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Departments of Pharmacology and Physiology, University of California School of Medicine, San Francisco, California 94143, U.S.A.

1. Experiments on the frog olfactory bulb have been performed in vitro in order to determine whether primary afferent transmission is modified by presynaptic inhibition.

2. Stimulation of the olfactory nerve resulted in a prolonged depolarization of the olfactory nerve as recorded across a sucrose gap. Unstimulated olfactory nerve fibres adjacent to the stimulated fibres were also depolarized.

3. An excitability increase of the olfactory nerve terminals was found that lasted the entire duration of the olfactory nerve depolarization, indicating that the terminals themselves were depolarized. Both the olfactory nerve depolarization and the excitability increase were blocked by cobalt and manganese ions.

4. Low concentrations of glutamate were found to produce a substantial depolarization of the olfactory nerve. Although gamma-aminobutyric acid (GABA) also elicited a depolarization of the olfactory nerve, picrotoxin, a GABA antagonist, did not reduce the stimulus-evoked olfactory nerve depolarization.

5. Recording with potassium-sensitive electrodes in the olfactory nerve terminal region demonstrated an increase in extracellular potassium with the same rise time and duration as the olfactory nerve depolarization. Cobalt and manganese blocked the potassium increase and the olfactory nerve depolarization without affecting the presynaptic action potential.

6. The focally recorded extracellular current resulting from orthodromic synaptic excitation of the secondary olfactory relay neurones was blocked at short intervals by paired stimulation and decreased for the duration of the olfactory nerve depolarization. This suggests a decreased release of transmitter from the olfactory nerve terminals.

7. The possible role of potassium and/or a neurotransmitter in generating the olfactory nerve depolarization and inhibition is discussed.

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