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Activation of Metabotropic Glutamate Receptors Inhibits High-Voltage-Gated Calcium Channel Currents of Chicken Nucleus Magnocellularis Neurons

Virginia Merrill Bloedel Hearing Research Center and Department of Otolaryngology-Head and Neck Surgery, University of Washington, Seattle, Washington

Submitted 30 June 2004; accepted in final form 13 September 2004

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 (HVA I_Ba²⁺). The N-type channel blocker (-conotoxin-GVIA) inhibited more than half of the total HVA I_Ba²⁺, whereas 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 (100 µM), 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 nonspecific mGluR agonist, (1S,3R)-1-aminocyclopentane-1,3-dicarbosylic acid (1S,3R-ACPD), mimicked the inhibitory effect of glutamate on HVA I_Ba²⁺. Group I–III mGluR agonists showed inhibition of the HVA current with the most potent being the group III agonist L(+)-2-amino-4-phosphonobutyric acid. 1S,3R-ACPD (200 µM) 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.

This article has been cited by other articles:

				Y. Lu Endogenous mGluR Activity Suppresses GABAergic Transmission in Avian Cochlear Nucleus Magnocellularis Neurons J Neurophysiol, February 1, 2007; 97(2): 1018 - 1029. [Abstract] [Full Text] [PDF]