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Background: Despite the widespread clinical use of acupuncture in painful situations, the use of this treatment should be further clarified. Nociception is mediated by the activation of nociceptors, such as transient receptor potentials (TRPs). The family of TRPs includes TRPV1, TRPM8, and TRPA1, which can be stimulated by substances such as capsaicin, menthol, and methyl salicylate, respectively. Objectives: This study aimed to investigate the role of TRPs in antinociception via the administration of agonists of these receptors in the Zusanli acupoint (ST36) in models of inflammatory, acute, and neuropathic pain. Methods: Male Wistar rats were used for this experiment. All rats received a subcutaneous injection of TRP agonists (capsaicin, menthol, or methyl salicylate) in ST36; saline was injected as control. Nociception was evaluated using the electronic mechanical threshold test and tail-flick test before the administration of complete Freund's adjunct or chronic constriction injury of the sciatic nerve and after the administration of TRP agonists. Results: Nociception was found to be attenuated after treatment with TRP agonists. The administration of different doses (0.03, 0.3, and 3.0 µg/20 µL) of capsaicin, menthol, and methyl salicylate in the different pain models (neuropathic, inflammatory, and nociceptive) induced antinociception in most of the evaluated time points. Conclusion: Based on the findings, we suggest that the activation of TRPV1, TRPM8, and TRPA1 receptors results in the antinociceptive effect of the stimulation of the ST36 acupoint. Thus, TRP receptors may present a new therapeutic opportunity for the control of inflammatory and neuropathic pain.

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The ability of the nervous system to detect a wide range of noxious stimuli is crucial to avoid life-threatening injury and to trigger protective behavioral and physiological responses. Pain represents a complex phenomenon, including nociception associated with cognitive and emotional processing. Animal experimental models have been developed to understand the mechanisms involved in pain response, as well as to discover novel pharmacological and non-pharmacological anti-pain therapies. Due to the genetic tractability, similar physiology, low cost, and rich behavioral repertoire, the zebrafish (Danio rerio) is a powerful aquatic model for modeling pain responses. Here, we summarize the molecular machinery of zebrafish responses to painful stimuli, as well as emphasize how zebrafish-based pain models have been successfully used to understand specific molecular, physiological, and behavioral changes following different algogens and/or noxious stimuli (e.g., acetic acid, formalin, histamine, Complete Freund's Adjuvant, cinnamaldehyde, allyl isothiocyanate, and fin clipping). We also discuss recent advances in zebrafish-based studies and outline the potential advantages and limitations of the existing models to examine the mechanisms underlying pain responses from evolutionary and translational perspectives. Finally, we outline how zebrafish models can represent emergent tools to explore pain behaviors and pain-related mood disorders, as well as to facilitate analgesic therapy screening in translational pain research.

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Whole-body vibration (WBV), which is widely used as a type of exercise, involves the use of vibratory stimuli and it is used for rehabilitation and sports performance programmes. This study aimed to investigate the effect of WBV treatment in a chronic pain model after 10 WBV sessions. An animal model (chronic pain) was applied in 60 male Wistar rats (±180 g, 12 weeks old) and the animals were treated with low intensity exercise (treadmill), WBV (vibrating platform), and a combined treatment involving both. The controls on the platform were set to a frequency of 42 Hz with 2 mm peak-to-peak displacement, g ≈ 7, in a spiral mode. Before and after the vibration exposure, sensitivity was determined. Aß-fibers-mediated mechanical sensitivity thresholds (touch-pressure) were measured using a pressure meter. C-fibers-mediated thermal perception thresholds (hot pain) were measured with a hot plate. After each session, WBV influenced the discharge of skin touch-pressure receptors, reducing mechanical sensitivity in the WBV groups (P < 0.05). Comparing the conditions "before vs. after", thermal perception thresholds (hot pain) started to decrease significantly after the third WBV session (P < 0.05). WBV decreases mechanical hyperalgesia after all sessions and thermal sensitivity after the third session with the use of WBV.

