EVIDENCE FOR GLUTAMATE AS THE OLFACTORY RECEPTOR CELL NEUROTRANSMITTER

1. Synaptic transmission between olfactory receptor neurons and mitral /tufted cells was examined using a whole-cell recording technique in a hemisected preparation of the turtle olfactory bulb. To determine the olfactory receptor neuron transmitter, we isolated components of the synaptic response of mitral/tufted cells to olfactory nerve stimulatio n using postsynaptic receptor antagonists. 2. Low-intensity stimulatio n of the olfactory nerve evoked monosynaptic excitatory postsynaptic p otentials in mitral/tufted cells that consisted of a rapid and prolong ed depolarization with little contribution from other bulb neurons. Th e exogeneous application of glutamate mimicked the response of mitral/ tufted cells to olfactory nerve stimulation. 3. Olfactory nerve stimul ation evoked in mitral/tufted cells a two component response that was reversibly blocked by glutamate receptor antagonists. The first, a rap id depolarization of short duration, was sensitive to the non-N-methyl -D-aspartate (NMDA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dio ne(DNQX);the second, a depolarization of slower onset but longer durat ion, was sensitive to the NMDA receptor antagonist DL-2-amino-5-phosph onovaleric acid (AP5). When DNQX and AP5 were both present the postsyn aptic response was completely abolished. These results strongly suppor t the notion that glutamate is the neurotransmitter at the olfactory n erve to mitral/tufted cell synapse.