Electrical coupling among Bergmann glial cells and its modulation by glutamate receptor activation

Müller, Thomas; Möller, Thomas; Neuhaus, Jochen; Kettenmann, Helmut

doi:10.1002/(sici)1098-1136(199608)17:4<274::aid-glia2>3.0.co;2-#

Cited by 98 publications

(50 citation statements)

References 41 publications

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“…This absence suggests that under many conditions in the intact neocortex, endogenous ATP release events may be relatively small or infrequent. Conversely, gap junction-mediated coupling, a known mechanism for the spread of glial waves in brain slices (39), may be unfavored in cerebellum because gap junction coupling between BG is blocked by calcium itself (41).…”

Section: Discussionmentioning

confidence: 99%

Radially expanding transglial calcium waves in the intact cerebellum

Hoogland

Kühn

Göbel

et al. 2009

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

148

133

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Multicellular glial calcium waves may locally regulate neural activity or brain energetics. Here, we report a diffusion-driven astrocytic signal in the normal, intact brain that spans many astrocytic processes in a confined volume without fully encompassing any one cell. By using 2-photon microscopy in rodent cerebellar cortex labeled with fluorescent indicator dyes or the calcium-sensor protein G-CaMP2, we discovered spontaneous calcium waves that filled approximately ellipsoidal domains of Bergmann glia processes. Waves spread in 3 dimensions at a speed of 4 -11 m/s to a diameter of Ϸ50 m, slowed during expansion, and were reversibly blocked by P2 receptor antagonists. Consistent with the hypothesis that ATP acts as a diffusible trigger of calcium release waves, local ejection of ATP triggered P2 receptor-mediated waves that were refractory to repeated activation. Transglial waves represent a means for purinergic signals to act with local specificity to modulate activity or energetics in local neural circuits.astrocytes ͉ Bergmann glia ͉ in vivo ͉ 2-photon microscopy ͉ G-CaMP2

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Section: Discussionmentioning

confidence: 99%

Radially expanding transglial calcium waves in the intact cerebellum

Hoogland

Kühn

Göbel

et al. 2009

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

148

133

View full text Add to dashboard Cite

show abstract

“…Moreover, GABAergic transmission is increased in the tg mouse (Zhou et al 2003) and increased inhibition can lead to synchronization of PCs (Cheron et al 2004). Another potential pathway for the propagation is the electrotonically coupled Bergmann glia (Muller et al 1996) because these cells can alter PC excitability (Araque and Perea 2004).…”

Section: Discussionmentioning

confidence: 99%

Low-Frequency Oscillations in the Cerebellar Cortex of the Tottering Mouse

Chen¹,

Popa²,

Wang

et al. 2009

Journal of Neurophysiology

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EJ, Ebner TJ. Low-frequency oscillations in the cerebellar cortex of the tottering mouse. J Neurophysiol 101: 234 -245, 2009. First published November 5, 2008 doi:10.1152/jn.90829.2008. The tottering mouse is an autosomal recessive disorder involving a missense mutation in the gene encoding P/Q-type voltage-gated Ca 2ϩ channels. The tottering mouse has a characteristic phenotype consisting of transient attacks of dystonia triggered by stress, caffeine, or ethanol. The neural events underlying these episodes of dystonia are unknown. Flavoprotein autofluorescence optical imaging revealed transient, low-frequency oscillations in the cerebellar cortex of anesthetized and awake tottering mice but not in wild-type mice. Analysis of the frequencies, spatial extent, and power were used to characterize the oscillations. In anesthetized mice, the dominant frequencies of the oscillations are between 0.039 and 0.078 Hz. The spontaneous oscillations in the tottering mouse organize into high power domains that propagate to neighboring cerebellar cortical regions. In the tottering mouse, the spontaneous firing of 83% (73/88) of cerebellar cortical neurons exhibit oscillations at the same low frequencies. The oscillations are reduced by removing extracellular Ca 2ϩ and blocking L-type Ca 2ϩ channels. The oscillations are likely generated intrinsically in the cerebellar cortex because they are not affected by blocking AMPA receptors or by electrical stimulation of the parallel fiber-Purkinje cell circuit. Furthermore, local application of an L-type Ca 2ϩ agonist in the tottering mouse generates oscillations with similar properties. The beam-like response evoked by parallel fiber stimulation is reduced in the tottering mouse. In the awake tottering mouse, transcranial flavoprotein imaging revealed low-frequency oscillations that are accentuated during caffeine-induced attacks of dystonia. During dystonia, oscillations are also present in the face and hindlimb electromyographic (EMG) activity that become significantly coherent with the oscillations in the cerebellar cortex. These low-frequency oscillations and associated cerebellar cortical dysfunction demonstrate a novel abnormality in the tottering mouse. These oscillations are hypothesized to be involved in the episodic movement disorder in this mouse model of episodic ataxia type 2.

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“…For instance, both endothelins and glutamate have been reported to control gap junctional communication among astrocytes (Giaume et al, 1992;Enkvist and McCarthy, 1994;Müller et al, 1996). However, this regulation occurs with a different time scale, as compared with the propagation of intercellular calcium waves (minutes vs seconds).…”

Section: Discussionmentioning

confidence: 99%

Mechanism Involved in Initiation and Propagation of Receptor-Induced Intercellular Calcium Signaling in Cultured Rat Astrocytes

et al. 1997

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The mechanisms involved in the initiation and the propagation of intercellular calcium signaling (calcium waves) were studied in cultured rat astrocytes. The analysis of calcium waves, induced either by mechanical stimulation or by focal application of ionomycin, indicated that initiation was dependent on the presence of external calcium. In addition, pharmacological experiments indicate that intercellular propagation required PLC activation, integrity of IP 3 -sensitive internal calcium stores, and functional gap junctions. An extracellular action of ATP or glutamate and participation of voltage-dependent Ca 2ϩ channels were tested by using enzymatic degradation, receptor antagonists, and channel blockers, respectively. Because neither the speed of propagation nor the extent of the calcium waves was affected by these treatments, these alternate mechanisms were excluded from playing a role in intercellular calcium signaling. Biochemical assays and focal applications of several agonists (methoxamine, carbachol, glutamate) of membrane receptors to neurotransmitters and peptides (endothelin 1) demonstrated that their ability to trigger regenerative calcium waves depended on phospholipase C activity and inositol phosphate production. Thus, in rat astrocytes, initiation and propagation of calcium waves involve a sequence of intra-and intercellular steps in which phospholipase C, inositol trisphosphate, internal calcium stores, and gap junction channels play a critical role. The identification of these different events allows us to determine several targets at which the level of long-range signaling in astrocytes may be controlled.

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Electrical coupling among Bergmann glial cells and its modulation by glutamate receptor activation

Cited by 98 publications

References 41 publications

Radially expanding transglial calcium waves in the intact cerebellum

Radially expanding transglial calcium waves in the intact cerebellum

Low-Frequency Oscillations in the Cerebellar Cortex of the Tottering Mouse

Mechanism Involved in Initiation and Propagation of Receptor-Induced Intercellular Calcium Signaling in Cultured Rat Astrocytes

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