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“It is generally believed that the hippocampus is not required for simple discrimination learning. However, a small number of studies have shown that hippocampus damage impairs retention of a previously learned visual discrimination task. selleck screening library We propose that, although simple discrimination learning may proceed in the absence of the hippocampus, it plays an important role in this type of learning when it is intact. In order to test the role of the hippocampus in simple discrimination

learning, we performed a series of experiments utilizing a two-choice picture discrimination task. Our experiments confirm that rats readily learn simple two-choice picture discriminations after hippocampus damage. However, if such discriminations are first learned while the hippocampus is intact, subsequent hippocampus damage causes severe retrograde amnesia for the discriminations. Furthermore, retrograde amnesia for simple picture discriminations was equally severe when the interval between training and damage was 1 d or 60 d; remote picture memories are not spared. Similarly, the rule or schema underlying

a recently or remotely acquired picture discrimination learning set was lost after hippocampus damage. The severity of retrograde amnesia for simple check details picture discriminations is negatively correlated with the volume of spared hippocampus tissue. Thus, the hippocampus plays an essential role in long-term memories supporting simple picture discriminations.”
“In pathological states, calpains in neurons Mephenoxalone easily degrade spectrin and yield specific fragments called spectrin breakdown products characterized by their high stabilities both in vitro and in vivo. In the present study, we investigated chronological changes in all-spectrin immunoreactivity and protein levels using the antibody to detect both the naive form and breakdown

products of alpha II-spectrin in the gerbil main olfactory bulb (MOB) after 5 min of transient forebrain ischemia. In sham-operated gerbils, weak all-spectrin immunoreactivity was detected in principal (mitral and tufted) cells. Ten days after ischemia/reperfusion, alpha II-spectrin immunoreactivity was increased in principal cells. Fifteen days after ischemia/reperfusion, all-spectrin immunoreactivity in the somata and processes of principal cells was markedly increased. Thereafter, alpha II-spectrin immunoreactivity in the principal cells in the ischemic MOB was decreased with time. In Western blot study, spectrin protein bands were detected in naive form (230 kDa) and its breakdown product (150 kDa). The breakdown product in MOB homogenates were significantly increased 15 days after ischemia/reperfusion and thereafter decreased with time after ischemia/reperfusion. Our results indicate that alpha II-spectrin breakdown product in the gerbil MOB is changed in principal cells after ischemic insult.