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Adequately localizing pain is crucial to protect the body against physical damage and react to the stimulus in external space having caused such damage. Accordingly, it is hypothesized that nociceptive inputs are remapped from a somatotopic reference frame, representing the skin surface, towards a spatiotopic frame, representing the body parts in external space. This ability is thought to be developed and shaped by early visual experience. To test this hypothesis, normally sighted and early blind participants performed temporal order judgment tasks during which they judged which of two nociceptive stimuli applied on each hand's dorsum was perceived as first delivered. Crucially, tasks were performed with the hands either in an uncrossed posture or crossed over body midline. While early blinds were not affected by the posture, performances of the normally sighted participants decreased in the crossed condition relative to the uncrossed condition. This indicates that nociceptive stimuli were automatically remapped into a spatiotopic representation that interfered with somatotopy in normally sighted individuals, whereas early blinds seemed to mostly rely on a somatotopic representation to localize nociceptive inputs. Accordingly, the plasticity of the nociceptive system would not purely depend on bodily experiences but also on crossmodal interactions between nociception and vision during early sensory experience.
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http://dx.doi.org/10.1016/j.cortex.2019.12.024 | DOI Listing |
Pain Rep
October 2025
Physiology, Pharmacology and Neuroscience, School of Life Sciences, The University of Nottingham, Nottingham, United Kingdom.
Introduction: The dorsal horn (DH) of the spinal cord is physiologically immature at birth. Spinal excitability increases and wide dynamic range (WDR) neurons in lamina V have lowered activation thresholds and larger receptive field sizes.
Objective: The DH is composed of 5 laminae containing diverse interneuronal populations yet our understanding of the physiology of the DH is based on behavioural studies or extrapolation of single cell WDR recordings to the whole network.
Psychophysiology
September 2025
Psychological Neuroscience Laboratory (PNL), Research Center in Psychology (CIPsi), School of Psychology, Universidade do Minho, Braga, Portugal.
Touch has an affective dimension, conveyed through low-threshold mechanoreceptors known as C-tactile (CT) afferents, which are activated by gentle, caress-like contact. While there is evidence that these fibers modulate nociceptive input, their influence on the processing of other somatosensory afferent activity remains largely unknown. In this study, we explored how slow brushing (CT-optimal stimulation) modulates somatosensory evoked potentials (SEPs) elicited by electrical stimulation of the median nerve (occurring at 0.
View Article and Find Full Text PDFEur J Pain
October 2025
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Background: Pain catastrophising is a maladaptive cognitive-emotional trait linked to greater pain severity and poorer outcomes, yet its neurophysiological correlates remain unclear.
Objectives: We tested whether pain catastrophising amplifies cortical responses to nociceptive input, independent of subjective pain intensity.
Methods: Fifty-two healthy adults underwent EEG during painful laser stimulation (n = 29; mean age 24.
Both the medial prefrontal cortex (mPFC) and thalamus have been implicated in pain regulation. However, the roles of the mPFC-thalamus connection in pain and how the mPFC modulates nociceptive processing within the brain remain unclear. Here, we show that the mPFC neurons that project to thalamus are marked by expression and deactivated in both acute and chronic pain.
View Article and Find Full Text PDFPain
September 2025
Division of Neurophysiology, Center for Brain Research, Medical University of Vienna, Wien, Austria.
Astrocytes are key players in chronic pain, driving maladaptive changes in neuronal circuits. Yet, their influence on acute nociception-the body's first line of defense against harmful stimuli-remains poorly understood. Using chemogenetic tools to mimic endogenous astrocytic G-protein-coupled receptor-mediated signaling, we reveal that astrocytes induce bidirectional plasticity at nociceptive synapses in the dorsal horn.
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