Electrical Activity During the Estrous Cycle of the Rat: Cyclic Changes in Limbic Structures

Terasawa, Ei; Timiras, Paola S.

doi:10.1210/endo-83-2-207

Cited by 218 publications

(97 citation statements)

References 23 publications

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“…Estradiol has been shown to increase hippocampal excitability as demonstrated by facilitation of kindled seizure acquisition in the hippocampus (Buterbaugh and Hudson, 1991), increased severity of kainic acid-induced seizures (Nicoletti et al, 1985), and decreased hippocampal seizure threshold (Terasawa and Timiras, 1968). Furthermore, during the estrous cycle, in which spine and synapse density fluctuate naturally with changing hormone levels , the threshold for hippocampal seizure activity decreases (Terasawa and Timiras, 1968) and LTP is enhanced (Warren et al, 1995) as spine and synapse density increase. Interestingly, Wong and Moss (1992) previously reported that ϳ20% of CA1 pyramidal cells in hippocampal slices from estradiol-treated rats showed prolonged EPSPs in response reduced to 0.6 mM; in addition, recorded cells were depolarized to approximately Ϫ40 mV and 200 mM QX-314 was included in the recording electrode to eliminate Na ϩ action potentials in the recorded cell.…”

Section: Discussionmentioning

confidence: 99%

“…With a time course very similar to spine and synapse changes, estradiol treatment facilitates acquisition of kindled seizures in the hippocampus (Buterbaugh and Hudson, 1991), increases severity of kainic acid-induced seizures (Nicoletti et al, 1985), and decreases hippocampal seizure threshold (Terasawa and Timiras, 1968). During the estrous cycle, in which spine and synapse density fluctuate naturally with changing hormone levels , the threshold for hippocampal seizure activity decreases (Terasawa and Timiras, 1968) and longterm potentiation (LTP) is enhanced (Warren et al, 1995) as estradiol levels increase.To address the relationship between estradiol-induced dif- …”

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Estradiol Increases the Sensitivity of Hippocampal CA1 Pyramidal Cells to NMDA Receptor-Mediated Synaptic Input: Correlation with Dendritic Spine Density

et al. 1997

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Previous studies have shown that estradiol induces new dendritic spines and synapses on hippocampal CA1 pyramidal cells. We have assessed the consequences of estradiolinduced dendritic spines on CA1 pyramidal cell intrinsic and synaptic electrophysiological properties. Hippocampal slices were prepared from ovariectomized rats treated with either estradiol or oil vehicle. CA1 pyramidal cells were recorded and injected with biocytin to visualize spines. The association of dendritic spine density and electrophysiological parameters for each cell was then tested using linear regression analysis. We found a negative relationship between spine density and input resistance; however, no other intrinsic property measured was significantly associated with dendritic spine density. Glutamate receptor autoradiography demonstrated an estradiol-induced increase in binding to NMDA, but not AMPA, receptors. We then used input/output (I/O) curves (EPSP slope vs stimulus intensity) to determine whether the sensitivity of CA1 pyramidal cells to synaptic input is correlated with dendritic spine density. Consistent with the lack of an estradiol effect on AMPA receptor binding, we observed no relationship between the slope of an I/O curve generated under standard recording conditions, in which the AMPA receptor dominates the EPSP, and spine density. However, recording the pharmacologically isolated NMDA receptor-mediated component of the EPSP revealed a significant correlation between I/O slope and spine density. These results indicate that, in parallel with estradiol-induced increases in spine/synapse density and NMDA receptor binding, estradiol treatment increases sensitivity of CA1 pyramidal cells to NMDA receptor-mediated synaptic input; further, sensitivity to NMDA receptor-mediated synaptic input is well correlated with dendritic spine density. Key words: estradiol; dendritic spines; hippocampal slice; CA1 pyramidal cells; biocytin; autoradiography; NMDA receptorSince the initial anatomical description of dendritic spines by Ramon y Cajal in the late 1800s, many investigators have speculated about dendritic spine function. Spines have been proposed to play primarily connective, electrical, and /or biochemical roles in neuronal physiology (for review, see Koch and Zador, 1992;Horner, 1993;Harris and Kater, 1994). Recent efforts to understand dendritic spine function based on imaging of dye-labeled spiny dendrites have yielded valuable information, particularly with regard to spines' potential for Ca 2ϩ compartmentalization (Guthrie et al., 1991;Muller et al., 1991). Such findings have been incorporated into proposals for dendritic spine function in synaptic integration (see, for example, Yuste and Denk, 1995) and neuroprotection (Harris and Kater, 1994;Segal, 1995). An additional approach to exploring dendritic spine function, which has not been used to date, is to assess the functional consequences of adding dendritic spines to the dendrites of spiny neurons.Hippocampal CA1 pyramidal cells are an ideal population of neurons in w...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Estradiol Increases the Sensitivity of Hippocampal CA1 Pyramidal Cells to NMDA Receptor-Mediated Synaptic Input: Correlation with Dendritic Spine Density

