Nociception: Difference between revisions
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'''Nociception''' is the neural processes of encoding and processing noxious stimuli.<ref name="1.">Loeser, J. D.; Treede, R. D. (2008). "The Kyoto protocol of IASP Basic Pain Terminology". Pain 137 (3): 473–7. doi:10.1016/j.pain.2008.04.025. PMID 18583048</ref> In another ways, it refers to signal arriving in the central nervous system resulting from activation of specialized sensor receptors celled nociceptors (peripheral nerves endings) by adequate noxious stimuli. Nociception is physiological process that protects tissue against damage. This process is also known as nocioception or nociperception, but is not synonym of pain sense. Term ‘‘nociception” and ‘‘pain” should not be confused, because each can occur without the other.<ref name="1." /> Pain arising from activation of nociceptors by actual or potentially harmful stimuli is called nociceptive pain. It is important to note that excitation of nociceptors does not always evoke pain.<br> | '''Nociception''' is the neural processes of encoding and processing noxious stimuli.<ref name="1.">Loeser, J. D.; Treede, R. D. (2008). "The Kyoto protocol of IASP Basic Pain Terminology". Pain 137 (3): 473–7. doi:10.1016/j.pain.2008.04.025. PMID 18583048</ref> In another ways, it refers to signal arriving in the central nervous system resulting from activation of specialized sensor receptors celled nociceptors (peripheral nerves endings) by adequate noxious stimuli. Nociception is physiological process that protects tissue against damage. This process is also known as nocioception or nociperception, but is not synonym of pain sense. Term ‘‘nociception” and ‘‘pain” should not be confused, because each can occur without the other.<ref name="1." /> Pain arising from activation of nociceptors by actual or potentially harmful stimuli is called nociceptive pain. It is important to note that excitation of nociceptors does not always evoke pain.<br> | ||
== Nociceptive pain can be classified by tissue origin:<br> == | == Nociceptive pain can be classified by tissue origin:<br> == | ||
*Superficial somatic (e.g. skin) | *Superficial somatic (e.g. skin) | ||
*Deep somatic (e.g. ligaments, tendons, bones and muscles) | *Deep somatic (e.g. ligaments, tendons, bones and muscles) | ||
*Visceral (e.g. internal organs)<br> | *Visceral (e.g. internal organs)<br> | ||
== Noxious stimuli is divided by type:<br> == | == Noxious stimuli is divided by type:<br> == | ||
*Thermal | *Thermal | ||
*Mechanical | *Mechanical | ||
*Chemical<br> | *Chemical<br> | ||
== Nociceptors<br> == | == Nociceptors<br> == | ||
'''Nociceptors''' (noci- is derived from the Latin for “hurt”) are sensory receptors capable of transducing and encoding noxious stimuli.<ref name="1." /> The initial reception of noxious input occurs in functionally specialized free nerve endings of the skin, muscles, joints, viscera, dura, blood vessels and in fascia. The cell bodies of nociceptors are located in the dorsal root ganglia (DRG) for the periphery and the trigeminal ganglion for the face. However, not every nociceptor responds to each type of the noxious stimuli. The apparent lack of a response to a noxious stimulus may result because of different receptors located on membrane of end terminal (free nerve ending) or the stimulus intensity is insufficient.<ref name="3.">Basbaum, AI.; Jessell, T. The Perception of Pain. In: Kandel, ER.; Schwartz, J.; Jessell, T., editors.Principles of Neuroscience. New York: Appleton and Lange; 2000. p. 472-491</ref> Usually, the stimulation threshold of a nociceptor is below tissue-damaging intensity. Nociceptors have heterogeneous properties, responding to multiple stimulus modalities (polymodal). However, application of noxious stimulus of one modality may alter the response properties of the nociceptor to other modalities. Also application of particular stimulus for given length of time may induce long-term changes in the response properties of the nociceptor.<ref name="4.">Meyer RA, Ringkamp M, Campbell JN, Raja SN. Peripheral mechanisms of cutaneous nociception. In: McMahon SB, Koltzenburg M, editors. Wall and Melzack’s Textbook of Pain. London: Elsevier; 2006. pp. 3–34.</ref> Injury and inflammation decrease the threshold and increase the magnitude of the response for a given stimulus, a phenomenon known as peripheral sensitization. Of particular interest are the heat responsive, but mechanically insensitive unmyelinated afferents that develop mechanical sensitivity only in the setting of injury | '''Nociceptors''' (noci- is derived from the Latin for “hurt”) are sensory receptors capable of transducing and encoding noxious stimuli.<ref name="1." /> The initial reception of noxious input occurs in functionally specialized free nerve endings of the skin, muscles, joints, viscera, dura, blood vessels and in fascia. The cell bodies of nociceptors are located in the dorsal root ganglia (DRG) for the periphery and the trigeminal ganglion for the face. However, not every nociceptor responds to each type of the noxious stimuli. The apparent lack of a response to a noxious stimulus may result because of different receptors located on membrane of end terminal (free nerve ending) or the stimulus intensity is insufficient.