title: The role of 5-hydroxytryptamine3 receptors in the vagal afferent activation-induced inhibition of the first cervical dorsal horn spinal neurons projected from tooth pulp in the rat.
abstract: To test the hypothesis that vagal afferent (VA) stimulation modulates the first cervical dorsal horn (C(1)) neuron activity, which is projected by tooth pulp (TP) afferent inputs through the activation of a local GABAergic mechanism via 5-hydroxytryptamine(3) (5-HT(3)) receptors, we used the technique of microiontophoretic application of drugs. In pentobarbital-anesthetized rats, we recorded C(1) spinal neuron activity responding to TP stimulation. The TP stimulation-evoked C(1) spinal neuron excitation was inhibited by VA stimulation, and this inhibition was significantly attenuated by iontophoretic application of the 5-HT(3) receptor antagonist ICS 205-930 (3-tropanyl-indole-3-carboxylate hydrochloride [endo-8-methyl-8-azabicyclo [3.2.1] oct-3-ol indol-3-yl-carboxylate hydrochloride]) (40 nA) or the GABA(A) receptor antagonist bicuculline (40 nA). In another series of experiments, we determined that 60 nA iontophoretic application of glutamate produced a maximal increase in the C(1) spinal neuron activity at a minimal current. In 53 of 65 neurons (81.5%), VA conditioning stimulation (1.0 mA x 0.1 ms, 50 Hz for 30 s) caused a significant inhibition (35.1%) of the glutamate (60 nA) application-evoked C(1) spinal neuron excitation. Iontophoretic application of ICS 205-930 (40 nA) or bicuculline (40 nA) significantly attenuated the VA stimulation-induced inhibition of glutamate iontophoretic application (60 nA)-evoked C(1) spinal neuron excitation. These results suggest that VA stimulation-induced suppression of C(1) spinal neuron activity, responding to TP stimulation, involve 5-HT(3) receptor activation, possibly originating in the descending serotonergic inhibitory system, and postsynaptic modulation of inhibitory GABAergic neurons.
authors.affiliation: Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo 102-8159, Japan. ttt1224@tokyo.ndu.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tanimoto
authors.forename: Mamoru
authors.initials: M
authors.lastname: Takeda
authors.forename: Toshimi
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Shigeji
authors.initials: S
authors.lastname: Matsumoto
mesh_terms: D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001016:Aortic Bodies / Q000187:drug effects / Q000502:physiology*; D003782:Dental Pulp / Q000166:cytology*; D004347:Drug Interactions; D004558:Electric Stimulation; D018698:Glutamic Acid / Q000494:pharmacology; D007211:Indoles / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D020671:Posterior Horn Cells; D051381:Rats; D044406:Receptors, Serotonin, 5-HT3 / Q000502:physiology*; D058831:Serotonin 5-HT3 Receptor Antagonists; D012702:Serotonin Antagonists / Q000494:pharmacology; D013131:Spine / Q000166:cytology*; D000077526:Tropisetron
chemical_list: D007211:Indoles; D044406:Receptors, Serotonin, 5-HT3; D058831:Serotonin 5-HT3 Receptor Antagonists; D012702:Serotonin Antagonists; D018698:Glutamic Acid; D000077526:Tropisetron