| Synaptic interactions between mitral/tufted (MT) and granule cells (GCs) in the olfactory bulb are important in determining the spatiotemporal pattern of output neuron firing, which forms an odor representation passed to higher brain centers. These synapses are modulated by several neurotransmitters, often released by centrifugal projections. I describe the effect of dopamine, which is presumably released by tyrosine hydroxylase-positive interneurons within the frog olfactory bulb, on the functioning of the MT-GC synapse. MT neurons express D2-like receptors, and D2 activation reduces GC field EPSCs, whole-cell EPSCs, and MT inhibitory feedback. The frequency of spontaneous, spike-independent, GC mEPSCs is also decreased by D2Rs, suggesting that these effects are due to a presynaptic mechanism in MTs that may act downstream of Ca2+ influx. Measurement of spike-generated Ca2+ transients in MT lateral dendrites, which drive release of glutamate onto GCs, shows that although action potentials normally propagate through their entire extent, D2 activation can reduce invasion at distal locations. This effect is coincident with a negative shift in MT membrane potential, and can be relieved by depolarizing current injection. Conversely, it is mimicked by hyperpolarization, and hyperpolarization-mediated effects are occluded by application of 4-AP, which blocks an inactivating A-current expressed by MTs. When the OB is physiologically activated with odor stimuli, block of D2 receptors increases the power of both evoked local field potential oscillations and unstimulated activity, while D2 stimulation produces the opposite effect. Thus, dopamine appears to play a role in normal odor processing in the frog olfactory bulb, by reducing synaptic excitation of GCs and subsequent feedback inhibition of MTs via both action potential-dependent and -independent mechanisms, as well as by decreasing MT excitability. These properties could function to regulate the sensitivity of the olfactory bulb to sensory inputs. Control of action potential invasion of lateral dendrites by transient K + currents also represents a possible site for modulation of this synapse on a dynamic basis through other mechanisms. |
