The extinction of electrophysiological activity in the acute phase of cerebral hypoperfusion appears to be consistent with the opinion on ischemic thresholds: as the CBF gradually decreases, the oligemia shifts to ischemia, which is defined by the affected electrical function of the neurons.Neurons can be rescued in the upper range of ischemia, before massive K efflux occurs. The retina of VO rats has been flashstimulated, and visual evoked potentials recorded from the occipital cortex.The latency of the positive peaks was increased, while the amplitude was diminished days after VO induction. Another set of experiments has furnished more reliable data on the electrophysiological activity of the hippocampus. In these Targetmol’s Tazobactam acid learning paradigms, substantial evidence has been compiled in support of learning being impaired by VO. Thus, it has been firmly established that experimental cerebral hypoperfusion compromises spatial learning in rats.The total distance covered by the VO animals in the open field did not differ from that for the controls, indicating that the locomotor activity remained intact. The latter explanation seems to be the more accurate since the VO rats did not appear less anxious as compared with their respective sham controls in the elevated plus maze. Finally, the nonspatial memory in an object recognition test evaluated with a discrimination index was also impaired in VO rats and days following occlusion of the vessels. These data suggest that not only the visuospatial learning, but also fear conditioning and nonspatial memory are impaired by VO.In view of the finding that the cerebral perfusion rate changes over time in the VO model, it is of interest to establish whether the learning impairment develops exclusively due to the sudden drop in blood flow in the acute phase or worsens in the chronic phase of VO.Hence, the learning performance has been compared at several time points in the VO model.Tests on rats in the arm radial maze week after VO induction revealed no difference in working and reference memory scores between the VO and control animals, but months later the VO animals committed significantly more errors. The VO rats performed significantly worse than the controls weeks after the onset of VO, and the learning impairment was considerably augmented as time passed.The escape latency at weeks was significantly longer than that at weeks after VO initiation, which was reflected in the time spent in the platform quadrant in the retention trial. In a nonspatial learning paradigm, the object recognition test, VO rats performed as well as the controls after days of VO, but a delayed learning impairment had developed by days, which was further enhanced after days. These results convincingly support the concept that the chronic phase of VO plays a major role in the gradual deterioration of the learning ability, though damage occurring in the acute phase of CBF reduction cannot be categorically excluded.A final point to consider here is whether the learning ability can return to the normal level on the cessation of cerebral hypoperfusion.First of all, the hippocampus is the area that displays the most characteristic neuropathological damage in AD.