Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons

Kang, Jian; Kang, Ning; Yu, Yong; Zhang, J.; Petersen, N.; Tian, Guo-Feng; Nedergaard, Maiken

doi:10.1016/j.neuroscience.2010.06.020

Cited by 50 publications

(40 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1C). Astrocytes were readily detected by two-photon imaging after the slice had been incubated with the fluorescent dye Texas red hydrazide, an approach similar to that described for sulphorhodamine 101 (11,12). Dye loading of slices obtained from transgenic mice that express EGFP under control of the Glt-1 promoter (Glt-1-EGFP BAC transgenic mice) (13) confirmed that Texas red hydrazide was selectively taken up by GFP-expressing astrocytes (Fig.…”

Section: Aqp4 Deletion Reduces Swelling Of Cortical Astrocytes Exposementioning

confidence: 81%

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema

Thrane

Rappold

Fujita

et al. 2010

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

240

247

View full text Add to dashboard Cite

Aquaporin-4 (AQP4) is a primary influx route for water during brain edema formation. Here, we provide evidence that brain swelling triggers Ca 2+ signaling in astrocytes and that deletion of the Aqp4 gene markedly interferes with these events. Using in vivo twophoton imaging, we show that hypoosmotic stress (20% reduction in osmolarity) initiates astrocytic Ca 2+ spikes and that deletion of Aqp4 reduces these signals. The Ca 2+ signals are partly dependent on activation of P2 purinergic receptors, which was judged from the effects of appropriate antagonists applied to cortical slices. Supporting the involvement of purinergic signaling, osmotic stress was found to induce ATP release from cultured astrocytes in an AQP4-dependent manner. Our results suggest that AQP4 not only serves as an influx route for water but also is critical for initiating downstream signaling events that may affect and potentially exacerbate the pathological outcome in clinical conditions associated with brain edema.endfeet | glial | two-photon

show abstract

Section: Aqp4 Deletion Reduces Swelling Of Cortical Astrocytes Exposementioning

confidence: 81%

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema

Thrane

Rappold

Fujita

et al. 2010

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

240

247

View full text Add to dashboard Cite

show abstract

“…1A) (11,17). Astrocytes were identified by enhanced green fluorescent protein (eGFP) expressed under the Glt1 promoter, which helped us avoid the use of the epileptogenic dye sulforhodamine (SR)101 (18,19). This labeling also Author contributions: A.S.T., V.R.T., E.A.N., and M.N.…”

Section: General Anesthetics Suppress Calcium Transients In Neocorticalmentioning

confidence: 99%

General anesthesia selectively disrupts astrocyte calcium signaling in the awake mouse cortex

Thrane

Zeppenfeld

et al. 2012

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

276

258

View full text Add to dashboard Cite

Calcium signaling represents the principle pathway by which astrocytes respond to neuronal activity. General anesthetics are routinely used in clinical practice to induce a sleep-like state, allowing otherwise painful procedures to be performed. Anesthetic drugs are thought to mainly target neurons in the brain and act by suppressing synaptic activity. However, the direct effect of general anesthesia on astrocyte signaling in awake animals has not previously been addressed. This is a critical issue, because calcium signaling may represent an essential mechanism through which astrocytes can modulate synaptic activity. In our study, we performed calcium imaging in awake head-restrained mice and found that three commonly used anesthetic combinations (ketamine/xylazine, isoflurane, and urethane) markedly suppressed calcium transients in neocortical astrocytes. Additionally, all three anesthetics masked potentially important features of the astrocyte calcium signals, such as synchronized widespread transients that appeared to be associated with arousal in awake animals. Notably, anesthesia affected calcium transients in both processes and soma and depressed spontaneous signals, as well as calcium responses, evoked by whisker stimulation or agonist application. We show that these calcium transients are inositol 1,4,5-triphosphate type 2 receptor (IP 3 R2)-dependent but resistant to a local blockade of glutamatergic or purinergic signaling. Finally, we found that doses of anesthesia insufficient to affect neuronal responses to whisker stimulation selectively suppressed astrocyte calcium signals. Taken together, these data suggest that general anesthesia may suppress astrocyte calcium signals independently of neuronal activity. We propose that these glial effects may constitute a nonneuronal mechanism for sedative action of anesthetic drugs.

show abstract

“…While it has been known for many years that astrocytes preferentially take up AM ester Ca 2+ indicators, the secondary marker SR-101 is often used to verify the loaded cells as astrocytes. SR-101 may in itself alter the intrinsic excitability of neurons 29 . Use of SR-101 corroborates the need to perform all astrocyte Ca 2+ measurements in TTX to limit possible SR-101 effects on neuronal excitability.…”

Section: Discussionmentioning

confidence: 99%

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

Xie

Lauderdale

Murphy

et al. 2014

JoVE

View full text Add to dashboard Cite

Close to two decades of research has established that astrocytes in situ and in vivo express numerous G protein-coupled receptors (GPCRs) that can be stimulated by neuronally-released transmitter. However, the ability of astrocytic receptors to exhibit plasticity in response to changes in neuronal activity has received little attention. Here we describe a model system that can be used to globally scale up or down astrocytic group I metabotropic glutamate receptors (mGluRs) in acute brain slices. Included are methods on how to prepare parasagittal hippocampal slices, construct chambers suitable for long-term slice incubation, bidirectionally manipulate neuronal action potential frequency, load astrocytes and astrocyte processes with fluorescent Ca 2+ indicator, and measure changes in astrocytic Gq GPCR activity by recording spontaneous and evoked astrocyte Ca 2+ events using confocal microscopy. In essence, a "calcium roadmap" is provided for how to measure plasticity of astrocytic GqGPCRs. Applications of the technique for study of astrocytes are discussed. Having an understanding of how astrocytic receptor signaling is affected by changes in neuronal activity has important implications for both normal synaptic function as well as processes underlying neurological disorders and neurodegenerative disease. Video LinkThe video component of this article can be found at

show abstract

Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons

Cited by 50 publications

References 30 publications

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema

General anesthesia selectively disrupts astrocyte calcium signaling in the awake mouse cortex

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

Contact Info

Product

Resources

About

Sulforhodamine 101 induces long-term potentiation of intrinsic excitability and synaptic efficacy in hippocampal CA1 pyramidal neurons

Cited by 50 publications

References 30 publications

Critical role of aquaporin-4 (AQP4) in astrocytic Ca 2+ signaling events elicited by cerebral edema

Critical role of aquaporin-4 (AQP4) in astrocytic Ca 2+ signaling events elicited by cerebral edema

General anesthesia selectively disrupts astrocyte calcium signaling in the awake mouse cortex

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

Contact Info

Product

Resources

About

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema

Critical role of aquaporin-4 (AQP4) in astrocytic Ca ²⁺ signaling events elicited by cerebral edema