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Introducción: El dolor proveniente de cabeza y cuello se vincula a la vía trigeminal, y participan tres neuronas: neurona de primer orden ubicada en ganglio trigeminal; neurona de segundo orden, en el subnúcleo caudal del nervio trigémino; y la neurona de tercer orden que parte de la zona medial del complejo ventrobasal de tálamo y termina en la corteza cerebral. Objetivo: Interpretar que el daño tisular, mediante impulsos nerviosos es transmitido por una cadena de neuronas hasta el encéfalo. Contenido: Las neuronas de primer orden, sus cuerpos neuronales se encuentran ubicados en el ganglio espinal del trigémino, en hueso temporal. En el subnúcleo caudal, se ubican las neuronas de segundo orden que reciben estímulos nociceptivos y de temperatura de la cara y la boca; sus axones se cruzan en la extensión de este subnúcleo, y ascienden contralateralmente, y establecen sinapsis en el tálamo con neuronas de tercer orden. En el encéfalo no hay un único "centro del dolor", las neuronas de tercer orden, terminan en diferentes áreas de la corteza cerebral que se reconocen como "matriz del dolor". Consideraciones finales: Tres conjuntos de neuronas conforman la vía nociceptiva trigeminal, la primera ubicada en el ganglio trigeminal fuera del sistema nervioso central y los otros dos conjuntos neuronales conforman núcleos dentro del mismo(AU)

Introduction: Pain from the head and neck is linked to the trigeminal pathway and three neurons participate: a first-order neuron located in the trigeminal ganglion, a second-order neuron from the subnucleus caudalis of the trigeminal nerve, and a third-order neuron which starts from the medial area of the ventrobasal thalamus complex and ends in the cerebral cortex. Objective: Describe the way in which a chain of neurons transmit tissue damage to the encephalon by means of nerve impulses. Content: In first-order neurons, their neuronal bodies are located in the trigeminal spinal ganglion, in temporal bone. In the subnucleus caudalis, second-order neurons are found which receive nociceptive and temperature stimuli from the face and mouth. Their axons cross over the extension of this subnucleus, ascend contralaterally and establish synapses with third-order neurons in the thalamus. In the encephalon there is not a single "pain center": third-order neurons end in different areas of the cerebral cortex recognized as the "pain matrix". Final considerations: Three sets of neurons make up the trigeminal nociceptive pathway. The first one is located in the trigeminal ganglion outside the central nervous system whereas the other two form nuclei within it(AU)

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Neuropathic and inflammatory pain results from cellular and molecular changes in dorsal root ganglion (DRG) neurons. The type-2 receptor for Angiotensin-II (AT2R) has been involved in this type of pain. However, the underlying mechanisms are poorly understood, including the role of the type-1 receptor for Angiotensin-II (AT1R). Here, we used a combination of immunohistochemistry and immunocytochemistry, RT-PCR and in vitro and in vivo pharmacological manipulation to examine how cutaneous inflammation affected the expression of AT1R and AT2R in subpopulations of rat DRG neurons and studied their impact on inflammation-induced neuritogenesis. We demonstrated that AT2R-neurons express C- or A-neuron markers, primarily IB4, trkA, and substance-P. AT1R expression was highest in small neurons and co-localized significantly with AT2R. In vitro, an inflammatory soup caused significant elevation of AT2R mRNA, whereas AT1R mRNA levels remained unchanged. In vivo, we found a unique pattern of change in the expression of AT1R and AT2R after cutaneous inflammation. AT2R increased in small neurons at 1 day and in medium size neurons at 4 days. Interestingly, cutaneous inflammation increased AT1R levels only in large neurons at 4 days. We found that in vitro and in vivo AT1R and AT2R acted co-operatively to regulate DRG neurite outgrowth. In vivo, AT2R inhibition impacted more on non-peptidergic C-neurons neuritogenesis, whereas AT1R blockade affected primarily peptidergic nerve terminals. Thus, cutaneous-induced inflammation regulated AT1R and AT2R expression and function in different DRG neuronal subpopulations at different times. These findings must be considered when targeting AT1R and AT2R to treat chronic inflammatory pain. Cover Image for this issue: doi: 10.1111/jnc.14737.

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Small nerve fibers that bind the isolectin B4 (IB4+ C-fibers) are a subpopulation of primary afferent neurons that are involved in nociceptive sensory transduction and do not express the neuropeptides substance P and calcitonin-gene related peptide (CGRP). Several studies have attempted to elucidate the functional role of IB4+-nociceptors in different models of pain. However, a functional characterization of the non-peptidergic nociceptors in mediating mechanical inflammatory hypersensitivity in mice is still lacking. To this end, in the present study, the neurotoxin IB4-Saporin (IB4-Sap) was employed to ablate non-peptidergic C-fibers. Firstly, we showed that intrathecal (i.t.) administration of IB4-Sap in mice depleted non-peptidergic C-fibers, since it decreased the expression of purinoceptor 3 (P2X3) and transient receptor potential cation channel subfamily V member 1 (TRPV1) in the dorsal root ganglia (DRGs) as well as IB4 labelling in the spinal cord. Non-peptidergic C-fibers depletion did not alter the mechanical nociceptive threshold, but it inhibited the mechanical inflammatory hypersensitivity induced by glial cell-derived neurotrophic factor (GDNF), but not nerve growth factor (NGF). Depletion of non-peptidergic C-fibers abrogated mechanical inflammatory hypersensitivity induced by carrageenan. Finally, it was found that the inflammatory mediators PGE2 and epinephrine produced a mechanical inflammatory hypersensitivity that was also blocked by depletion of non-peptidergic C-fibers. These data suggest that IB4-positive nociceptive nerve fibers are not involved in normal mechanical nociception but are sensitised by inflammatory stimuli and play a crucial role in mediating mechanical inflammatory hypersensitivity.

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Small nerve fibers that bind the isolectin B4 (IB4+ C-fibers) are a subpopulation of primary afferent neurons that are involved in nociceptive sensory transduction and do not express the neuropeptides substance P and calcitonin-gene related peptide (CGRP). Several studies have attempted to elucidate the functional role of IB4+-nociceptors in different models of pain. However, a functional characterization of the non-peptidergic nociceptors in mediating mechanical inflammatory hypersensitivity in mice is still lacking. To this end, in the present study, the neurotoxin IB4-Saporin (IB4-Sap) was employed to ablate non-peptidergic C-fibers. Firstly, we showed that intrathecal (i.t.) administration of IB4-Sap in mice depleted non-peptidergic C-fibers, since it decreased the expression of purinoceptor 3 (P2X3) and transient receptor potential cation channel subfamily V member 1 (TRPV1) in the dorsal root ganglia (DRGs) as well as IB4 labelling in the spinal cord. Non-peptidergic C-fibers depletion did not alter the mechanical nociceptive threshold, but it inhibited the mechanical inflammatory hypersensitivity induced by glial cell-derived neurotrophic factor (GDNF), but not nerve growth factor (NGF). Depletion of non-peptidergic C-fibers abrogated mechanical inflammatory hypersensitivity induced by carrageenan. Finally, it was found that the inflammatory mediators PGE2 and epinephrine produced a mechanical inflammatory hypersensitivity that was also blocked by depletion of non-peptidergic C-fibers. These data suggest that IB4-positive nociceptive nerve fibers are not involved in normal mechanical nociception but are sensitised by inflammatory stimuli and play a crucial role in mediating mechanical inflammatory hypersensitivity.

