抄録
Inhibitory synaptic transmission and its modulation in neurons of the area postrema (AP), one of autonomic nuclei in the medulla, were studied using whole-cell patch-electrodes applied to slices from newborn rats. When external saline containing 20 mM KCl was applied from a "Y tube" to AP neurons, which were whole-cell clamped at -10 mV, massive inhibitory postsynaptic currents (IPSCs) were induced. Most of the evoked IPSCs were blocked by bicuculline, indicating GABAergic identity, while the remaining minority of synaptic currents was sensitive to strychnine. When nicotine (5-100 μM) or capsaicin (0.1-1 μM) was applied to AP neurons, robust appearance of IPSCs with GABAergic identity was induced. After blocking action potential generation in the slice with tetrodotoxin (1 μM), nicotine or capsaicin could still induce GABAergic IPSCs. The nicotine-induced presynaptic facilitation was significantly inhibited by mecamylamine, and it was slightly inhibited by dihydro-β-erythroidine and negligibly inhibited by α-bungarotoxin. Interestingly, responses to capsaicin of the synaptic facilitation showed marked desensitization; even after five minutes of rigorous washout, the magnitude of synaptic facilitation by capsaicin was 10-30% of that evoked by the first application. It is concluded that nicotinic receptors, as well as capsaicin receptors (presumably TRPV1), are expressed at GABAergic presynaptic terminals in area postrema neurons and play a distinctive role in controlling excitability of these neurons for their proper function in the autonomic system. [J Physiol Sci. 2006;56 Suppl:S172]