<ref name="3.">Basbaum, AI.; Jessell, T. The Perception of Pain. In: Kandel, ER.; Schwartz, J.; Jessell, T., editors.Principles of Neuroscience. New York: Appleton and Lange; 2000. p. 472-491</ref> Usually, the stimulation threshold of a nociceptor is below tissue-damaging intensity. Nociceptors have heterogeneous properties, responding to multiple stimulus modalities (polymodal). However, application of noxious stimulus of one modality may alter the response properties of the nociceptor to other modalities. Also application of particular stimulus for given length of time may induce long-term changes in the response properties of the nociceptor.<ref name="4.">Meyer RA, Ringkamp M, Campbell JN, Raja SN. Peripheral mechanisms of cutaneous nociception. In: McMahon SB, Koltzenburg M, editors. Wall and Melzack’s Textbook of Pain. London: Elsevier; 2006. pp. 3–34.</ref> Injury and inflammation decrease the threshold and increase the magnitude of the response for a given stimulus, a phenomenon known as peripheral sensitization. Of particular interest are the heat responsive, but mechanically insensitive unmyelinated afferents that develop mechanical sensitivity only in the setting of injury. | ||
<br>'''Nociceptors''' have the morphological appearance of free nerve endings. The term “free nerve ending” indicates that in the light microscope no (corpuscular) receptive structure can be recognized. At present, there are no clear ultrastructural differences between non-nociceptive free nerve endings (e.g., sensitive mechanoreceptors and thermoreceptors) and nociceptive ones. Functionally, different free nerve endings are assumed to possess different sets of receptor molecules in their axonal membrane. Receptor molecules that are particularly important for the function of muscle nociceptors are acid-sensing ion channels (ASICs) that open at a low tissue pH, P2X3 receptors that are activated by binding adenosine triphosphate (ATP), and the transient receptor potential receptor subtype 1 (TRPV1) that is sensitive to high temperatures, capsaicin chemical and low pH. The neuropeptide substance P has been reported to be present predominantly in nociceptive afferent fibres. While there are numerous neurotransmitters within nervous system, the three most common participating in nociceptive transmission are peptides, purines, and excitatory amino acids (EAA). The EAA, particularly glutamate, produce the initial excitatory response on the postsynaptic, second-order, neuron, followed by the release of peptides, including substance P, causing a more prolonged depolarization and sustained nociceptive transmission. | |||
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'''Nociceptors''' are present in many body tissue but has not been found in articular cartridge, synovial membranes, visceral pleura, lung parenhyma, pericardium, brain and spinal cord tissue. | '''Nociceptors''' are present in many body tissue but has not been found in articular cartridge, synovial membranes, visceral pleura, lung parenhyma, pericardium, brain and spinal cord tissue. | ||
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Several classes of nociceptors have been described. Some nociceptors respond to noxious cold, noxious heat and high threshold mechanical stimuli as well as a variety of chemical mediators. Nociceptors, although polymodal, can be further divided into two main classes on the basis of response to mechanical stimuli, leading to distinction between mechanically sensitive afferents (MSA) and mechanically insensitive afferents (MIA) defined as afferents that have very high mechanical thresholds or are unresponsive to mechanical stimuli.<br> | Several classes of nociceptors have been described. Some nociceptors respond to noxious cold, noxious heat and high threshold mechanical stimuli as well as a variety of chemical mediators. Nociceptors, although polymodal, can be further divided into two main classes on the basis of response to mechanical stimuli, leading to distinction between mechanically sensitive afferents (MSA) and mechanically insensitive afferents (MIA) defined as afferents that have very high mechanical thresholds or are unresponsive to mechanical stimuli.<br> | ||
<br> | == <br> == | ||
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== References == | == References == | ||
<br> | <br> | ||
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References will automatically be added here, see [[Adding References|adding references tutorial]]. | References will automatically be added here, see [[Adding References|adding references tutorial]]. | ||
<references /> | <references /> | ||
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[[Category:Pain]] [[Category:PPA_Project]] | [[Category:Pain]] [[Category:PPA_Project]] | ||
Revision as of 23:41, 16 October 2014
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- Define and describe the physiological process and purpose of nociception
- Describe different nocipetors and explain the need for adequate stimuli to activate nociceptors in different tissue types (i.e. skin, muscle, joint, viscera)
Original Editor - Przemyslaw Jaczun
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Nociception[edit | edit source]
Content ...
