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Physiology (Bethesda, Md.) Jan 2018The study of diverse animal groups allows us to discern the evolution of the neurobiology of nociception. Nociception functions as an important alarm system alerting the... (Comparative Study)
Comparative Study Review
The study of diverse animal groups allows us to discern the evolution of the neurobiology of nociception. Nociception functions as an important alarm system alerting the individual to potential and actual tissue damage. All animals possess nociceptors, and, in some animal groups, it has been demonstrated that there are consistent physiological mechanisms underpinning the nociceptive system. This review considers the comparative biology of nociception and pain from an evolutionary perspective.
Topics: Animals; Biological Evolution; Humans; Nociception; Nociceptors; Pain; Species Specificity
PubMed: 29212893
DOI: 10.1152/physiol.00022.2017 -
Neuron Aug 2015Recent neuroimaging studies suggest that the brain adapts with pain, as well as imparts risk for developing chronic pain. Within this context, we revisit the concepts... (Review)
Review
Recent neuroimaging studies suggest that the brain adapts with pain, as well as imparts risk for developing chronic pain. Within this context, we revisit the concepts for nociception, acute and chronic pain, and negative moods relative to behavior selection. We redefine nociception as the mechanism protecting the organism from injury, while acute pain as failure of avoidant behavior, and a mesolimbic threshold process that gates the transformation of nociceptive activity to conscious pain. Adaptations in this threshold process are envisioned to be critical for development of chronic pain. We deconstruct chronic pain into four distinct phases, each with specific mechanisms, and outline current state of knowledge regarding these mechanisms: the limbic brain imparting risk, and the mesolimbic learning processes reorganizing the neocortex into a chronic pain state. Moreover, pain and negative moods are envisioned as a continuum of aversive behavioral learning, which enhance survival by protecting against threats.
Topics: Affect; Animals; Avoidance Learning; Brain; Humans; Nociception; Pain; Pain Perception
PubMed: 26247858
DOI: 10.1016/j.neuron.2015.06.005 -
Best Practice & Research. Clinical... Sep 2019Opioid-free anesthesia (OFA) is emerging as a new stimulating research perspective. The rationale to propose OFA is based on the aim to avoid the negative impact of... (Review)
Review
Opioid-free anesthesia (OFA) is emerging as a new stimulating research perspective. The rationale to propose OFA is based on the aim to avoid the negative impact of intraoperative opioid on a patient's postoperative outcomes and also on the physiology of pathways involved in intraoperative nociception. It is based on the concept of multimodal anesthesia. OFA has been shown to be feasible but the literature is still scarce on the clinically meaningful benefits for patients as well as on the side effects and/or complications that might be associated with it. This review focused first on the physiology of nociception, the reasons for using or not using opioids during anesthesia, and then on the literature reporting evidence-based proofs of benefits/risks associated with OFA.
Topics: Analgesics, Opioid; Anesthesia; Humans; Nociception; Pain, Postoperative
PubMed: 31785720
DOI: 10.1016/j.bpa.2019.09.002 -
Current Biology : CB Feb 2017Nociception, the sensory mechanism that allows animals to sense and avoid potentially tissue-damaging stimuli, is critical for survival. This process relies on...
Nociception, the sensory mechanism that allows animals to sense and avoid potentially tissue-damaging stimuli, is critical for survival. This process relies on nociceptors, which are specialized neurons that detect and respond to potentially damaging forms of energy - heat, mechanical and chemical - in the environment. Nociceptors accomplish this task through the expression of molecules that function to detect and signal the presence of potential harm. Downstream of the nociceptive sensory input, the neural signals trigger protective (nocifensive) behaviors, and the sensory stimuli that reach the brain may be perceived as painful.
Topics: Animals; Cold Temperature; Hot Temperature; Mechanical Phenomena; Nociception; Nociceptors; Noxae
PubMed: 28222285
DOI: 10.1016/j.cub.2017.01.037 -
British Journal of Anaesthesia Aug 2019Nociception, in contrast to pain, is not a subjective feeling, but the physiological encoding and processing of nociceptive stimuli. However, monitoring nociception... (Review)
Review
Nociception, in contrast to pain, is not a subjective feeling, but the physiological encoding and processing of nociceptive stimuli. However, monitoring nociception remains a challenge in attempts to lower the incidence of acute postoperative pain and the move towards a more automated approach to analgesia and anaesthesia. To date, several commercialised devices promise a more accurate reflection of nociception than the traditionally used vital signs, blood pressure and heart rate. This narrative review presents an overview of existing technologies and commercially available devices, and offers a perspective for future research. Although firm conclusions about individual methods may be premature, none currently appears to offer a sufficiently broad applicability. Furthermore, there is currently no firm evidence for any clinically relevant influence of such devices on patient outcome. However, the available monitors have significantly aided the understanding of underlying mechanisms and identification of potential pitfalls.
Topics: Humans; Monitoring, Intraoperative; Nociception; Nociceptive Pain
PubMed: 31047645
DOI: 10.1016/j.bja.2019.03.024 -
Nature Mar 2021The innate immune regulator STING is a critical sensor of self- and pathogen-derived DNA. DNA sensing by STING leads to the induction of type-I interferons (IFN-I) and...
