central administration of GYY4137 (3 mg/kg) also caused hypothermia and hypometabolism. The hypothermic response to both H2S donors was significantly (p < 0.001) attenuated in Trpa1−/− mice compared to their Trpa1+/+ littermates. Trpa1 mRNA transcripts could be detected with RNAscope in hypothalamic and other brain neurons within the autonomic thermoeffector pathways. In conclusion, slow- and fast-releasing H2S donors induce hypothermia through hypometabolism and cutaneous vasodilation in mice that is mediated by TRPA1 channels located in the brain, presumably in hypothalamic neurons within the autonomic thermoeffector pathways.

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Section: Discussionmentioning

confidence: 93%

The Hypothermic Effect of Hydrogen Sulfide Is Mediated by the Transient Receptor Potential Ankyrin-1 Channel in Mice

et al. 2021

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“…Admittedly, our findings do not alternatively indicate that cold and noxious sensations share the same spinal pathway. Indeed, indirect evidence in humans indicates the presence of cold‐specific nuclei in the thalamus (Kim, Greenspan, Coghill, Ohara, & Lenz, 2007), and animal studies have consistently identified cold‐specific neurons in the dorsal horn lamina I (Bud Craig, 2018). Further studies are, therefore, needed to distinctly identify cold and nociceptive afferent pathways within the spinothalamic tract.…”

Section: Discussionmentioning

confidence: 99%

Conduction velocity of the cold spinal pathway in healthy humans

Leone

Lionardo

Diotallevi

et al. 2020

European Journal of Pain

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Neurophysiological assessment of the spinothalamic system currently relies on noxious heat-and warm-mediated evoked potential recordings related to Aδ-and C-fibres, using laser and contact heat stimulation (Iannetti et al., 2003; Wydenkeller, 2008). A new device based on micro-Peltier elements that is able to produce steep cooling ramps up to 300°C/s has been developed to activate selectively cold-mediating fibres (De Keyser, van den Broeke, Courtin, Dufour, & Mouraux, 2018). This tool, which provides rapid and painless skin cooling, elicits cold-evoked potentials at latencies compatible with Aδ-fibres conduction velocity (De Keyser et al., 2018; Leone et al., 2019). Previous studies-using heat and warm laser stimulation of the skin overlying the vertebral spinous processes-have investigated the spinothalamic tract in healthy humans and patients and provided information on nociceptive and warm spinal pathway conduction velocities (

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“…Neuroimaging studies have contributed increasing knowledge to facilitate the understanding on pain processing 32–34. Thereby, thermal allodynia has been investigated in experimental pain models32,35 and in neuropathic pain patients 36–40.…”

Section: Discussionmentioning

confidence: 99%

<p>Neuroimaging Of Cold Allodynia Reveals A Central Disinhibition Mechanism Of Pain</p>

Forstenpointner¹,

Binder²,

Maag³

et al. 2019

JPR

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PurposeAllodynia refers to pain evoked by physiologically innocuous stimuli. It is a disabling symptom of neuropathic pain following a lesion within the peripheral or central nervous system. In fact, two different pathophysiological mechanisms of cold allodynia (ie, hypersensitivity to innocuous cold) have been proposed. The peripheral sensitization of nociceptive neurons can produce cold allodynia, which can be induced experimentally by a topical application of menthol. An alternative mechanism involves reduced inhibition of central pain processing by innocuous cold stimuli. A model to induce the latter type of allodynia is the conduction block of peripheral A-fiber input.Patients and methodsIn the presented study, functional MRI was used to analyze these two different experimental models of cold allodynia. In order to identify the underlying cerebral activation patterns of both mechanisms, the application of menthol and the induction of a mechanical A-fiber blockade were studied in healthy volunteers.ResultsThe block-induced cold allodynia caused significantly stronger activation of the medial polymodal pain processing pathway, including left medial thalamus, anterior cingulate cortex, and medial prefrontal cortex. In contrast, menthol-induced cold allodynia caused significantly stronger activity of the left lateral thalamus as well as the primary and secondary somatosensory cortices, key structures of the lateral discriminative pathway of pain processing. Mean pain intensity did not differ between both forms of cold allodynia.ConclusionExperimental cold allodynia is mediated in different cerebral areas depending on the underlying pathophysiology. The activity pattern associated with block-induced allodynia confirms a fundamental integration between painful and non-painful temperature sensation, ie, the cold-induced inhibition of cold pain.

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Central neural substrates involved in temperature discrimination, thermal pain, thermal comfort, and thermoregulatory behavior

Cited by 22 publications

References 206 publications

The Hypothermic Effect of Hydrogen Sulfide Is Mediated by the Transient Receptor Potential Ankyrin-1 Channel in Mice

The Hypothermic Effect of Hydrogen Sulfide Is Mediated by the Transient Receptor Potential Ankyrin-1 Channel in Mice

Conduction velocity of the cold spinal pathway in healthy humans

<p>Neuroimaging Of Cold Allodynia Reveals A Central Disinhibition Mechanism Of Pain</p>

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