Changes in PKCγ lmmunoreactivity in Mouse Hippocampus Induced by Spatial Discrimination Learning

In the present study, we examined changes in immunoreactivity (ir) for the γ-isoform of protein kinase C (PKCγ) in mouse hippocampus in relation to spatial memory processes employing the monoclonal antibody 36G9 raised against purified PKCγ. Learning and memory were assessed by performance in a free-choice spatial pattern paradigm in a hole board in which the animals learned the pattern of 4 baited holes out of 16 holes. Adult male house mice were used, divided in four groups. Three control groups were formed: group N, naive (blank controls); group H, habituated (animals were for 5 consecutive days introduced to the hole board with all holes baited); and group PT, pseudotrained (animals were for 13 consecutive days introduced to the hole board with all holes baited). The T (trained) group was for 5 consecutive days introduced to the hole board with all holes baited (similar to the H and PT groups) followed by 6 successive days with only four holes baited in a fixed pattern. Behaviorally, following the first 5 d, the PT group crossed the hole board randomly, whereas the T group gradually learned to orientate in the hole board. The mice were killed 24 hr after the last performance. A shift in 36G9-ir appeared from the cell somata to the dendrites of hippocampal principal neurons when comparing the H and PT group, respectively. In contrast, the T group showed strong PKCγ-ir in both cell somata and dendrites, which clearly exceeded that of the H and PT mice. In this way, 36G9-ir reveals the physiologically activated neurons involved in hole board learning. The present results, showing changes in PKCγ-ir and redistribution of hippocampal PKCγ induced by hole board learning, are consistent with the observation that PKC is involved in spatial memory processes.