Learning-Induced Suboptimal Compensation for PKCι/λ Function in Mutant Mice.

has been proposed to be crucial in the early expression of long-term potentiation (LTP). Here, we further investigate the potential role of duanyu1531ι/λ in learning and memory by generating duanyu1531ι/λ conditional knockout mice specifically lacking duanyu1531ι/λ in the hippocampal CA1 pyramidal cells. Surprisingly, duanyu1531ι/λ cKO mice show normal hippocampal LTP and memory. Further close-up observation reveals compensation for duanyu1531ι/λ expression by PKMζ in duanyu1531ι/λ cKO mice. This compensation was not observed under basal conditions, but was detected either after LTP induction or learning-associated behavioral training. Accordingly, in the early stage of LTP expression, a switch from to PKMζ-dependent molecular mechanisms was detected in duanyu1531ι/λ cKO mice. Notably, when cKO mice were challenged with more difficult hippocampus-dependent learning tasks, moderate learning deficits were detected, suggesting a suboptimal compensation for function in duanyu1531ι/λ cKO mice. Thus, under physiological conditions, duanyu1531ι/λ is essential for hippocampal early-LTP and long-term memory (LTM).

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