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NEUROPHARMACOLOGY

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

Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, Tokyo, Japan

To test the hypothesis that vagal afferent (VA) stimulation modulates the first cervical dorsal horn (C₁) neuron activity, which is projected by tooth pulp (TP) afferent inputs through the activation of a local GABAergic mechanism via 5-hydroxytryptamine₃ (5-HT₃) receptors, we used the technique of microiontophoretic application of drugs. In pentobarbital-anesthetized rats, we recorded C₁ spinal neuron activity responding to TP stimulation. The TP stimulation-evoked C₁ spinal neuron excitation was inhibited by VA stimulation, and this inhibition was significantly attenuated by iontophoretic application of the 5-HT₃ 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 C₁ 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 C₁ 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 C₁ spinal neuron excitation. These results suggest that VA stimulation-induced suppression of C₁ spinal neuron activity, responding to TP stimulation, involve 5-HT₃ receptor activation, possibly originating in the descending serotonergic inhibitory system, and postsynaptic modulation of inhibitory GABAergic neurons.

Address correspondence to: Dr. Takeshi Tanimoto, Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo 102-8159, Japan. E-mail: ttt1224{at}tokyo.ndu.ac.jp

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