Impacts that threaten or indeed compromise the integrity of tissues trigger the development of a defence response, which through the activity of the nociceptive system includes pain. If the noxious impact does not induce tissue damage, the pain, called “nociceptive” pain, ceases within seconds after the impact is withdrawn. In contrast, if tissue damage does occur, a pain experience that usually persists until the injury is resolved and includes two major pathological sensory experiences, hypersensitivity to heat stimuli (i.e. heat hyperalgesia) and/or hypersensitivity to mechanical stimuli (i.e. mechanical allodynia) develop.
The cellular and molecular mechanisms underlying the development of nociceptive pain are fairly well understood. Our understanding of the development of pain associated with tissue injury has also significantly improved in the last decades. Hence, two fundamental mechanisms, interactions between the nervous and immune systems both within and without the central nervous system and sensitization that is a use-dependent increase in the sensitivity and activity of neurons involved in nociceptive processing have been identified being pivotal for the development of tissue injury-associated pain. However, important details of the cellular and molecular mechanisms, which account for the development of the pathological sensory experiences and those experiences becoming persistent, still await elucidation.
In this Research Topic we will gather original research as well as review papers presenting and discussing the latest advances in our understanding of the physiology of the nociceptive system. We encourage authors to submit papers describing their novel discoveries and views on novel cellular and molecular mechanisms of neuron-immune interactions and sensitization following somatic and visceral tissue injuries, as well as injuries of peripheral nerves, of various origins including pathological processes, medical interventions and accidents.
Impacts that threaten or indeed compromise the integrity of tissues trigger the development of a defence response, which through the activity of the nociceptive system includes pain. If the noxious impact does not induce tissue damage, the pain, called “nociceptive” pain, ceases within seconds after the impact is withdrawn. In contrast, if tissue damage does occur, a pain experience that usually persists until the injury is resolved and includes two major pathological sensory experiences, hypersensitivity to heat stimuli (i.e. heat hyperalgesia) and/or hypersensitivity to mechanical stimuli (i.e. mechanical allodynia) develop.
The cellular and molecular mechanisms underlying the development of nociceptive pain are fairly well understood. Our understanding of the development of pain associated with tissue injury has also significantly improved in the last decades. Hence, two fundamental mechanisms, interactions between the nervous and immune systems both within and without the central nervous system and sensitization that is a use-dependent increase in the sensitivity and activity of neurons involved in nociceptive processing have been identified being pivotal for the development of tissue injury-associated pain. However, important details of the cellular and molecular mechanisms, which account for the development of the pathological sensory experiences and those experiences becoming persistent, still await elucidation.
In this Research Topic we will gather original research as well as review papers presenting and discussing the latest advances in our understanding of the physiology of the nociceptive system. We encourage authors to submit papers describing their novel discoveries and views on novel cellular and molecular mechanisms of neuron-immune interactions and sensitization following somatic and visceral tissue injuries, as well as injuries of peripheral nerves, of various origins including pathological processes, medical interventions and accidents.
