Astrocytes in 17β-estradiol treated mixed hippocampal cultures show attenuated calcium response to neuronal activity

Rao, Shilpa P.; Sikdar, SK

doi:10.1002/glia.20341

Cited by 18 publications

(19 citation statements)

References 66 publications

(67 reference statements)

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“…For example, estradiol can block cannabinoid-induced presynaptic inhibition of fast synaptic transmission in pro-opiomelanocortin neurons (Nguyen and Wagner 2006). Estradiol reduced the ability of neuronal activity to increase intracellular calcium levels in astrocytes in hippocampal cultures (Rao and Sikdar, 2006). This process is dependent upon activation of astrocyte mGluRs; consistent with this, the ability of 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), a broad-spectrum mGluR agonist, to increase astrocytic calcium levels was also decreased in estradiol-treated cultures.…”

Section: Discussionmentioning

confidence: 99%

Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits

Glanowska

Moenter

2011

Journal of Neurophysiology

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Gonadotropin-releasing hormone (GnRH) neurons form the final common pathway for central control of fertility. Regulation of GnRH neurons by long-loop gonadal steroid feedback through steroid receptor-expressing afferents such as GABAergic neurons is well studied. Recently, local central feedback circuits regulating GnRH neurons were identified. GnRH neuronal depolarization induces short-term inhibition of their GABAergic afferents via a mechanism dependent on metabotropic glutamate receptor (mGluR) activation. GnRH neurons are enveloped in astrocytes, which express mGluRs. GnRH neurons also produce endocannabinoids, which can be induced by mGluR activation. We hypothesized the local GnRH-GABA circuit utilizes glia-derived and/or cannabinoid mechanisms and is altered by steroid milieu. Whole cell voltage-clamp was used to record GABAergic postsynaptic currents (PSCs) from GnRH neurons before and after action potential-like depolarizations were mimicked. In GnRH neurons from ovariectomized (OVX) mice, this depolarization reduced PSC frequency. This suppression was blocked by inhibition of prostaglandin synthesis with indomethacin, by a prostaglandin receptor antagonist, or by a specific glial metabolic poison, together suggesting the postulate that prostaglandins, potentially glia-derived, play a role in this circuit. This circuit was also inhibited by a CB1 receptor antagonist or by blockade of endocannabinoid synthesis in GnRH neurons, suggesting an endocannabinoid element, as well. In females, local circuit inhibition persisted in androgen-treated mice but not in estradiol-treated mice or young ovary-intact mice. In contrast, local circuit inhibition was present in gonad-intact males. These data suggest GnRH neurons interact with their afferent neurons using multiple mechanisms and that these local circuits can be modified by both sex and steroid feedback.

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Section: Discussionmentioning

confidence: 99%

Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits

Glanowska

Moenter

2011

Journal of Neurophysiology

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“…When t-ACPD-evoked astrocyte [Ca 21 ] i responses were examined, it was observed that the number of astrocytes responding to t-ACPD and the amplitude of the response were lower in presence of estradiol, suggesting that estradiol rapidly inhibited astrocyte mGluRs. Effects of estradiol on mGluRs have been previously reported (Boulware et al, 2005;Hilton et al, 2006;Rao and Sikdar, 2006), and the rapid inhibitory actions described in our study could be instrumental in causing the impaired [Ca 21 ] i response seen in astrocytes around a stimulated cell.…”

Section: Discussionmentioning

confidence: 75%

“…Cumulative distributions were compared using Kolmogorov-Smirnov (K-S) test. (Rao and Sikdar, 2006). The fluorescence of the stimulated astrocyte recovered to baseline levels in all experiments indicating that mechanical stimulus did not irreversibly damage the cells.…”

Section: Discussionmentioning

confidence: 90%

“…Increase in fluorescence value 1 SD above the baseline that persisted for five successive frames was taken as a [Ca 21 ] i response (Umemiya et al, 1999). The maximum wave radius was the farthest distance traveled by the [Ca 21 ] i wave in any direction and wave velocity was obtained by dividing the maximum wave radius by the time taken to reach that distance (Rao and Sikdar, 2006).…”