Definition/Descrition
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Nociception is the neural processes of encoding and processing noxious stimuli.[1] In another ways, it refers to signal arriving in the central nervous system resulting from activation of specialized sensor receptors celled nociceptors (peripheral nerves endings) by adequate noxious stimuli. Nociception is physiological process that protects tissue against damage. This process is also known as nocioception or nociperception, but is not synonym of pain sense. Term ‘‘nociception” and ‘‘pain” should not be confused, because each can occur without the other.[1] Pain arising from activation of nociceptors by actual or potentially harmful stimuli is called nociceptive pain. It is important to note that excitation of nociceptors does not always evoke pain.
Nociceptive pain can be classified by tissue origin:
[edit | edit source]
- Superficial somatic (e.g. skin)
- Deep somatic (e.g. ligaments, tendons, bones and muscles)
- Visceral (e.g. internal organs)
Noxious stimuli is divided by type:
[edit | edit source]
- Thermal
- Mechanical
- Chemical
Nociceptors
[edit | edit source]
Nociceptors (noci- is derived from the Latin for “hurt”) are sensory receptors capable of transducing and encoding noxious stimuli.[1] The initial reception of noxious input occurs in functionally specialized free nerve endings of the skin, muscles, joints, viscera, dura, blood vessels and in fascia. The cell bodies of nociceptors are located in the dorsal root ganglia (DRG) for the periphery and the trigeminal ganglion for the face. However, not every nociceptor responds to each type of the noxious stimuli. The apparent lack of a response to a noxious stimulus may result because of different receptors located on membrane of end terminal (free nerve ending) or the stimulus intensity is insufficient.[2] Usually, the stimulation threshold of a nociceptor is below tissue-damaging intensity. Nociceptors have heterogeneous properties, responding to multiple stimulus modalities (polymodal). However, application of noxious stimulus of one modality may alter the response properties of the nociceptor to other modalities. Also application of particular stimulus for given length of time may induce long-term changes in the response properties of the nociceptor.[3] Injury and inflammation decrease the threshold and increase the magnitude of the response for a given stimulus, a phenomenon known as peripheral sensitization. Of particular interest are the heat responsive, but mechanically insensitive unmyelinated afferents that develop mechanical sensitivity only in the setting of injury.
Nociceptors have the morphological appearance of free nerve endings. The term “free nerve ending” indicates that in the light microscope no (corpuscular) receptive structure can be recognized. At present, there are no clear ultrastructural differences between non-nociceptive free nerve endings (e.g., sensitive mechanoreceptors and thermoreceptors) and nociceptive ones. Functionally, different free nerve endings are assumed to possess different sets of receptor molecules in their axonal membrane. Receptor molecules that are particularly important for the function of muscle nociceptors are acid-sensing ion channels (ASICs) that open at a low tissue pH, P2X3 receptors that are activated by binding adenosine triphosphate (ATP), and the transient receptor potential receptor subtype 1 (TRPV1) that is sensitive to high temperatures, capsaicin chemical and low pH. The neuropeptide substance P has been reported to be present predominantly in nociceptive afferent fibres. While there are numerous neurotransmitters within nervous system, the three most common participating in nociceptive transmission are peptides, purines, and excitatory amino acids (EAA). The EAA, particularly glutamate, produce the initial excitatory response on the postsynaptic, second-order, neuron, followed by the release of peptides, including substance P, causing a more prolonged depolarization and sustained nociceptive transmission.
Nociceptors are present in many body tissue but has not been found in articular cartridge, synovial membranes, visceral pleura, lung parenhyma, pericardium, brain and spinal cord tissue.
Several classes of nociceptors have been described. Some nociceptors respond to noxious cold, noxious heat and high threshold mechanical stimuli as well as a variety of chemical mediators. Nociceptors, although polymodal, can be further divided into two main classes on the basis of response to mechanical stimuli, leading to distinction between mechanically sensitive afferents (MSA) and mechanically insensitive afferents (MIA) defined as afferents that have very high mechanical thresholds or are unresponsive to mechanical stimuli.
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[edit | edit source]
[edit | edit source]
References[edit | edit source]
References will automatically be added here, see adding references tutorial.
- ↑ 1.0 1.1 1.2 Loeser, J. D.; Treede, R. D. (2008). "The Kyoto protocol of IASP Basic Pain Terminology". Pain 137 (3): 473–7. doi:10.1016/j.pain.2008.04.025. PMID 18583048
- ↑ Basbaum, AI.; Jessell, T. The Perception of Pain. In: Kandel, ER.; Schwartz, J.; Jessell, T., editors.Principles of Neuroscience. New York: Appleton and Lange; 2000. p. 472-491
- ↑ Meyer RA, Ringkamp M, Campbell JN, Raja SN. Peripheral mechanisms of cutaneous nociception. In: McMahon SB, Koltzenburg M, editors. Wall and Melzack’s Textbook of Pain. London: Elsevier; 2006. pp. 3–34.
