Estrogen induces a rapid increase of calcium-calmodulin-dependent protein kinase II activity in the hippocampus.
Molecular genetics experiments using gene targeting and transgenic technology demonstrated the importance of alpha-calcium-calmodulin-dependent protein kinase II (alphaCaMKII) in long-term potentiation (LTP) and memory. Little information is available though on how CaMKII activity may be regulated in vivo. We show that estradiol benzoate activates CaMKII in a dose and time-dependent manner in mouse hippocampus after 30 min stimulation. The effect of estrogen is via a very rapid nongenomic mechanism that is blocked in vitro in hippocampal primary neurons by the pure estrogen receptor antagonist, ICI 182,780. These results suggest that estrogen action in the hippocampus is linked to CaMKII activation.
Sawai
T
T
Tsukuba Research Laboratories, Eisai Co., Ltd., 5-1-3 Tokodai, Ibaraki 300-2635, Tsukuba City, Japan.
Bernier
F
F
Fukushima
T
T
Hashimoto
T
T
Ogura
H
H
Nishizawa
Y
Y
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology*; D005260:Female; D006624:Hippocampus / Q000187:drug effects* / Q000201:enzymology*; D051379:Mice; D008813:Mice, Inbred ICR; D009474:Neurons / Q000187:drug effects / Q000201:enzymology
C074283:estradiol 3-benzoate; D004958:Estradiol; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases