1. Metabotropic glutamate receptors (mGluRs) have been suggested to modulate neurotransmission of glutamatergic pathways via autoreceptive action. Visceral sensory afferents and baroreceptor afferents in particular are thought to utilize L-glutamate (L-glu) as a primary neurotransmitter. The purpose of this study was to investigate whether visceral sensory afferents possess a mGluR and determine the effect of mGluR activation on voltage- gated calcium currents in these neurons. 2. Activation of mGluRs by the selective agonist trans-(±)-1-amino-1,3-cyclopentanedicarboxylic acid (t- ACPD) reversibly suppressed the voltage-gated calcium currents in visceral sensory afferents of the nodose ganglion. Concentrations of t-ACPD ranging from 50 to 1,000 μM consistently decreased the evoked calcium current with a maximum suppression of the peak current of 25-30%. This response was repeatable and reversible within a given cell. 3. Metabotropic GluR activation selectively decreased the high-threshold calcium current evoked from step potentials greater than -30 mV and had no effect on the low- threshold calcium current. The inhibitory effects of t-ACPD on the high- threshold channel was partially blocked by ω-conotoxin (ω-CTx-GVIA) suggesting that at least part of the effects of mGluR inhibition of the voltage-gated calcium current is because of a modulation of the ω-CTx-GVIA sensitive high-threshold current. 4. Finally, the inhibitory effects of quisqualate (quis) on the high-threshold calcium current were blocked by pretreatment of the neurons with pertussis toxin (PTX). These results suggest that visceral sensory afferents do possess a PTX-sensitive mGluR and activation of this receptor results in the inhibition of a ω-CTx-GVIA sensitive high-threshold calcium channel.
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