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Suppression of neurokinin‐1 receptor in trigeminal ganglia attenuates central sensitization following inflammation
Author(s) -
Takeda Mamoru,
Takahashi Masayuki,
Matsumoto Shigeji
Publication year - 2012
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2012.00404.x
Subject(s) - substance p , tachykinin receptor 1 , inflammation , nociception , medicine , stimulation , sensitization , antagonist , nk1 receptor antagonist , spinal trigeminal nucleus , receptor antagonist , neuroscience , receptor , anesthesia , neuropeptide , immunology , psychology
This study examined whether local application of a neurokinin‐1 (NK1) receptor antagonist into the trigeminal ganglia (TRGs) modulates hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) wide‐dynamic range (WDR) neuron activity innervating both the temporomandibular joint (TMJ) region and facial skin following TMJ inflammation. Extracellular single unit recording combined with multibarrel electrodes was used. TMJ inflammation was induced by the injection of complete Freund's adjuvant (CFA). WDR neurons responding to electrical stimuli of the TMJ region and facial skin were recorded from the SpVc in anesthetized rats. The spontaneous and mechanical stimulation‐induced discharge frequencies of WDR neurons were significantly larger in inflamed rats than in control rats. The spontaneous WDR activities were current‐dependently decreased by local iontophoretic application of an NK1 receptor antagonist into the TRGs after 1 and 2 days of inflammation. The firing frequency of WDR neurons and threshold evoked by mechanical stimulation of facial skin returned to control levels by application of the NK1 receptor antagonist into TRGs after 1 day, but not 2 days, of inflammation. These results suggest that in the early stages of inflammation suppression of the NK1 receptor mechanism in TRGs may prevent central sensitization of SpVc nociceptive neurons.