Trace eyeblink conditioning requires the hippocampus but not autophosphorylation of alphaCaMKII in mice.
Little is known about signaling mechanisms underlying temporal associative learning. Here, we show that mice with a targeted point mutation that prevents autophosphorylation of alphaCaMKII (alphaCaMKII(T286A)) learn trace eyeblink conditioning normally. This forms a sharp contrast to the severely impaired spatial learning in the water maze and contextual fear conditioning observed in alphaCaMKII(T286A) mutants. Importantly, hippocampal lesions impaired trace eyeblink conditioning in alphaCaMKII(T286A) mice, suggesting a potential role of hippocampal alphaCaMKII-independent mechanisms. These results indicate that hippocampal signaling mechanisms that underlie temporal associative learning as assessed by trace eyeblink conditioning may differ from those of spatial and contextual learning.
Ohno
Masuo
M
Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611-3008, USA. ohno@northwestern.edu
Tseng
Wilbur
W
Silva
Alcino J
AJ
Disterhoft
John F
JF
D000818:Animals; D001245:Association Learning / Q000502:physiology*; D001767:Blinking / Q000502:physiology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000235:genetics / Q000378:metabolism*; D003213:Conditioning, Psychological / Q000502:physiology*; D005239:Fear / Q000523:psychology; D005838:Genotype; D006624:Hippocampus / Q000502:physiology*; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010766:Phosphorylation; D017354:Point Mutation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases