TY - JOUR
T1 - Synaptic remodeling induced by gonadal hormones
T2 - Neuronal plasticity as a mediator of neuroendocrine and behavioral responses to steroids
AU - Parducz, A.
AU - Hajszan, T.
AU - MacLusky, N. J.
AU - Hoyk, Z.
AU - Csakvari, E.
AU - Kurunczi, A.
AU - Prange-Kiel, J.
AU - Leranth, C.
N1 - Funding Information:
This work was supported by grants from the Hungarian Scientific Research Fund (OTKA T043436 to A.P.), the Hungarian National Office for Research and Technology (RET 08/2004 to A.P.), as well as from the NIH (MH60858 and NS42644 to C.L.).
PY - 2006
Y1 - 2006
N2 - During recent decades, it has become a generally accepted view that structural neuroplasticity is remarkably involved in the functional adaptation of the CNS. Thus, cellular morphology in the brain is in continuous transition throughout the life span, as a response to environmental stimuli. The effects of the environment on neuroplasticity are mediated by, to some extent, the changing levels of circulating gonadal steroid hormones. Today, it is clear that the function of gonadal steroids in the brain extends beyond simply regulating reproductive and/or neuroendocrine events. In addition, or even more importantly, gonadal steroids participate in the shaping of the developing brain, while their actions during adult life are implicated in higher brain functions such as cognition, mood and memory. A large body of evidence indicates that gonadal steroid-induced functional changes are accompanied by alterations in neuron and synapse numbers, as well as in dendritic and synaptic morphology. These structural modifications are believed to serve as a morphological basis for changes in behavior and cellular activity. Due to their growing functional and clinical significance, the specificity, timeframe, as well as the molecular and cellular mechanisms of hormone-induced neuroplasticity have become the focus of many studies. In this review, we briefly summarize current knowledge and the most significant recent discoveries from our laboratories on estrogen- and dehydroepiandrosterone-induced synaptic remodeling in the hypothalamus and hippocampus, two important brain areas heavily involved in autonomic and cognitive operations, respectively.
AB - During recent decades, it has become a generally accepted view that structural neuroplasticity is remarkably involved in the functional adaptation of the CNS. Thus, cellular morphology in the brain is in continuous transition throughout the life span, as a response to environmental stimuli. The effects of the environment on neuroplasticity are mediated by, to some extent, the changing levels of circulating gonadal steroid hormones. Today, it is clear that the function of gonadal steroids in the brain extends beyond simply regulating reproductive and/or neuroendocrine events. In addition, or even more importantly, gonadal steroids participate in the shaping of the developing brain, while their actions during adult life are implicated in higher brain functions such as cognition, mood and memory. A large body of evidence indicates that gonadal steroid-induced functional changes are accompanied by alterations in neuron and synapse numbers, as well as in dendritic and synaptic morphology. These structural modifications are believed to serve as a morphological basis for changes in behavior and cellular activity. Due to their growing functional and clinical significance, the specificity, timeframe, as well as the molecular and cellular mechanisms of hormone-induced neuroplasticity have become the focus of many studies. In this review, we briefly summarize current knowledge and the most significant recent discoveries from our laboratories on estrogen- and dehydroepiandrosterone-induced synaptic remodeling in the hypothalamus and hippocampus, two important brain areas heavily involved in autonomic and cognitive operations, respectively.
KW - DHEA
KW - Electron microscopic stereology
KW - Estrogen
KW - Hippocampus
KW - Hypothalamus
KW - Synaptogenesis
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U2 - 10.1016/j.neuroscience.2005.07.008
DO - 10.1016/j.neuroscience.2005.07.008
M3 - Article
C2 - 16310961
AN - SCOPUS:33644518240
SN - 0306-4522
VL - 138
SP - 977
EP - 985
JO - Neuroscience
JF - Neuroscience
IS - 3
ER -