Dopaminergic modulation at the olfactory nerve synapse

Dopamine can change the membrane potential, regulate cyclic nucleotides, an d modulate transmitter release in central neurons. In the olfactory bulb (O B), the dopamine synthetic enzyme, tyrosine hydroxylase, is largely confine d to neurons in the glomerular layer. After demonstrating dopamine D2 recep tors in the glomerular and olfactory nerve (ON) layers, Nickell et al. [W.T . Nickell, A.B. Norman, L.M. Wyatt, M.T. Shipley, Olfactory bulb DA recepto rs may be located on terminals of the olfactory nerve, NeuroReport, 2 (1991 ) 9-12.] proposed that these receptors may reduce transmitter release due t o their localization to ON presynaptic boutons. We have previously demonstr ated that olfactory, receptor neurons use glutamate to excite OB neurons th rough activation of glutamate receptors subtypes, NMDA and AMPA/kainate [D. A. Berkowicz, P.Q. Trombley, G.M. Shepherd, Evidence for glutamate as the o lfactory receptor cell neurotransmitter. J. Neurophysiol., 71 (1994) 2557-2 561]. Here, we used a hemisected turtle OB preparation and patch-clamp reco rding techniques to assess dopamine modulation of the ON/OB neuron synapse. We found that dopamine (10-300 mu M) reversibly decreased the excitatory p ostsynaptic response to ON stimulation. This effect could be overcome by re cruiting additional nerve fibers by increasing the intensity of ON stimulat ion. Quinpirole (10 mu M), a D2 agonist, mimicked the effects of dopamine. Conversely, sulpiride (300 mu M), a D2 antagonist, prevented the inhibitory effects of dopamine on synaptic transmission. `Whereas dopamine appeared t o equally affect the NMDA and AMPA/kainate receptor-mediated components of the synaptically evoked response, it had no diner effect on membrane curren ts evoked by exogenous glutamate, kainate or NMDA applied to cultured OB ne urons. Our data, therefore, support the notion that dopamine modulates syna ptic transmission between olfactory receptor neurons and OB neurons via a p resynaptic mechanism involving D2 receptor activation. Our abstract (Berkow icz et al. (1994) Neuroscience Abs. 20:328) is the first report of these re sults. (C) 2000 Elsevier Science B.V. All rights reserved.