Functional type I vanilloid receptor expression by substantia gelatinosa neurons of trigeminal subnucleus caudalis in mice.
The aim of this study was to investigate the existence of functional TRPV1 receptor by substantia gelatinosa (SG) neurons of the trigeminal subnucleus caudalis (Vc), which is implicated in the processing of nociceptive information from orofacial regions. The direct membrane effects of a TRPV1 receptor agonist, capsaicin, were examined by gramicidin-perforated patch clamp recording using a trigeminal brainstem slice preparation containing Vc from immature mice. Capsaicin (1-2 microM) induced a membrane depolarization in 58 out of 71 SG neurons tested (82%). Capsaicin-induced depolarization was maintained in 20 out of 32 (63%) SG neurons in the presence of amino acid and voltage-dependent sodium channel blockers (10 microM CNQX, 20 microM AP-5, 0.5 microM TTX, 50 microM picrotoxin and 2 microM strychnine). In addition, capsaicin-induced depolarization was maintained in the presence of L-732,138 (1 microM), an NK1 receptor antagonist, in 14 out of 17 neurons (82%) tested. The capsaicin-induced depolarizing effects were blocked by a TRPV1 receptor antagonist, capsazepine (10 microM). These results indicate that a sub-population of SG neurons in the Vc express functional TRPV1 receptors, and that capsaicin can directly activate the TRPV1 receptor on the postsynaptic membrane of SG neurons.
Department of Oral Physiology, School of Dentistry, Chonbuk National University, Jeonju, Republic of Korea.
Seong Kyu
SK
Han
Seon Ah
SA
Park
Jae Gyu
JG
Jeon
Kee Wan
KW
Chang
Dong Kuk
DK
Ahn
Seok Bae
SB
Oh
Soo Joung
SJ
Park
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology*; D002211:Capsaicin / Q000031:analogs & derivatives / Q000494:pharmacology; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D003292:Convulsants / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D064729:Neurokinin-1 Receptor Antagonists; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010852:Picrotoxin / Q000494:pharmacology; D018689:Sensory System Agents / Q000494:pharmacology; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013331:Strychnine / Q000494:pharmacology; D013376:Substantia Gelatinosa / Q000187:drug effects / Q000378:metabolism*; D050916:TRPV Cation Channels / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D014364:Tryptophan / Q000031:analogs & derivatives / Q000494:pharmacology
D015763:2-Amino-5-phosphonovalerate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D002211:Capsaicin; D000697:Central Nervous System Stimulants; D003292:Convulsants; D018691:Excitatory Amino Acid Antagonists; D064729:Neurokinin-1 Receptor Antagonists; D010852:Picrotoxin; D018689:Sensory System Agents; D026941:Sodium Channel Blockers; D013331:Strychnine; D050916:TRPV Cation Channels; D013779:Tetrodotoxin; D014364:Tryptophan; C493921:TRPV1 protein, mouse; C086089:3,5-bis(trifluoromethyl)benzyl N-acetyltryptophan; C071423:capsazepine