Fig. 6.

LTP in double-mutant mice (cGKI−/− cGKII−/−) is normal and reduced in the presence of the NOS inhibitor NOArg.Top, Double-mutant mice were generated by mating heterozygous cGKI+/ånd cGKII+/− mice. WT and mutant alleles of the cGKI and cGKII genes were identified by specific PCR products as illustrated for four offsprings (lanes 2–5). The DNA sample used as template for PCRs in lane 5 was derived from a double-mutant homozygous animal (cGKI−/− cGKII−/−). Lane 1, One kilobase DNA ladder (Life Technologies, Gaithersburg, MD). Middle, Average potentiation of the fEPSP slope in response to theta burst stimulation in slices from WT (▪; n = 18) and double-mutant (○;n = 15) animals. The mean baseline slope (pretetanus control) was −0.34 ± 0.02 and −0.29 ± 0.03 mV/msec in slices from WT and double-mutant animals, respectively. Representative fEPSP recordings are shown in the insets. Calibration: 20 msec, 0.5 mV. Bottom, Average potentiation of the fEPSP slope in slices from double-mutant mice bathed in normal ACSF (control) (▪;n = 7 slices) and ACSF containing 100 μm NOArg (○; n = 7 slices). The mean baseline slope (pretetanus control) was −0.46 ± 0.12 and −0.37 ± 0.10 mV/msec in control and NOArg-treated slices, respectively. Representative fEPSP recordings are shown in theinset. Calibration: 20 msec, 0.5 mV.