Age-related increase in nitric oxide synthase activity in senescence accelerated mouse brain and the effect of long-term administration of superoxide radical scavenger

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition

“…In conclusion, there is growing literature linking the effects of age and age-related cognitive decline with changes in NO and NOS activity (Arnaiz et al 2004;Cha et al 1998;Chalimoniuk and Strosznajder 1998;de la Torre et al 2003;Dere et al 2002;Inada et al 1996Inada et al , 1997Kuo et al 1997;Law et al 2003;Liu et al 2004;Noda et al 1997;Reddy and Kulkarni 1998;Strolin Benedetti et al 1993;Yamada et al 1996). In the present study, downstream upregulation of the NO-cGMP pathway with the PDE5 inhibitor sildenafil citrate attenuated the complex maze impairment produced by NOS inhibition, a model of agerelated cognitive decline (Ingram et al 1994a(Ingram et al ,b, 1996Meyer et al 1998a).…”

Norepinephrine promotes long-term potentiation in the adult rat hippocampus in vitro

“…Although the biological targets of NO responsible for LTP inhibition in young animals have not yet been determined, one potential candidate is suppression of PI turnover through an increase in cyclic-GMP (Oliva and Garcia, 1995;Samochocki et al, 1996;Yu and Chuang, 1996). In this case, the increase in NO synthase activity in older animals (Inada et al, 1996) would be consistent with a decline in LTP generation. However, in slices from PND 120 rats LTP could not be produced in the presence of either 10 µM APV or 100 µM L-NMMA, suggesting that untimely NMDA receptor activation and NO release do not contribute to the decline in LTP generating ability in older animals.…”

Age-related changes in the brains of senescence-accelerated mice (SAM): Association with glial and endothelial reactions

“…Excessive oxidation of cortical synaptosomal protein was found in the brain in aged SAMP8 but not aged SAMR1 mice (Butterfield et al, 1997). The activity of NOS but not the content of nitric oxide (NO), a radical product of NOS, was increased with age in the cerebral cortex of SAMP8, suggesting reduced sensitivity of the NO reaction system during the aging process (Inada et al, 1996). These free radical-mediated alterations could be prevented by administering a radical scavenger.…”