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. 2005 Jul 20;25(29):6887–6897. doi: 10.1523/JNEUROSCI.5291-04.2005

Figure 4.

Figure 4.

cGK is involved in the beneficial effect by cGMP analogs on Aβ-induced LTP impairment. A, When KT5823 (2 μm), a specific cGK inhibitor, is added to the slices treated with Aβ and 8-Br-cGMP, the beneficial effect of 8-Br-cGMP is blocked (F(1, 10) = 18.16; p < 0.05, compared with 8-Br-cGMP plus Aβ plus tetanus). B, Similar to 8-Br-cGMP, 10 min of perfusion with 8-pCPT-cGMP (2 μm) reverses the Aβ-induced LTP impairment (F(1, 16) = 87.81; p < 0.001, compared with Aβ plus tetanus) without affecting basal neurotransmission in nontetanized slices (F(1, 5) = 0.67; p > 0.1 in slices treated with 8-pCPT-cGMP compared with vehicle-treated slices). C, Perfusion with KT5720 paired with 8-Br-cGMP and Aβ does not block LTP (F(1, 11) = 0.44; p > 0.5, compared with 8-Br-cGMP plus Aβ plus tetanus). D, KT5720 paired with 8-Br-cGMP does not produce normal LTP (F(1, 7) = 7.22; p < 0.05, compared with vehicle plus tetanus). LTP is inhibited by KT5823 plus 8-Br-cGMP (F(1, 7) = 22.72; p < 0.01, compared with vehicle plus tetanus).