Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are stimulated by glutamate, released from the auditory nerve, and GABA, released from both interneurons surrounding NM and from cells located in the superior olivary nucleus. In this study, the Ca 2ุ indicator dye Fura-2 was used to measure Ca 2ุ responses in NM stimulated by glutamate-and GABA-receptor agonists using a chicken brainstem slice preparation. Glutamatergically stimulated Ca 2ุ responses were evoked by kainic acid (KA), โฃ-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid (AMPA), and N-methyl-D-aspartate (NMDA). KA-and AMPA-stimulated changes in [Ca 2ุ ] i were also produced in NM neurons stimulated in the presence of nifedipine, an L-type Ca 2ุ channel blocker, suggesting that KA-and AMPA-stimulated changes in [Ca 2ุ ] i were carried by Ca 2ุ -permeable receptor channels. Significantly smaller changes in [Ca 2ุ ] i were produced by NMDA. When neurons were stimulated in an alkaline (pH 7.8) superfusate, NMDA responses were potentiated. KA-and AMPA-stimulated responses were not affected by pH. Several agents known to stimulate metabotropic receptors in other systems were tested on NM neurons bathed in a Ca 2ุ free-EGTA-buffered media, including L-cysteine sulfinic acid (L-CSA), transazetidine dicarboxylic acid (t-ADA), trans-aminocyclopentanedicarboxylic acid (t-ACPD), and homobromoibotenic acid (HBI). The only agent to reliably and dosedependently increase [Ca 2ุ ] i was HBI, an analog of ibotenate. GABA also stimulated increases in [Ca 2ุ ] i in NM neurons. GABA-stimulated responses were reduced by agents that block voltage-operated channels and by agents that inhibit Ca 2ุ release from intracellular stores. Whereas GABA-A receptor agonist produced increases in [Ca 2ุ ] i GABA-B and GABA-C receptor agonists had no effect. There appear to be several ways for [Ca 2ุ ] i to increase in NM neurons. Presumably, each route represents a means by which Ca 2ุ can alter cellular processes.