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Schwann cells are glial cells that support axonal development, maintenance, defense, and regeneration in the peripheral nervous system. There is limited knowledge regarding the organization, plasticity, and aging of Schwann cells within the dental pulp in adult permanent teeth. The present study sought to relate changes in the pattern of Schwann cell phenotypes between young and old adult teeth with neuronal, immune, and vascular components of the dental pulp. Schwann cells are shown to form a prominent glial network at the dentin-pulp interface, consisting of nonmyelinating and myelinating phenotypes, forming a multicellular neuroimmune interface in association with nerve fibers and dendritic cells. Schwann cell phenotypes are recognized by the expression of S100, glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), Sox10, GAP43, and p75NTR markers. In young adult teeth, a dense population of nonmyelinating Schwann cells projects processes in close association with sensory nerve terminals through the odontoblast layer, reaching the adjacent predentin/dentin domain. While GAP43 and p75NTR are highly expressed in nonmyelinating Schwann cells from young adult teeth, the presence of these markers declines significantly in old adult teeth. Myelinated axons, identified by MBP expression, are mainly present at the Raschkow plexus and within nerve bundles in the dental pulp, but their density is significantly reduced in old adult versus young adult teeth. These data reveal age-related changes within the glial network of the dental pulp, in association with a reduction of coronal dental pulp innervation in old adult versus young adult teeth. The prominence of Schwann cells as a cellular component at the dentin-pulp interface supports the notion that their association with sensory nerve terminals and immune system components forms part of an integrated multicellular barrier for defense against pathogens and dentin repair.

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INTRODUCTION: IL-33 signals through ST2 receptor and promotes inflammation by activating downstream pathways culminating in the production of pro-inflammatory mediators such as IL-1ß, TNF-α, and IL-6 in an NF-κB-dependent manner. In fact, compelling evidence has demonstrated the importance of IL-33/ST2 in both innate and adaptive immune responses in diseases presenting pain as an important clinical symptom. Areas covered: IL-33 is a pleiotropic cytokine with varied immune functions. Dysregulation of this pathway has been described as a key step in varied immune responses. Further, IL-33 contributes to peripheral and spinal cord nociceptor neuron sensitization in innate and adaptive inflammatory immune responses as well as in neuropathic and cancer pain. In this sense, targeting IL-33/ST2 signaling is a promising therapeutic approach. Expert opinion: The modulation of IL-33/ST2 signaling represents a possible approach in regulating immune functions. In addition to immune function, strategies targeting IL-33/ST2 signaling pathway display a favorable preclinical analgesic profile in both acute and chronic models of pain. Therefore, IL-33-targeting therapies represent a potential target for the development of novel analgesic drugs given that IL-33 activates, for instance, neutrophils, mast cells, macrophages, astrocytes, and microglia that are important cells in the induction and maintenance of chronic pain states.

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To evaluate corneal sensitivity by using the Cochet-Bonnet® esthesiometer in normal canine eyes at different time points following instillation of three different topical non-steroidal anti-inflammatory drugs (flurbiprofen sodium 0.03%, diclofenac sodium 0.1% and ketorolac tromethamine 0.5%) and benzalkonium chloride 0.01%. Six healthy mixed breed dogs from the same litter were used in two different stages. First, one drop of flurbiprofen sodium 0.03% and diclofenac sodium 0.1% in each eye; second, one drop of ketorolac tromethamine 0.5% and benzalkonium chloride 0.01% in each eye. Baseline esthesiometry was obtained before eye drop application and every 15 minutes thereafter until a total of 105 minutes of evaluation time. A one-week interval was allowed between the two treatment phases. Statistical analysis was used to compare means according to time of evaluation and drug used. Diclofenac sodium 0.1% decreased corneal sensitivity at 75 and 90 minutes (P > 0.015) with possible interference on neuronal nociceptive activity and analgesic effect while ketorolac tromethamine 0.5% did not show any variation for esthesiometry means along the evaluation. Flurbiprofen sodium 0.03% resulted in increased esthesiometry values 30 minutes after instillation (P > 0.013), increasing corneal sensitivity and possibly producing a greater irritant corneal effect over its analgesic properties. Benzalkonium chloride 0.01% significantly increased corneal sensitivity at 15 minutes of evaluation (P > 0.001), most likely resulting from its irritating effect. Esthesiometry did not allow a definite conclusion over the analgesic effect of the NSAIDs tested; however it was effective in detecting fluctuations in corneal sensitivity.

