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Nociceptor plasticity: A closer look
Author(s) -
Pace Maria Caterina,
Passavanti Maria Beatrice,
De Nardis Lorenzo,
Bosco Fabio,
Sansone Pasquale,
Pota Vincenzo,
Barbarisi Manlio,
Palagiano Antonio,
Iannotti Fabio Arturo,
Panza Elisabetta,
Aurilio Caterina
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25993
Subject(s) - nociceptor , neuroscience , neuroplasticity , sensitization , stimulation , stimulus (psychology) , nervous system , medicine , hyperalgesia , nociception , psychology , receptor , cognitive psychology
Nociceptors are receptors specifically involved in detecting a tissue damage and transducing it in an electrical signal. Nociceptor activation provoked by any kind of acute lesion is related to the release of several mediators of inflammation, within the framework of a process defined as “peripheral sensitization.” This results in an exaggerated response to the painful stimulus, clinically defined as “primary hyperalgesia.” The concept of “neuroplasticity” may explain the adaptive mechanisms carried out by the Nervous System in relation to a “harmful” damage; also, neuroplasticity mechanisms are also fundamental for rehabilitative intervention protocols. Here we review several studies that addressed the role of different receptors and ionic channels discovered on nociceptor surface and their role in pain perception. The changes in expression, distribution, and functioning of receptors and ionic channels are thought to be a part of the neuroplasticity property, through which the Nervous System constantly adapts to external stimuli. Moreover, some of the reviewed mediators are also been associated to “central sensitization,” a process that results in pain chronicization when the painful stimulation is particularly prolonged or intense, and lastly leads to the memorization of the uncomfortable painful perception.