Electrophysiological effects on taste receptor cells were investigated using whole-cell patch clamp technique. The taste buds were isolated from the fungiform papilla of rat tongue. In the bath solution containingCa
2+(10 mM), the inward Ca
2+current(I
Ca(L))was observed. Holding potential was -60 mV. The threshold potential was -40 mV, and the peak amplitude at 0 mV was-69.8 ±11.0 pA (n=5). The I
Ca(L)was rapidly inactivated. The capacitance was 3-5 pF. The I
Ca(L)was inhibited by 78.4±4.9%(n=4, P<0.001) by MnCl
2(2 mM), and by 67.3±3.6%(n=5, P<0.001) by C
oCl
2(3 mM), but NiCl
2(40μM), an antagonist of T-type Ca
2+channel, did not significantly affect I
Ca (L) (by 6.7±, 2.0%, n=4). On the other hand, nifedipine (2μM) blocked the I
Ca(L)current almost completely (by 97.2±3.2%, n=4, P<0.001), and garapamil (D-600)(1μM) inhibited it by 55.1±3.0%(n=4, P<0.001). Application of Na-saccharin (20 mM) increased I
Ca(L)by 19.6±3.1%(n=5, P<0.01). The effect was reversible. These results indicate that the slow in ward current is I
Ca(L)current, and the I
Ca(L)is enhanced by Na-saccharin, suggesting that the enhancement of I
Ca(L)would electrically transmit the signals to sensory neurons and modulate physiological functions.
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