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Myosin-Va, widely distributed throughout the developing nervous system, is involved in the transport of vesicles and other intracellular components with its globular tail domain (GTD) implicated in cargo recognition/interaction. Inactivation of myosin-Va in dorsal root ganglia (DRG) neurons of chick embryos, in vitro, decreases the rate of filopodial extension. MYO5A mutant mice have severe neurological defects. We have found that the overexpression of GTD in DRG cultures reduces the number of neurons with long neurites (above fourfold cell body length) and increased the number of neurons with short or no neurites. However, if transfection occurred after the onset of neuritogenesis, this was not seen. In embryo, we characterized the expression pattern of myosin-Va during neuritogenesis of TrkA-positive cells at different stages of chick DRG development. Myosin-Va expression was detected starting from HH25. At this stage, it was present in cells both with and without neurites. The presence of myosin-Va in DRG neurites persisted throughout the last stage analysed (HH34). The data suggest that Myosin Va can participate in embryonic DRG neuritogenesis.

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Nervous System Mobilization is used to restore the biomechanics of the nervous system and adjacent structures, promoting the return to their duties. This study evaluated the pain threshold to pressure, to cold, and the cold pain intensity in healthy subjects that underwent intervention with neural mobilization. The sample consisted of 20 volunteers with a mean age of 19.5 ± 1.0 years. The participants were divided randomly into two groups: group 1 (G1) and group 2 (G2); the first group received intervention by means of neural mobilization, and the second, by means of conventional stretching exercises, on the first day; on the subsequent day the procedures were reversed for the groups. The volunteers were evaluated using the pain threshold to pressure and to cold, and the cold pain intensity, prior, immediately after, 20, and 40 minutes after the intervention. No significant differences were found between any assessments. In conclusion, the pain threshold to pressure and to cold, and the cold pain intensity had no significantly change after neural mobilization.

A mobilização do Sistema Nervoso é utilizada para restabelecer a biomecânica do sistema nervoso e também de estruturas adjacentes, o que promove o retorno às suas funções. O objetivo do presente estudo foi avaliar o limiar de dor à pressão e ao frio e a intensidade da dor ao frio, em indivíduos saudáveis submetidos à intervenção com mobilização neural. A amostra foi composta por 20 voluntárias, com idade média de 19,5 ± 1,0 anos. As participantes foram divididas, aleatoriamente, em dois grupos, o grupo 1 (G1) e o grupo 2 (G2), sendo que o primeiro recebeu intervenção por meio de mobilização neural e o segundo por meio de alongamentos convencionais, no primeiro dia, já no dia posterior os grupos inverteram os procedimentos. As voluntárias foram avaliadas por meio do limiar de dor à pressão e ao frio, além da intensidade de dor ao frio, antes das intervenções, imediatamente após, 20 e 40 minutos depois das intervenções. Os resultados demonstraram que em todas as avaliações não houve diferenças significantes. Desta maneira concluiu-se que o limiar de dor à pressão e ao frio e a intensidade de dor ao frio não foram alterados significativamente após mobilização neural.

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Background: Painful polyneuropathy may result from selective impairment of small diameter nerve fibers, while tactile and motor functions are preserved. In these patients clinical and electrophysiological assessment is usually unrevealing. We report three patients with a pure painful polyneuropathy. One of them had neurogenic pruritus additionally. Quantitative sensory analysis disclosed a slight warm hypoesthesia (3/3) and paradoxical hot sensation (2/3) in the feet. Intraneural recordings from the peroneal nerve demonstrated abnormal spontaneous activity in 8 of 17 nociceptive afferents. One of them displayed double firing reflecting impulse multiplication. These results support the notion that patients with pain or pruritus with a distal distribution similar to a polyneuropathy, could have small diameter afferent fiber damage, despite normal function of large diameter fibers.

