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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on June 23, 2004; DOI: 10.1124/jpet.104.070300

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Received for publication April 20, 2004.
Revised June 22, 2004.
Accepted for publication June 23, 2004.

The Role of 5-HT3 Receptors in the Vagal Afferent Activation-Induced Inhibition of C1 Spinal Neurons Projected from Tooth-Pulp in the Rat

Takeshi Tanimoto 1*, Mamoru Takeda 1, Toshimi Nishikawa 1, Shigeji Matsumoto 1

1 Nippon Dental University, School of Dentistry at Tokyo

* Address correspondence to: E-mail: ttt1224{at}tokyo.ndu.ac.jp

Abstract

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-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 (40 nA) or the GABAA 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, involves 5-HT3 receptor activation, possibly originating in the descending serotonergic inhibitory system, and post synaptic modulation of inhibitory GABAergic neurons.


Key words: 5-HT3 receptor, C1 spinal neuron, descending pain inhibition, iontophoresis, tooth-pulp, vagal afferent


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