The innate immune regulator STING is a critical sensor of self- and pathogen-derived DNA. DNA sensing by STING leads to the induction of type-I interferons (IFN-I) and other cytokines, which promote immune-cell-mediated eradication of pathogens and neoplastic cells. STING is also a robust driver of antitumour immunity, which has led to the development of STING activators and small-molecule agonists as adjuvants for cancer immunotherapy. Pain, transmitted by peripheral nociceptive sensory neurons (nociceptors), also aids in host defence by alerting organisms to the presence of potentially damaging stimuli, including pathogens and cancer cells. Here we demonstrate that STING is a critical regulator of nociception through IFN-I signalling in peripheral nociceptors. We show that mice lacking STING or IFN-I signalling exhibit hypersensitivity to nociceptive stimuli and heightened nociceptor excitability. Conversely, intrathecal activation of STING produces robust antinociception in mice and non-human primates. STING-mediated antinociception is governed by IFN-Is, which rapidly suppress excitability of mouse, monkey and human nociceptors. Our findings establish the STING-IFN-I signalling axis as a critical regulator of physiological nociception and a promising new target for treating chronic pain.
Topics: Analgesia; Animals; Female; Humans; Interferon Type I; Macaca mulatta; Male; Membrane Proteins; Mice; Nociception; Pain; Sensory Receptor Cells; Signal Transduction
PubMed: 33442058
DOI: 10.1038/s41586-020-03151-1 -
Brazilian Journal of Physical Therapy 2023
Topics: Humans; Nociception; Neuralgia; Chronic Pain
PubMed: 37639943
DOI: 10.1016/j.bjpt.2023.100537 -
Proceedings of the National Academy of... Mar 2022Acute nociception is essential for survival by warning organisms against potential dangers, whereas tissue injury results in a nociceptive hypersensitivity state that is...
Acute nociception is essential for survival by warning organisms against potential dangers, whereas tissue injury results in a nociceptive hypersensitivity state that is closely associated with debilitating disease conditions, such as chronic pain. Transient receptor potential (Trp) ion channels expressed in nociceptors detect noxious thermal and chemical stimuli to initiate acute nociception. The existing hypersensitivity model suggests that under tissue injury and inflammation, the same Trp channels in nociceptors are sensitized through transcriptional and posttranslational modulation, leading to nociceptive hypersensitivity. Unexpectedly and different from this model, we find that in Drosophila larvae, acute heat nociception and tissue injury-induced hypersensitivity involve distinct cellular and molecular mechanisms. Specifically, TrpA1-D in peripheral sensory neurons mediates acute heat nociception, whereas TrpA1-C in a cluster of larval brain neurons transduces the heat stimulus under the allodynia state. As a result, interfering with synaptic transmission of these brain neurons or genetic targeting of TrpA1-C blocks heat allodynia but not acute heat nociception. TrpA1-C and TrpA1-D are two splicing variants of TrpA1 channels and are coexpressed in these brain neurons. We further show that Gq-phospholipase C signaling, downstream of the proalgesic neuropeptide Tachykinin, differentially modulates these two TrpA1 isoforms in the brain neurons by selectively sensitizing heat responses of TrpA1-C but not TrpA1-D. Together, our studies provide evidence that nociception and noncaptive sensitization could be mediated by distinct sensory neurons and molecular sensors.
Topics: Animals; Drosophila; Neurons; Nociception; Nociceptors; Transducers; Transient Receptor Potential Channels
PubMed: 35294287
DOI: 10.1073/pnas.2113645119 -
The Journal of Pain Sep 2019Congenital insensitivity to pain is an umbrella term used to describe a group of rare genetic diseases also classified as hereditary sensory autonomic neuropathies.... (Review)
Review
Congenital insensitivity to pain is an umbrella term used to describe a group of rare genetic diseases also classified as hereditary sensory autonomic neuropathies. These conditions are intriguing, with the potential to shed light on the poorly understood relationship concerning nociception and the experience of pain. However, the term congenital insensitivity to pain is epistemologically incorrect and is the product of historical circumstances. The term conflates pain and nociception and, thus, prevents researchers and caregivers from grasping the full dimensions of these conditions. The aims of this article were to review the epistemological problems surrounding the term, to demonstrate why the term is inaccurate and to suggest a new term, namely, congenital nociceptor deficiency. The suggested term better reflects the nature of the conditions and incorporates current understandings of nociception. PERSPECTIVE: The umbrella term congenital insensitivity to pain conflates pain and nociception, which is epistemologically unacceptable. We suggest a new term, namely, congenital nociceptor deficiency, that overcomes this problem and is concordant with current neurobiological knowledge.
Topics: Humans; Nociception; Pain Insensitivity, Congenital; Pain Perception
PubMed: 30716471
DOI: 10.1016/j.jpain.2019.01.331 -
Medecine Sciences : M/S Feb 2021Autistic subjects frequently display sensory anomalies. Those regarding nociception and its potential outcome, pain, are of crucial interest. Indeed, because of numerous... (Review)
Review
Autistic subjects frequently display sensory anomalies. Those regarding nociception and its potential outcome, pain, are of crucial interest. Indeed, because of numerous comorbidities, autistic subjects are more often exposed to painful situation. Despite being often considered as less sensitive, experimental studies evaluating this point are failing to reach consensus. Using animal model can help reduce variability and bring, regarding autism, an overview of potential alterations of the nociceptive system at the cellular and molecular level.
Topics: Animals; Autistic Disorder; Disease Models, Animal; Humans; Nociception; Pain; Pain Measurement; Pain Threshold
PubMed: 33591257
DOI: 10.1051/medsci/2020280