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JUSTIFICATIVA E OBJETIVOS: As citocinas são substâncias necessárias para a resposta inflamatória, favorecendo a cicatrização apropriada da ferida. No entanto, a produção exagerada de citocinas pró-inflamatórias a partir da lesão pode manifestar-se sistemicamente com instabilidade hemodinâmica ou distúrbios metabólicos. O objetivo desta revisão foi descrever os efeitos das citocinas na dor. CONTEÚDO: Este artigo faz uma revisão dos efeitos das citocinas na dor. Em doenças que cursam com processo inflamatório agudo ou crônico, as citocinas podem ser reconhecidas por neurônios e utilizadas para desencadear diversas reações celulares que influenciam na atividade, proliferação e sobrevida da célula imunológica, bem como na produção e atividade de outras citocinas. As citocinas podem ser pró-inflamatórias e anti-inflamatórias. As pró-inflamatórias estão relacionadas com a fisiopatologia das síndromes dolorosas. Foram descritas as células que secretam as citocinas, as citocinas pró-inflamatórias (IL-1, IL-2, IL-6, IL-7 e FNT) e anti-inflamatórias (IL-4, IL-10, IL-13 e FTCβ), as funções de cada citocina e como ocorre a ação dessas substâncias no processamento da dor. CONCLUSÕES: As citocinas desempenham importante papel na dor, agindo através de diferentes mecanismos em vários locais das vias de transmissão da dor.

BACKGROUND AND OBJECTIVES: Cytokines are necessary for the inflammatory response, favoring proper wound healing. However, exaggerated proinflammatory cytokine production can manifest systemically as hemodynamic instability or metabolic derangements. The objective of this review was to describe the effects of cytokines in pain. CONTENTS: This article reviews the effects of cytokines in pain. In diseases with acute or chronic inflammation, cytokines can be recognized by neurons and used to trigger several cell reactions that influence the activity, proliferation, and survival of immune cells, as well as the production and activity of other cytokines. Cytokines can be proinflammatory and anti-inflammatory. Proinflammatory cytokines are related with the pathophysiology of pain syndromes. Cells that secrete proinflammatory (IL-1, IL-2, IL-6, IL-7, and TNF) and anti-inflammatory (IL-4, IL-10, IL-13, and TGFβ) cytokines, the functions of each cytokine, and the action of those compounds on pain processing, have been described. CONCLUSIONS: Cytokines have an important role in pain through different mechanisms in several sites of pain transmission pathways.

JUSTIFICATIVA Y OBJETIVOS: Las citocinas son sustancias necesarias para la respuesta inflamatoria, favoreciendo la cicatrización apropiada de la herida. Sin embargo, la producción exagerada de citocinas proinflamatorias a partir de la lesión puede manifestarse sistémicamente con la inestabilidad hemodinámica o disturbios metabólicos. El objetivo de esta revisión fue describir los efectos de las citocinas en el dolor. CONTENIDO: Este artículo intenta hacer una revisión de los efectos de las citocinas en el dolor. En enfermedades que se manifiestan con un proceso inflamatorio agudo o crónico, las citocinas pueden ser reconocidas por las neuronas y utilizadas para desencadenar diversas reacciones celulares que influyen en la actividad, proliferación y sobrevida de la célula inmunológica, como también en la producción y en la actividad de otras citocinas. Las citocinas pueden ser proinflamatorias y antiinflamatorias. Las proinflamatorias tienen una relación con la fisiopatología de los síndromes dolorosos. Ya se han descrito las células que segregan las citocinas, las citocinas proinflamatorias (IL-1, IL-2, IL-6, IL-7 y FNT) y antiinflamatorias (IL-4, IL-10, IL-13 y FTCβ), las funciones de cada citocina y también cómo ocurre la acción de esas sustancias en el proceso del dolor. CONCLUSIONES: Las citocinas desempeñan un rol muy importante en el dolor, actuando por medio de diferentes mecanismos en varios locales de las vías de transmisión del dolor.

