抄録
Young rats show aversion to the odor which has been exposed with foot shock. We previously reported that the main olfactory bulb (OB) is a critical site for this olfactory learning. There is, however, little electrophysiological evidence on synaptic plasticity in the OB. Using brain slices, we found that 5 trains of tetanic stimulation of the lateral olfactory tract induced NMDA receptor-dependent long-term potentiation (LTP) of field potentials recorded in the granule cell layer of the OB. Although 3 tetani were subthreshold for LTP, application of noradrenaline (NA) paired with the tetani was capable of inducing LTP (NA-LTP). This NA-LTP was partially reduced by the NMDA receptor antagonist, AP5, and completely blocked by the L-type voltage-dependent calcium channel (VDCC) blocker, nifedipine. NA-LTP was blocked by the beta-adrenoceptor antagonist, timolol but not by the alpha-adrenoceptor antagonist, phentolamine. The NA effect on induction of LTP was mimicked by the beta-adrenoceptor agonist, isoproterenol. Moreover, our results showed that paired-pulse facilitation was significantly decreased by application of NA as well as isoproterenol in the presence of the GABAA receptor antagonist, bicuculline. These results indicate that (1) tetanic stimulation-induced LTP in the OB is dependent on NMDA receptors, (2) NA-LTP requires the activation of NMDA receptors and L-type VDCCs, (3) a presynaptic mechanism underlies the effect of NA on LTP, and (4) NA-LTP is induced via beta-adrenoceptors. Taken together with behavioral data, these results suggest a connection between NA-LTP in the OB and olfactory learning. [Jpn J Physiol 54 Suppl:S161 (2004)]
