Using whole-cell patch clamp recordings, we pharmacologically characterized the voltage-gated Ca²⁺ channel (VGCC) currents of chicken nucleus magnocellularis (NM) neurons, using barium as the charge carrier. NM neurons possessed both low- and high-voltage activated Ca²⁺ channel currents (LVA and HVA I-Ba²⁺). The N-type channel blocker (-Conotoxin-GVIA) inhibited more than half of the total HVA I-Ba²⁺, while blockers of L- and P/Q-type channels each inhibited a small fraction of the current. Metabotropic glutamate receptor (mGluR)-mediated modulation of the HVA I-Ba²⁺ was examined by bath application of glutamate (100µM), which inhibited the HVA I-Ba²⁺ by an average of 16%. The inhibitory effect was dose-dependent and was partially blocked by -Conotoxin-GVIA, indicating that mGluRs modulate N- and other type HVA I-Ba²⁺ . The non-specific mGluR agonist, 1S,3R-ACPD, mimicked the inhibitory effect of glutamate on HVA I-Ba²⁺. Group I, II, III mGluR agonists showed inhibition of the HVA current, with the most potent being the group III agonist L-AP4. 1S,3R-ACPD (200µM) had no effect on K⁺ or Na⁺ currents. The firing properties of NM neurons were also not altered by 1S,3R-ACPD. We propose that the inhibition of VGCC currents by mGluRs limits depolarization-induced Ca²⁺ entry into these highly active NM neurons, and regulates their Ca²⁺ homeostasis.