TY - JOUR
T1 - Ketamine, not fentanyl, suppresses pain-related magnetic fields associated with trigeminally innervated area following CO2 laser stimulation
AU - Matsuura, Nobuyuki
AU - Shibukawa, Yoshiyuki
AU - Kato, Motoichiro
AU - Ichinohe, Tatsuya
AU - Suzuki, Takashi
AU - Kaneko, Yuzuru
N1 - Funding Information:
This work was supported in part by grants (HRC3A07 and HRC6A01 to TI, HRC6A03 to YS, and HRC6A08 to MN) for the High-Tech Research Center Project from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan. YS is a recipient of a grant-in-aid (nos. 18592050 and 20592187) for Scientific Research from the MEXT of Japan and a Grant from the Dean of Tokyo Dental College. The author would like to greatly thank Prof. Tatsuya Ishikawa for his valuable comments on this manuscript, and Associate Prof. Jeremy Williams, Tokyo Dental College, for his editing of the English.
PY - 2008/10
Y1 - 2008/10
N2 - A variety of pharmacological agents are clinically used to treat pain-related diseases, including in the orofacial region. The effects of analgesics upon cerebral sites responsible for pain perception have yet to be determined. The aim of the present study was to examine the effects of ketamine, an N-methyl-d-aspartate (NMDA) antagonist, and fentanyl, a narcotic analgetic, on pain-related somatosensory-evoked magnetic fields (pain-SEFs) induced by CO2 laser stimulation of the trigeminally innervated area. Two peaks with latencies of approximately 120 and 200 ms were observed in pain-SEFs after CO2 laser stimulation. Peaks with approximately 120 ms latency were detected in the bilateral secondary somatosensory cortices. Amplitude of pain-SEFs after CO2 laser stimulation increased in an intensity-dependent manner. Ketamine suppressed amplitude and prolonged latency of pain-SEFs, whilst fentanyl did not. This suggests that ketamine inhibits NMDA receptor-mediated neurotransmission in a pain input pathway to the cerebral cortex, thereby exerting an analgesic effect. Fentanyl, which acts via opioid receptors, is believed to act differently to ketamine in the pain input process.
AB - A variety of pharmacological agents are clinically used to treat pain-related diseases, including in the orofacial region. The effects of analgesics upon cerebral sites responsible for pain perception have yet to be determined. The aim of the present study was to examine the effects of ketamine, an N-methyl-d-aspartate (NMDA) antagonist, and fentanyl, a narcotic analgetic, on pain-related somatosensory-evoked magnetic fields (pain-SEFs) induced by CO2 laser stimulation of the trigeminally innervated area. Two peaks with latencies of approximately 120 and 200 ms were observed in pain-SEFs after CO2 laser stimulation. Peaks with approximately 120 ms latency were detected in the bilateral secondary somatosensory cortices. Amplitude of pain-SEFs after CO2 laser stimulation increased in an intensity-dependent manner. Ketamine suppressed amplitude and prolonged latency of pain-SEFs, whilst fentanyl did not. This suggests that ketamine inhibits NMDA receptor-mediated neurotransmission in a pain input pathway to the cerebral cortex, thereby exerting an analgesic effect. Fentanyl, which acts via opioid receptors, is believed to act differently to ketamine in the pain input process.
KW - CO laser
KW - Fentanyl
KW - Ketamine
KW - Magnetoencephalography
KW - Secondary somatosensory area
KW - Somatosensory-evoked magnetic field
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U2 - 10.1016/j.neures.2008.06.006
DO - 10.1016/j.neures.2008.06.006
M3 - Article
C2 - 18655812
AN - SCOPUS:50449099125
SN - 0168-0102
VL - 62
SP - 105
EP - 111
JO - Neuroscience Research
JF - Neuroscience Research
IS - 2
ER -