The SBP, DBP and HR SpO2 EtCO2 were defined as major parameters to assess the hemodynamic response to nociceptive
stimuli during the following periods.
Enhancement of nociceptive
reactions by naloxone in mice and rats.
Medication overuse including opioids and triptans could induce central sensitization and impair the descending pain modulation from the RVM and limited the migraineur's ability to tolerate nociceptive
inputs. Therefore, the inability to tolerate the nociceptive
inputs would increase headache intensity, which could reasonably explain that the left RVM was positively related to the headache intensity in MOH patients.
Although studies have reported the outcomes of PSH, no study has explored potential contributing environmental nociceptive
factors in children who develop PSH.
input, in its course from the peripheral to the central nervous system (PNS and CNS, respectively) is constantly regulated by highly specialized modulatory systems.
To ensure that nociceptive
afferent information from the lower limb had reached the cortex prior to evoking MEPs (SEP latency to thermal pain stimulation = 532 [+ or -] 19 ms ), TMS was triggered with a 750 ms delay after the onset of the thermode plateau temperature.
Two types of VGSCs, Nav1.7 and Nav1.8, are known to contribute to pain transduction in nociceptive
neurons [21, 22].
pain is caused by a painful stimulus on special nerve endings called nociceptors.
Cannabinoid receptor 1 is the principal receptor of the central nervous system (CNS) and is densely expressed in several areas of the brain and supraspinal regions involved with nociceptive
 It is well known that inflammatory mediators are involved in nociceptive
processing at the perivascular nociceptors level.
It is known that the TCC is a key relay center for conveying sensory and visceral information, particularly nociceptive
, from the head and orofacial region, including cranial vasculature, to higher pain processing centers in the brain, along the trigeminohypothalamic tract to the hypothalamus and trigeminothalamic (or quintothalamic) tract to the thalamus.
In this paper, to elicit translocation, as well as bradykinin [12, 22], we use the peptide prokineticin 2 (PK2), involved in both inflammatory [23-25] and neuropathic  states, which activate PKC[epsilon] via Gq-coupled receptors in nociceptive
neurons [16, 23].