Abstract
Pheromonal memory formation is associated with an increase in the length of the postsynaptic densities, of the excitatory part of the reciprocal dendrodendritic synapses between mitral and granule cells in the accessory olfactory bulb (AOB). Behavioral experiments have implicated noradrenaline (NA) and α-receptors in the AOB in the formation of the pheromonal memory. We have demonstrated, in slice preparations of the AOB, that long-term theta frequency stimulation of the lateral olfactory tract (LOT) induces NMDA dependent LTP at the mitral-to-granule cell synapses and NA facilitates induction of LTP via α2-receptors. To clarify the cellular mechanisms of α2-adrenergic enhancement of LTP, we performed whole cell recordings from visually identified mitral and granule cells. NA and clonidine diminished voltage-gated calcium currents in mitral cells. Both drugs reduced the frequencies of spontaneous and miniature EPSCs without affecting their amplitudes and also reduced LOT-evoked EPSCs in granule cells. In contrast, clonidine had no effect on miniature IPSCs in mitral cells. In granule cells, NA and clonidine decreased plateau depolarization and increased number of action potential firing during theta frequency stimulation. These results indicate that NA inhibits mitral-to-granule cell synaptic transmission via presynaptic α2-receptors, thereby leading to a smaller depolarizing plateau and thus to increased firing probability in granule cells that may contribute to LTP induction during theta frequency stimulation. [Jpn J Physiol 54 Suppl:S161 (2004)]
