The neural circuits of thermal perception

Bokiniec, Phillip; Zampieri, Niccolò; Lewin, Gary R.; Poulet, James F.A.

doi:10.1016/j.conb.2018.04.006

Cited by 38 publications

(25 citation statements)

References 102 publications

(139 reference statements)

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“…While the afferent neurons and ion channels necessary for cool perception have been studied extensively (Bubb et al, 1994;Dhaka et al, 2007Dhaka et al, , 2008Knowlton et al, 2013;McKemy et al, 2002;Milenkovic et al, 2014;Pogorzala et al, 2013), far less is known about non-noxious warm perception (Bokiniec et al, 2018;Filingeri, 2016). Here, we show that mice have similar perceptual thresholds for warm as humans.…”

Section: Discussionmentioning

confidence: 46%

The Sensory Coding of Warm Perception

Paricio-Montesinos

Schwaller

Udhayachandran

et al. 2020

Neuron

127

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Section: Discussionmentioning

confidence: 46%

The Sensory Coding of Warm Perception

Paricio-Montesinos

Schwaller

Udhayachandran

et al. 2020

Neuron

127

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“…The mitigated AD and immune dysfunction observed in the T3Tx-XPro1595 correlated well with histological evidence that XPro1595 diminished plasticity implicated in increasing excitability of the SSR circuit. Normally, CGRP ϩ nociceptors predominantly synapse on neurons in superficial dorsal horn laminae that then project up the spinothalamic tract to relay nociceptive information to the brain (Bokiniec et al, 2018). We know from current and previous experiments that sTNF␣ drives plasticity of nociceptors (Wheeler et al, 2014;Mironets et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Attenuating Neurogenic Sympathetic Hyperreflexia Robustly Improves Antibacterial Immunity After Chronic Spinal Cord Injury

et al. 2019

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Spinal cord injury (SCI) disrupts critical physiological systems, including the cardiovascular and immune system. Plasticity of spinal circuits below the injury results in abnormal, heightened sympathetic responses, such as extreme, sudden hypertension that hallmarks life-threatening autonomic dysreflexia. Moreover, such sympathetic hyperreflexia detrimentally impacts other effector organs, including the spleen, resulting in spinal cord injury-induced immunodeficiency. Consequently, infection is a leading cause of mortality after SCI. Unfortunately, there are no current treatments that prophylactically limit sympathetic hyperreflexia to prevent subsequent effector organ dysfunction. The cytokine soluble tumor necrosis factor ␣ (sTNF␣) is upregulated in the CNS within minutes after SCI and remains elevated. Here, we report that commencing intrathecal administration of XPro1595, an inhibitor of sTNF␣, at a clinically feasible, postinjury time point (i.e., 3 d after complete SCI) sufficiently diminishes maladaptive plasticity within the spinal sympathetic reflex circuit. This results in less severe autonomic dysreflexia, a real-time gauge of sympathetic hyperreflexia, for months postinjury. Remarkably, delayed delivery of the sTNF␣ inhibitor prevents sympathetic hyperreflexia-associated splenic atrophy and loss of leukocytes to dramatically improve the endogenous ability of chronic SCI rats to fight off pneumonia, a common cause of hospitalization after injury. The improved immune function with XPro1595 correlates with less noradrenergic fiber sprouting and normalized norepinephrine levels in the spleen, indicating that heightened, central sTNF␣ signaling drives peripheral, norepinephrine-mediated organ dysfunction, a novel mechanism of action. Thus, our preclinical study supports intrathecally targeting sTNF␣ as a viable strategy to broadly attenuate sympathetic dysregulation, thereby improving cardiovascular regulation and immunity long after SCI.

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“…While the afferent pathways and ion channels necessary for cooling perception have been studied extensively (Dhaka et al, 2007(Dhaka et al, , 2008Knowlton et al, 2013;McKemy et al, 2002;Milenkovic et al, 2014), far less is known about the molecular and neuronal pathways mediating innocuous warmth perception (Bokiniec et al, 2018;Filingeri, 2016). Here we show that mice learn to report warming stimuli delivered to the paw with similar perceptual thresholds to humans, and easily discriminate forelimb skin warming from cooling.…”

Section: Discussionmentioning

confidence: 99%

The sensory coding of warm perception

Paricio-Montesinos

Schwaller

Udhayachandran

et al. 2018

Preprint

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Humans easily discriminate tiny skin temperature changes that are perceived as warming or cooling. Dedicated thermoreceptors forming distinct thermosensory channels or "labelled lines" are thought to underlie thermal perception. We show that mice have similar perceptual thresholds for forepaw warming to humans (~1 o C change) and do not mistake warming for cooling. Mice perform warm discrimination tasks without dedicated thermoreceptors, but use information carried by unmyelinated polymodal C-fibers. Deletion of the heat-sensitive transduction channels TRPM2 and TRPV1 did not impact warming perception or afferent coding of warm. However, without the cold sensitive TRPM8 channel, afferent coding of cooling was impaired and these mice cannot perceive warming or cooling. Our data is incompatible with the existence of thermospecific labelled lines, but can be reconciled by the existence of central circuits that compare and integrate the input from at least two types of polymodal afferents, hitherto thought to exclusively signal pain.

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The neural circuits of thermal perception

Cited by 38 publications

References 102 publications

The Sensory Coding of Warm Perception

The Sensory Coding of Warm Perception

Attenuating Neurogenic Sympathetic Hyperreflexia Robustly Improves Antibacterial Immunity After Chronic Spinal Cord Injury

The sensory coding of warm perception

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