We studied the effects of training on DNA synthesis intensity in mouse brain. Brain cells where DNA synthesis-associated processes took place under the infl uence of training were detected by immunohistochemical labeling of DNA molecules with synthetic thymine analogue 5-bromo-2'-deoxyuridine. The number of 5-bromo-2'-deoxyuridine-positive cell increased in various structures of the brain under the infl uence of training. The key feature of long-term memory is its persistence over the protracted period. The hypothesis of DNA-dependent mechanisms of memory maintenance was put forward in 1970s, since DNA is the only permanent information carrier in eukaryotic cell, which lifetime corresponds to cell lifetime [2,3]. Key Words: DNA synthesis; 5-bromo-2'-deoxyuridine; long-term memory; dentate gyrusAutoradiographic method of [methyl-3H]-thymidine detection in brain cells was employed to obtain results concerning the presence of permanent DNA synthesis in the brain, that can be intensifi ed during learning. This hypothesis was confi rmed in later studies [1] conducted using immunohistochemical labeling of cell DNA containing nucleoside analogue molecule (e.g., 5-bromo-2'-deoxyuridine, BrdU). BrdU is a synthetic analogue of thymine and can be incorporated into DNA instead of thymine during the synthesis [9].

No abstract

No abstract

Possible mechanisms of recovery of the memory impaired during consolidation process were investigated. In mice, amnesia was induced by intraperitoneal cycloheximide (100 mg/kg) administration 20 min before exposure to tone signal combined with footshock (2 sec, 0.5 mA). Reminder by the footshock (2 sec, 0.5 mA) 24 h after the learning procedure resulted in recovery of impaired memory in amnestic animals up to the level of control animals. Analysis of c-Fos expression in response to reminder indicated increased number of c-Fos-positive cells in prelimbic cortex in the animals with unaffected memory in comparison with corresponding parameter in amnestic animals. These findings are indicative of impairment in prelimbic cortex activity in experimental amnesia as well as for reminder ability to recover the memory impaired in that way.