The hippocampus has long been presumed the primary site of action of estrogen on cognition; and explicit memory is considered the cognitive function most vulnerable tomenopausal loss of estrogen [222,233–235]. Supportive evidence includes increased hippocampal neuronal excitability after estradiol administration to ovariectomized rats [233], and a positive correlation of hippocampal CA1 dendritic spine and synapse density with estrogen levels, in which exogenous estrogen was administered in ovariectomized rats and monkeys [236–245], or endogenous estrogen levels fluctuated across the rat estrous cycle [235]. The beneficial effect of estrogen upon hippocampal synaptic plasticity was confirmed via a variety of approaches in these studies, including Golgi analysis, light microscopic or electron microscopic analysis of synapses or synaptic proteins, dye-filling techniques, and radioimmunochemistry [235–245].
The hippocampus has long been presumed the primary site of action of estrogen on cognition; and explicit memory is considered the cognitive function most vulnerable tomenopausal loss of estrogen [222,233–235]. Supportive evidence includes increased hippocampal neuronal excitability after estradiol administration to ovariectomized rats [233], and a positive correlation of hippocampal CA1 dendritic spine and synapse density with estrogen levels, in which exogenous estrogen was administered in ovariectomized rats and monkeys [236–245], or endogenous estrogen levels fluctuated across the rat estrous cycle [235]. The beneficial effect of estrogen upon hippocampal synaptic plasticity was confirmed via a variety of approaches in these studies, including Golgi analysis, light microscopic or electron microscopic analysis of synapses or synaptic proteins, dye-filling techniques, and radioimmunochemistry [235–245].
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