Progesterone regulation of synaptic transmission and plasticity in rodent hippocampus

Foy, Michael R.; Akopian, Garnik; Thompson, Richard F.

doi:10.1101/lm.1124708

Cited by 44 publications

(30 citation statements)

References 13 publications

(11 reference statements)

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“…However, like E 2 , P 4 can also enhance hippocampal LTP [84], neurogenesis [85; 86], ERK signaling, and mTOR-dependent local protein synthesis [87]. Nevertheless, understanding how P 4 influences memory is considerably more challenging than E 2 because P 4 serves as an obligatory precursor for the synthesis of other steroids including estrogens, androgens, and glucocorticoids.…”

Section: Effects Of Ovarian Hormones In the Hippocampus: A Generalmentioning

confidence: 99%

Regulation of object recognition and object placement by ovarian sex steroid hormones

Tuscher

Fortress

Kim

et al. 2015

Behavioural Brain Research

111

102

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The ovarian hormones 17β-estradiol (E2) and progesterone (P4) are potent modulators of hippocampal memory formation. Both hormones have been demonstrated to enhance hippocampal memory by regulating the cellular and molecular mechanisms thought to underlie memory formation. Behavioral neuroendocrinologists have increasingly used the object recognition and object placement (object location) tasks to investigate the role of E2 and P4 in regulating hippocampal memory formation in rodents. These one-trial learning tasks are ideal for studying acute effects of hormone treatments on different phases of memory because they can be administered during acquisition (pre-training), consolidation (post-training), or retrieval (pre-testing). This review synthesizes the rodent literature testing the effects of E2 and P4 on object recognition (OR) and object placement (OP), and the molecular mechanisms in the hippocampus supporting memory formation in these tasks. Some general trends emerge from the data. Among gonadally intact females, object memory tends to be best when E2 and P4 levels are elevated during the estrous cycle, pregnancy, and in middle age. In ovariectomized females, E2 given before or immediately after testing generally enhances OR and OP in young and middle-aged rats and mice, although effects are mixed in aged rodents. Effects of E2 treatment on OR 7and OP memory consolidation can be mediated by both classical estrogen receptors (ERα and ERβ), and depend on glutamate receptors (NMDA, mGluR1) and activation of numerous cell signaling cascades (e.g., ERK, PI3K/Akt, mTOR) and epigenetic processes (e.g., histone H3 acetylation, DNA methylation). Acute P4 treatment given immediately after training also enhances OR and OP in young and middle-aged ovariectomized females by activating similar cell signaling pathways as E2 (e.g., ERK, mTOR). The few studies that have administered both hormones in combination suggest that treatment can enhance OR and OP, but that effects are highly dependent on factors such as dose and timing of administration. In addition to providing more detail on these general conclusions, this review will discuss directions for future avenues of research into the hormonal regulation of object memory.

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Section: Effects Of Ovarian Hormones In the Hippocampus: A Generalmentioning

confidence: 99%

Regulation of object recognition and object placement by ovarian sex steroid hormones

Tuscher

Fortress

Kim

et al. 2015

Behavioural Brain Research

111

102

View full text Add to dashboard Cite

show abstract

“…Specifically, several laboratories have shown that brief infusions of 17β-estradiol (E2), at concentrations found in the blood during phases of the estrus cycle, result in an almost immediate enhancement of fast excitatory postsynaptic potentials (EPSPs) in hippocampal slices from male (Foy et al, 1999; Bi et al, 2000; Sharrow et al, 2002; Kim et al, 2006; Foy et al, 2008; Kramár et al, 2009a) and female (ovariectomized; OVX) rats (Smejkalova and Woolley, 2010). Notably, this facilitation involves both the slope and amplitude, but not the waveform, of monosynaptic potentials and reverses quickly upon washout (Fig 1A).…”

Section: Introductionmentioning

confidence: 99%

Estrogen promotes learning-related plasticity by modifying the synaptic cytoskeleton

et al. 2013

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Estrogen's acute, facilitatory effects on glutamatergic transmission and long-term potentiation (LTP) provide a potential explanation for the steroid's considerable influence on behavior. Recent work has identified mechanisms underlying these synaptic actions. Brief infusion of 17β-estradiol (E2) into adult male rat hippocampal slices triggers actin polymerization within dendritic spines via a signaling cascade beginning with the GTPase RhoA and ending with inactivation of the filament severing protein cofilin. Blocking this sequence, or actin polymerization itself, eliminates E2's effects on synaptic physiology. Notably, the theta burst stimulation used to induce LTP activates the same signaling pathway as E2 plus events that stabilize the reorganization of the sub-synaptic cytoskeleton. These observations suggest that E2 elicits a partial form of LTP, resulting in an increase of fast EPSP's and a reduction in the threshold for lasting synaptic changes. While E2's effects on the cytoskeleton could be direct, results described here indicate that the hormone activates synaptic TrkB receptors for Brain Derived Neurotrophic Factor, a releasable neurotrophin that stimulates the RhoA to cofilin pathway. It is therefore possible that E2 acts via transactivation of neighboring receptors to modify the composition and structure of excitatory contacts. Finally, there is the question of whether a loss of acute synaptic actions contributes to the memory problems associated with estrogen depletion. Initial tests found that ovariectomy in middle-aged rats disrupts RhoA signaling, actin polymerization, and LTP consolidation. Acute applications of E2 reversed these defects, a result consistent with the idea that disturbances to actin management are one cause of behavioral effects that emerge with reductions in steroid levels.

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“…Numerous studies indicate that neurosteroids have important neurotrophic, neuroprotective roles and can regulate advanced brain function. Neurosteroids not only promote development and maturation of neurons and glial cells [3], but also promote myelin regeneration and synapse formation [4], reduce calcium overload and neuron damage caused by reactive oxygen species (ROS) and regulate a variety of advanced brain functions including learning, memory, mood and sleep [5][6][7]. Memory dysfunction is one of the symptoms of aging-related degenerative diseases.…”

Section: Introductionmentioning

confidence: 99%

Effects of pregnenolone intervention on the cholinergic system and synaptic protein 1 in aged rats

2013

International Journal of Neuroscience

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Progesterone regulation of synaptic transmission and plasticity in rodent hippocampus

Cited by 44 publications

References 13 publications

Regulation of object recognition and object placement by ovarian sex steroid hormones

Regulation of object recognition and object placement by ovarian sex steroid hormones

Estrogen promotes learning-related plasticity by modifying the synaptic cytoskeleton

Effects of pregnenolone intervention on the cholinergic system and synaptic protein 1 in aged rats

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