2006
DOI: 10.1016/j.brainres.2006.06.115
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Central sensitization induced in thalamic nociceptive neurons by tooth pulp stimulation is dependent on the functional integrity of trigeminal brainstem subnucleus caudalis but not subnucleus oralis

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Cited by 26 publications
(11 citation statements)
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“…In these studies we and others have shown that acute or chronic dental pulpitis or trigeminal nerve damage induced functional neuroplasticity reflecting an increased glutamate-mediated excitability (“ central sensitization ”) of nociceptive neurons within the brainstem trigeminal subnucleus caudalis that process orofacial nociceptive afferent inputs (for review see Sessle, 2011), and increased neuronal activity in the trigeminal motor nucleus (Sunakawa et al, 1999; Mostafeezur et al, 2014). Central sensitization following dental manipulations has also been documented in the rodent somatosensory thalamus (Park et al, 2006; Zhang S. et al, 2006; Kaneko et al, 2011). Central sensitization contributes to increased pain sensitivity (allodynia and hyperalgesia) and extraterritorial spread or referral of pain hypersensitivity that characterize many acute and chronic pain conditions (for review, see Sessle, 2011).…”
Section: Discussionmentioning
confidence: 94%
“…In these studies we and others have shown that acute or chronic dental pulpitis or trigeminal nerve damage induced functional neuroplasticity reflecting an increased glutamate-mediated excitability (“ central sensitization ”) of nociceptive neurons within the brainstem trigeminal subnucleus caudalis that process orofacial nociceptive afferent inputs (for review see Sessle, 2011), and increased neuronal activity in the trigeminal motor nucleus (Sunakawa et al, 1999; Mostafeezur et al, 2014). Central sensitization following dental manipulations has also been documented in the rodent somatosensory thalamus (Park et al, 2006; Zhang S. et al, 2006; Kaneko et al, 2011). Central sensitization contributes to increased pain sensitivity (allodynia and hyperalgesia) and extraterritorial spread or referral of pain hypersensitivity that characterize many acute and chronic pain conditions (for review, see Sessle, 2011).…”
Section: Discussionmentioning
confidence: 94%
“…Data about the exact location of these regions varies, depending on the sensory modality studied. For example, representations of periodontal mechanosensitive neurons occurred in the most ventral part of the intermediate portion of the VPM (Tabata et al, 2002 ), while oral nociceptive sensations were relayed mostly by the rostral half of the VPM (Park et al, 2006 ; Zhang et al, 2006 ). So the intermediate segment of the VPM differs from the other two VPM segments by relaying sensory pathways of different modalities.…”
Section: Discussionmentioning
confidence: 99%
“…Several research studies have been conducted to examine neuronal sensitization at higher levels along the interoceptive pathway, in particular: (a) spinothalamic tract (Simone et al, 1991 ; Willis, 2002 ); (b) brainstem: rostroventral medulla (Porreca et al, 2002 ); and trigeminal nuclei (Hu et al, 1992 )—especially trigeminal subnucleus caudalis (Cao et al, 2013 ; Wang et al, 2013 ); (c) diencephalum, thalamic neurons (Park et al, 2006 ; Kaneko et al, 2011 ), in the thalamic-anterior cingulate pathway (Shyu and Vogt, 2009 ), hypothalamic neurons (Peng et al, 2011 ; Daviu et al, 2014 ; Donnerer and Liebmann, 2015 ), in the hypothalamic-pituitary-adrenal axis (Daviu et al, 2014 ); (d) telencephalic level, including the anterior cingulate cortex (Wei and Zhuo, 2001 ), amygdala (Neugebauer and Li, 2003 ), and insular cortex (Qiu et al, 2014 ).…”
Section: Central Elaboration: the Sensitization Statementioning
confidence: 99%