Advances are hampered by the difficulties inherent in studying neuronal processes in humans, cellular changes in nociceptors induced by invasive methods, the inability to record directly from the tiny structures where transduction of noxious stimuli occurs, and the uncertainty in model systems that an animal’s behavior is due to its perception of pain ( 15, 17). Significant insights into the cellular and molecular basis of cutaneous nociception have been realized from studies on conscious humans and surrogate animal models ( 15, 16), although we are far from understanding the cell biology of pain perception. Since maladaptive changes in normal physiological mechanisms underlie a variety of pathologies leading to chronic pain, a thorough understanding of nociception is required to identify the interventions most likely to provide therapeutic benefit.Īnatomy and physiology of cutaneous nociception We further discuss innovations using genetic and pharmacological tools that begin to address how particular nociceptor populations contribute to the perception of specific pain qualities. Since recent reviews have described in detail the molecules involved in detecting noxious stimuli ( 10– 13) and contributing to protective mechanisms mediating enhanced pain at the site of injury ( 14), we take an integrative approach that highlights recently discovered cellular transduction/conduction mechanisms in the context of different nociceptor fiber types identified in vivo and ex vivo. We provide an overview of how noxious stimuli are detected, encoded, and conveyed to the CNS. Discussion of the similarities and differences among cutaneous, visceral, muscle, and joint nociception can be found elsewhere ( 7– 9). Here, we review the nociceptive aspect of pain perception, focusing on nociceptors innervating the skin and subserving exteroception of noxious stimuli. As opposed to the relatively more objective nature of other senses, pain is highly individual and subjective ( 4, 5) and the translation of nociception into pain perception can be curtailed by stress or exacerbated by anticipation ( 6). The intensity of these global reactions underscores the importance of avoiding damaging situations for survival and maintaining homeostasis. Pain is described as having different qualities and temporal features depending on the modality and locality of the stimulus, respectively: first pain is described as lancinating, stabbing, or pricking second pain is more pervasive and includes burning, throbbing, cramping, and aching and recruits sustained affective components with descriptors such as “sickening” ( 3). This is in contrast to the high sensitivity of visual, auditory, olfactory, taste, and somatosensory organs to their adequate stimuli. These high threshold physical and noxious chemical stimuli are detected by specialized peripheral sensory neurons (nociceptors). Normally, nociception (see Glossary, Sidebar 1) and the perception of pain are evoked only at pressures and temperatures extreme enough to potentially injure tissues and by toxic molecules and inflammatory mediators. The benefit of these unpleasant sensations, however, is underscored by extreme cases: patients lacking the ability to perceive pain due to hereditary neuropathies often maintain unrealized infections, self mutilate, and have curtailed life spans ( 2). Mechano-thermal: Mechano-thermal nociceptors respond to both mechanical and thermal stimuli.Pain, as a submodality of somatic sensation, has been defined as a “complex constellation of unpleasant sensory, emotional and cognitive experiences provoked by real or perceived tissue damage and manifested by certain autonomic, psychological, and behavioral reactions” ( 1).Polymodal: Polymodal nociceptors respond to mechanical, thermal, and chemical stimuli.Most visceral nociceptors (those located on organs inside the body) are silent nociceptors. Silent: Silent nociceptors must be first activated or "awakened" by tissue inflammation before responding to a mechanical, thermal, or chemical stimulus.Chemical: Chemical nociceptors respond to chemicals released from tissue damage (for example, prostaglandins and substance P) or from external chemicals (for example, topical capsaicin).The muscles or tendons are stretched beyond their ability, stimulating nociceptors and sending pain signals to the brain. Mechanical: Mechanical nociceptors respond to intense stretch or strain, like when you pull a hamstring or strain your Achilles tendon.For instance, if you touch a hot stove, nociceptors signaling pain are activated right away, sometimes before you're even aware of what you've done. Thermal: Thermal nociceptors respond to extreme hot or cold temperatures.
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