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. 1998 Apr 1;18(7):2458–2466. doi: 10.1523/JNEUROSCI.18-07-02458.1998

Table 1.

Characteristics of inward current and [Ca2+]i rise evoked by 2 sec pulse of nicotine are not affected by drugs regulating protein kinase/phosphatase activity

Apeak(nA) Aend/Apeak(%) τ1 (msec) τ2(msec) [Ca2+]i decay (%)
Control (n = 10) 1.1  ± 0.2 8  ± 5 110  ± 20 660  ± 100 50  ± 9
PMA (n = 14) 1.2  ± 0.2 11  ± 2 90  ± 10 760  ± 140 44  ± 7
Staurosporine (n = 13) 0.9  ± 0.2 12  ± 1 140  ± 20 730  ± 100 40  ± 6
Forskolin (n = 4) 1.0  ± 0.2 12  ± 7 110  ± 30 620  ± 60 47  ± 9
Rp-cAMPS (n = 10) 0.8  ± 0.2 15  ± 4 80  ± 10 640  ± 120 54  ± 13
CC complex (n = 3) 1.1  ± 0.2 15  ± 5 100  ± 10 430  ± 80 58  ± 9
Calyculin A (n = 5) 1.3  ± 0.3 10  ± 7 90  ± 30 510  ± 50 47  ± 13

Note that Apeak,Aend/Apeak, τ1, and τ2 values (measured as indicated in Materials and Methods) as well as the rate of [Ca2+]i clearance (measured as percentage of its decay from peak value 30 sec after the conditioning pulse of nicotine) were independent of the above treatments.