抄録
The mice lacking alpha1B subunit of N-type voltage dependent calcium channels (VDCC) show manifest hypertension and lack of baroreflex (Ino et. al. PNAS USA, 2001). The caudal part of the nucleus tractus solitarii (NTS) is the primary integrative center of the cardiovascular control. To determine whether modulation of transmitter release in the NTS underlies these autonomic failures, non-NMDA receptor-mediated EPSCs (eEPSCs) evoked by the primary afferent stimulation were recorded in brainstem slices (3-5 wks). Adenosine (100 μM), which we have shown to suppress glutamate release in this synapse through activation of A1 receptors, decreased eEPSC amplitude to 73.3% of the control in the wild type (CaV2.2+/+; 7 of 8 cells tested) and to 72.5% in the heterozygotes (CaV2.2+/-; n=14/21). Adenosine was ineffective in the homozygotes (CaV2.2-/-; n=4). The effect of adenosine was occluded by ω-conotoxin GVIA (CgTX, 3 μM) in all of CaV2.2+/+ neurons and in 33% of CaV2.2+/- neurons, but not in 77% of neurons responding to adenosine in CaV2.2+/-. CgTX exerted no effect in CaV2.2-/-.These results suggest that the coupling between presynaptic G-protein-coupled receptors and N-type calcium channels underlying transmitter release is perturbed by the decrease in the channel protein expression. [Jpn J Physiol 54 Suppl:S160 (2004)]
