Glutamate metabotropic receptor inhibition of voltage-gated calcium currents in visceral sensory neurons

M. Hay, D. L. Kunze

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)421-430
Number of pages10
JournalJournal of neurophysiology
Issue number1
StatePublished - 1994

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology


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