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  • 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.
    Author: Tanimoto T, Takeda M, Nishikawa T, Matsumoto S.
    Journal: J Pharmacol Exp Ther; 2004 Nov; 311(2):803-10. PubMed ID: 15215286.
    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.
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