Section: Image Analysismentioning

confidence: 99%

“…Astrocyte-neuron signaling involves integration of neuronal inputs by astrocytes and modulation of neurotransmission (Carmignoto, 2000;Newman, 2003;Perea and Araque, 2005). The presence of ERs on both neurons and astrocytes suggests a complex interplay between the two in mediating the effects of estradiol (Garcia-Ovejero et al, 2005;Garcia-Segura and McCarthy, 2004;Rao and Sikdar, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Acute treatment with 17β‐estradiol attenuates astrocyte–astrocyte and astrocyte–neuron communication

Rao

Sikdar

2007

Glia

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Astrocytes are now recognized as dynamic signaling elements in the brain. Bidirectional communication between neurons and astrocytes involves integration of neuronal inputs by astrocytes and release of gliotransmitters that modulate neuronal excitability and synaptic transmission. The ovarian steroid hormone, 17beta-estradiol, in addition to its rapid actions on neuronal electrical activity can rapidly alter astrocyte intracellular calcium concentration ([Ca2+]i) through a membrane-associated estrogen receptor. Using calcium imaging and electrophysiological techniques, we investigated the functional consequences of acute treatment with estradiol on astrocyte-astrocyte and astrocyte-neuron communication in mixed hippocampal cultures. Mechanical stimulation of an astrocyte evoked a [Ca2+]i rise in the stimulated astrocyte, which propagated to the surrounding astrocytes as a [Ca2+]i wave. Following acute treatment with estradiol, the amplitude of the [Ca2+]i elevation in astrocytes around the stimulated astrocyte was attenuated. Further, estradiol inhibited the [Ca2+]i rise in individual astrocytes in response to the metabotropic glutamate receptor agonist, trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid. Mechanical stimulation of astrocytes induced [Ca2+]i elevations and electrophysiological responses in adjacent neurons. Estradiol rapidly attenuated the astrocyte-evoked glutamate-mediated [Ca2+]i rise and slow inward current in neurons. Also, the incidence of astrocyte-induced increase in spontaneous postsynaptic current frequency was reduced in the presence of estradiol. The effects of estradiol were stereo-specific and reversible following washout. These findings may indicate that the regulation of neuronal excitability and synaptic transmission by astrocytes is sensitive to rapid estradiol-mediated hormonal control.

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Corticosterone treatment results in enhanced release of peptidergic vesicles in astrocytes via cytoskeletal rearrangements

Chatterjee

Sikdar

2013

Glia

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While the effect of stress on neuronal physiology is widely studied, its effect on the functionality of astrocytes is not well understood. We studied the effect of high doses of stress hormone corticosterone, on two physiological properties of astrocytes, i.e., gliotransmission and interastrocytic calcium waves. To study the release of peptidergic vesicles from astrocytes, hippocampal astrocyte cultures were transfected with a plasmid to express pro-atrial natriuretic peptide (ANP) fused with the emerald green fluorescent protein (ANP.emd). The rate of decrease in fluorescence of ANP.emd on application of ionomycin, a calcium ionophore was monitored. Significant increase in the rate of calcium-dependent exocytosis of ANP.emd was observed with the 100 nM and 1 μM corticosterone treatments for 3 h, which depended on the activation of the glucocorticoid receptor. ANP.emd tagged vesicles exhibited increased mobility in astrocyte culture upon corticosterone treatment. Increasing corticosterone concentrations also resulted in concomitant increase in the calcium wave propagation velocity, initiated by focal ATP application. Corticosterone treatment also resulted in increased GFAP expression and F-actin rearrangements. FITC-Phalloidin immunostaining revealed increased formation of cross linked F-actin networks with the 100 nM and 1 μM corticosterone treatment. Alternatively, blockade of actin polymerization and disruption of microtubules prevented the corticosterone-mediated increase in ANP.emd release kinetics. This study reports for the first time the effect of corticosterone on gliotransmission via modulation of cytoskeletal elements. As ANP acts on both neurons and blood vessels, modulation of its release could have functional implications in neurovascular coupling under pathophysiological conditions of stress.

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Astrocytes in 17β-estradiol treated mixed hippocampal cultures show attenuated calcium response to neuronal activity

Cited by 18 publications

References 66 publications

Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits

Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits

Acute treatment with 17β‐estradiol attenuates astrocyte–astrocyte and astrocyte–neuron communication

Corticosterone treatment results in enhanced release of peptidergic vesicles in astrocytes via cytoskeletal rearrangements

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