Journal of Neuroscience, Vol 15, 214-222, Copyright © 1995 by Society for Neuroscience
Activation of a metabotropic glutamate receptor increases intracellular calcium concentrations in neurons of the avian cochlear nucleus
L Zirpel, EA Lachica and EW Rubel
Department of Physiology and Biophysics, School of Medicine, University of Washington, Seattle 98195.
Metabotropic glutamate receptors have been shown to stimulate
phosphatidylinositol metabolism, and subsequently liberate Ca2+ from
intracellular stores, in a variety of tissue and cell types. We previously
demonstrated that glutamate could stimulate phosphatidylinositol
metabolism, generating inositol-1,4,5- trisphosphate (IP3), in isolated
cochlear nucleus tissue from the chick. Using the calcium indicator dye
fura-2 and ratiometric fluorescent imaging, this study examined the ability
of glutamate and its analogs to liberate Ca2+ from intracellular stores of
neurons of the avian cochlear nucleus, and qualitatively characterized the
pharmacological profile of such an action. In normal, Ca(2+)-containing
medium, glutamate, kainate (KA), alpha-amino-3-hydroxy-5-methyl-
isoxazole-4-propionate (AMPA), NMDA, quisqualate (QUIS), and (+/-)-
aminocyclopentane-trans-dicarboxylate (ACPD) elicited increases in
intracellular calcium concentrations ([Ca2+]i). In the absence of external
Ca2+, glutamate, quisqualate, and ACPD evoked increases in [Ca2+]i. In
normal medium, the ionotropic glutamate receptor antagonist
6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the NMDA receptor
antagonist 2-amino-5-phosphonovalerate (APV) attenuated but did not abolish
the glutamate-evoked response and had no effect on the ACPD- evoked
response. The putative metabotropic glutamate receptor antagonist
2-amino-3-phosphonopropionate (AP3) was without effect on the glutamate-
and ACPD-evoked increases in [Ca2+]i in Ca(2+)-free medium. We conclude
that a metabotropic glutamate receptor (mGluR) is present on cochlear
nucleus neurons and is able to stimulate the phosphatidylinositol
metabolism--Ca2+ signal transduction cascade.
Previous Article | Next Article
