GLUTAMATE AS A PUTATIVE NEUROTRANSMITTER IN THE BUCCAL CENTRAL PATTERN GENERATOR OF HELISOMA-TRIVOLVIS

1. The effects Of L-glutamate superfusion over identified neurons within the buccal ganglia of Helisoma trivolvis were examined. Glutamate mirrored the effect of activity of subunit 2 (S2) of the tripartite feeding central pattern generator (CPG) on S2 postsynaptic neurons. Neurons that are excited by S2 are depolarized by glutamate, whereas neurons that are inhibited by S2 are hyperpolarized by glutamate. Glutamate also stimulated rhythmic S2 activity. 2. Different glutamate agonists could mimic specific components of the effects of glutamate on buccal neurons. Kainate produced depolarizations in neurons that receive S2 excitatory postsynaptic potentials (EPSPs) and activated rhythmic S2 activity. Quisqualate produced hyperpolarizations in neurons that receive S2 inhibitory postsynaptic potentials (IPSPs). 3. The non-N-methyl-D-aspartate glutamate receptor antagonist cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked the effects of S2 EPSPs and depolarizations produced by application of glutamate and kainate, but was ineffective in blocking S2 IPSPs or hyperpolarizations produced by application of glutamate and quisqualate. 4. These data support the hypothesis that glutamate is the transmitter of S2 of the feeding CPG in Helisoma, acting at CNQX-sensitive kainate-like receptors at excitatory synapses and CNQX-insensitive quisqualate-like receptors at inhibitory synapses.