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El dolor es un signo de enfermedad y un motivo frecuente de consulta; se clasifica en agudo o crónico, nociceptivo o neuropático, y según la velocidad de conducción en rápido o lento. Los estímulos causantes del dolor son detectados por receptores nociceptores; los cuales son identificados como fibras C y fibras Aδ. El proceso neural de la transmisiσn del dolor comprende: La transducciσn; es el proceso por el cual el estνmulo nociceptivo es convertido en seρal elιctrica en los nociceptores. La transmisiσn; es el proceso por el cual los estímulos nociceptivos son referidos al asta dorsal de la medula espinal, donde se liberan los neurotransmisores del dolor: Glutamato, sustancia P, péptido relacionado al gen de la calcitonina. Seguidamente el estímulo cruza al lado contralateral de la medula espinal y viaja en el haz espinotálamico hasta el tálamo y luego a la corteza cerebral. La modulación; es el proceso por el cual la señal nociceptiva en el asta dorsal de la medula puede ser inhibida y modificada para los centros superiores del dolor. Los opiodes endógenos y exógenos dan lugar a un bloqueo indirecto de los canales de calcio y apertura de los canales de potasio, con hiperpolarización celular e inhibición de la liberación de mediadores del dolor. La activación del sistema neural descendente da lugar a la liberación de b endorfinas, encefalinas, dinorfinas; que alivian el dolor.

Pain is a sign of illness and a common complain that bring patients to a health care facility. It is classified in acute or chronic pain, nociceptive or neuropathic, and according to conduction velocity, fast or slowly. C and Aδ- fibers respond to stimuli and produce the experience of pain, this defines them as nociceptors. Central pathways of pain include: nociceptors respond to stimuli and produce the experience of pain when they are electrically stimulated (Transduction); axons of nociceptors enter the spinal cord via the dorsal root, where Glutamate are Substance P are released, spinal neurons send their axons to the contralateral thalamus (Transmission); the perceived intensity of pain can be modulated by brain circuits (Modulation). Pain inhibition is achieved by calcium channel blockage and open potassium channel by endogenous and exogenous opioids, due hyperpolarization of the cell and inhibition of pain mediators. b endorphins, enkephalins and dinorphins are released due to activation of neural descending pathway causing pain relief.

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El dolor es probablemente el principal motivo de consulta en las urgencias estomatológicas y es precisamente el dolor de la pulpitis aguda el que comentamos en este trabajo. El dolor pulpar en sí mismo es similar al dolor que resulta por inflamación de los órganos viscerales y, por lo tanto, podrían ser inadecuados los intentos de explicarlos por comparación con los nociceptores de estructuras somáticas. Se propone analizar el comportamiento del dolor como consecuencia de una pulpitis aguda, con un nuevo enfoque, asimilándolo como el dolor proveniente de estructuras viscerales con manifestaciones dolorosas alejadas del sitio o zona dañada y en el propio diente en que el tejido ha sido injuriado y evoluciona rápidamente hacia la necrosis. Establecemos una analogía entre el dolor visceral como el generado de la pulpa y el del tipo somático profundo como el correspondiente a la afectación periapical por rápida evolución de la inflamación hacia la necrosis.

Pain is probably the chief complaint in dental emergencies and this paper deals precisely with the pain caused by acute pulpitis. The pulpar pain itself is similar to the one resulting from inflammation of the visceral organs and, therefore, the attempts to explain these pains by comparing them with the nociceptors of somatic structures may be inappropiate. It is our objective to analyze the behaviour of pain caused by acute pulpitis with a new approach, assimilating it as the pain from visceral structures with painful manifestations far from the damaged site or zone and it is the own tooth whose tissue has been affected and evolves rapidly to necrosis.We establish an analogy between the visceral pain as the one generated by the pulpa and that of deep somatic type as the corresponding to the periapical affection by the fast evolution of inflammation to necrosis.