et al. 1997

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“…Estrogen has profound effects on synaptic structure and function in CA1, yet few neurons in this region express a nuclear ER (Hart et al, 2001;Blurton-Jones and Tuszynski, 2002;Mitra et al, 2003). Estrogen increases dendritic spine and excitatory synapse numbers in CA1 (Woolley and McEwen, 1992;Adams et al, 2001), increases the sensitivity of CA1 pyramidal cells to excitatory synaptic input (Woolley et al, 1997;Rudick and Woolley, 2001), and increases dorsal hippocampal seizure susceptibility (Terasawa and Timiras, 1968). Both in vitro (Murphy et al, 1998) and in vivo (Rudick and Woolley, 2001; studies suggest that estrogen regulates excitatory synaptic connectivity through an initial suppression of inhibitory GABAergic synaptic transmission.…”

Section: Introductionmentioning

confidence: 99%

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

Hart

Snyder²,

Smejkalová³

et al. 2007

J. Neurosci.

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Although the classical mechanism of estrogen action involves activation of nuclear transcription factor receptors, estrogen also has acute effects on neuronal signaling that occur too rapidly to involve gene expression. These rapid effects are likely to be mediated by extranuclear estrogen receptors associated with the plasma membrane and/or cytoplasmic organelles. Here we used a combination of serialsection electron microscopic immunocytochemistry, immunofluorescence, and Western blotting to show that estrogen receptor-␣ is associated with clusters of vesicles in perisomatic inhibitory boutons in hippocampal CA1 and that estrogen treatment mobilizes these vesicle clusters toward synapses. Estrogen receptor-␣ is present in approximately one-third of perisomatic inhibitory boutons, and specifically in those that express cholecystokinin, not parvalbumin. We also found a high degree of extranuclear estrogen receptor-␣ colocalization with neuropeptide Y. Our results suggest a novel mode of estrogen action in which a subset of vesicles within a specific population of inhibitory boutons responds directly to estrogen by moving toward synapses. The mobilization of these vesicles may influence acute effects of estrogen mediated by estrogen receptor-␣ signaling at inhibitory synapses.

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“…But another possible functional consequence of the neural rewiring centers on a disadvantageous effect of estrogen. Estrogen treatment can decrease the threshold for hippocampal seizures (15). The simultaneous excitation of two different CA1 cells by the same terminal bouton in estrogen-treated animals would be expected to increase the synchronization of firing that can lead to seizure (16).…”

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confidence: 99%

The increasingly plastic, hormone-responsive adult brain

Breedlove

Jordan

2001

Proc. Natl. Acad. Sci. U.S.A.

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Electrical Activity During the Estrous Cycle of the Rat: Cyclic Changes in Limbic Structures

Cited by 218 publications

References 23 publications

Estradiol Increases the Sensitivity of Hippocampal CA1 Pyramidal Cells to NMDA Receptor-Mediated Synaptic Input: Correlation with Dendritic Spine Density

Estradiol Increases the Sensitivity of Hippocampal CA1 Pyramidal Cells to NMDA Receptor-Mediated Synaptic Input: Correlation with Dendritic Spine Density

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

The increasingly plastic, hormone-responsive adult brain

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