Receptor-mediated calcium signalling in glial cells from mouse corpus callosum slices

Bernstein, Maurice; Lyons, Susan A.; Möller, Thomas; Kettenmann, Helmut

doi:10.1002/(sici)1097-4547(19961015)46:2<152::aid-jnr3>3.0.co;2-g

Cited by 72 publications

(52 citation statements)

References 45 publications

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“…Individual components of a purinergic extracellular signaling system have been demonstrated in diverse systems and by different investigators. Cultured astrocytes can release ATP in response to glutamatergic receptor stimulation (Queiroz et al, 1997) and respond to ATP with calcium elevations both in vitro (McCarthy and Salm, 1991;van den Pol et al, 1992;Salter and Hicks, 1994;Centemeri et al, 1997) and in situ (Kriegler and Chiu, 1993;Bernstein et al, 1996;Newman and Zahs, 1997). Additionally, suramin, which blocks purinergic receptors [although it has other biological effects (Chahdi et al, 1998)], blocks glial calcium waves (Guan et al, 1997;Zanotti and Charles, 1997).…”

Section: Atp Is the Primary Extracellular Messengermentioning

confidence: 86%

“…Individual astrocytes can respond to different subsets of neurotransmitters both in vivo (Bernstein et al, 1996) and in culture (McCarthy and Salm, 1991). The sensitivity of astrocytes seems to be developmentally regulated (Bernstein et al, 1996) and even altered by specific pathological conditions (Enkvist et al, 1996;Gottlieb and Matute, 1997;McKeon et al, 1997).…”

Section: There Are Multiple Mechanisms Involved In Calcium Wave Propamentioning

confidence: 99%

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ATP Released from Astrocytes Mediates Glial Calcium Waves

et al. 1999

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Calcium waves represent a widespread form of intercellular communication. Although they have been thought for a long time to require gap junctions, we recently demonstrated that mouse cortical astrocytes use an extracellular messenger for calcium wave propagation. The present experiments identify ATP as a major extracellular messenger in this system. Medium collected from astrocyte cultures during (but not before) calcium wave stimulation contains ATP. The excitatory effects of medium samples and of ATP are blocked by purinergic receptor antagonists and by pretreatment with apyrase; these same purinergic receptor antagonists block propagation of electrically evoked calcium waves. ATP, applied at the concentration measured in medium samples, evokes responses that are qualitatively and quantitatively similar to those evoked by those medium samples. These data implicate ATP as an important transmitter between CNS astrocytes.Key words: glia; astrocytes; calcium waves; ATP; extracellular signal; suramin; apyrase; purinergic; electrical stimulation Intercellular calcium waves, i.e., rises in intracellular free calcium that propagate between neighboring cells, occur widely among different cell types throughout the animal kingdom (Cornell-Bell et al., 1990;Boitano et al., 1992;Enomoto et al., 1992;Demer et al., 1993;Nathanson et al., 1995;C ao et al., 1997;Young et al., 1996;Jørgensen et al., 1997;Newman and Z ahs, 1997). Although we are at an early stage of understanding the f unction of such waves, one must consider that glial calcium waves may provide an information-processing system operating in parallel with neuronal circuits within the nervous system. There is clear evidence of interaction between glial calcium waves and neurons; neuronal activity can directly evoke glial calcium waves (Dani et al., 1992), and glial calcium waves can directly evoke calcium transients and electrical activity in neurons (Nedergaard, 1994;Parpura et al., 1994;Hassinger et al., 1995;Newman and Z ahs, 1998). Understanding how glial calcium waves could contribute to information processing requires an understanding of the mechanisms underlying calcium wave propagation.For some years, glial calcium waves have been thought to propagate through gap junctions (Boitano et al., 1992;Charles et al., 1993;Sanderson et al., 1994;Sneyd et al., 1994Sneyd et al., , 1995. We demonstrated recently that an extracellular communication system can provide a dominant path for glial calcium wave propagation (Hassinger et al., 1996), because calcium waves can propagate between physically separated astrocytes, and the extent and direction of calcium wave propagation are significantly influenced by movement of the extracellular medium. T wo subsequent publications now confirm that astrocytes do not absolutely require functional gap junction coupling for calcium wave propagation (Guan et al., 1997;Naus et al., 1997). Taken together, the newer literature supports the idea that substance(s) released from astrocytes can activate receptor systems on adjacent astroc...

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Section: Atp Is the Primary Extracellular Messengermentioning

confidence: 86%

Section: There Are Multiple Mechanisms Involved In Calcium Wave Propamentioning

confidence: 99%

ATP Released from Astrocytes Mediates Glial Calcium Waves

et al. 1999

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“…Functional AMPA/ kainate receptors are known to be present on glia (Gallo and Russell, 1995;Bernstein et al, 1996;Chen et al, 1997). The AMPA subunits GluR1-4 have been detected in glia in vivo using reverse transcription-PCR analysis in combination with immuno- histochemistry (Garcia-Barcina and Matute, 1998).…”

Section: Discussionmentioning

confidence: 99%

2,3-Dihydroxy-6-Nitro-7-Sulfamoyl-Benzo(f)Quinoxaline Reduces Glial Loss and Acute White Matter Pathology after Experimental Spinal Cord Contusion

1999

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Focal microinjection of 2,3-dihyro-6-nitro-7-sulfamoylbenzo( f )quinoxaline (NBQX), an antagonist of the AMPA/kainate subclass of glutamate receptors, reduces neurological deficits and tissue loss after spinal cord injury. Dose-dependent sparing of white matter is seen at 1 month after injury that is correlated to the dose-related reduction in chronic functional deficits. To determine whether NBQX exerts an acute effect on white matter pathology, female, adult Spague Dawley rats were subjected to a standardized weight drop contusion at T-8 (10 gm ϫ 2.5 cm) and NBQX (15 nmol) or vehicle (VEH) solution focally injected into the injury site 15 min later. At 4 and 24 hr, tissue from the injury epicenter was processed for light and electron microscopy, and the histopathology of ventromedial white matter was compared. The axonal injury index, a quantitative representation of axoplasmic and myelinic pathologies, was significantly lower in the NBQX group at 4 hr (2.7 Ϯ 0.24, mean Ϯ SE) and 24 hr (1.4 Ϯ 0.19) than in VEH controls (3.8 Ϯ 0.33 and 2.1 Ϯ 0.20, respectively). Counts of glial cell nuclei indicated a loss of at least 60% at 4 and 24 hr after injury in the VEH group compared with uninjured controls. NBQX treatment reduced this glial loss by half. Immunohistochemistry revealed that the spared glia were primarily oligodendrocytes. Thus, the chronic effects of NBQX in reducing white matter loss after spinal cord injury appear to be attributable to the reduction of acute pathology and may be mediated through the protection of glia, particularly oligodendrocytes. Key words: spinal cord injury; NBQX; CC1; oligodendrocytes; astrocytes; microglia; white matterTraumatic injury to the spinal cord produces loss of gray matter and white matter (W M) that leads to permanent neurological deficits. Most injuries are the result of spinal cord contusion, i.e., a bruising caused by the impact of vertebral bone onto the dura after rapid flexion -extension of the spinal column. Approximately half are initially classified as "incomplete," in that some function can be detected below the injury site (Bracken et al., 1990). E xperimental models of such incomplete contusion spinal cord injury (SCI) have been developed to investigate the basic pathophysiological mechanisms involved and to test potential therapeutic approaches to mitigate the long-term neurological consequences. From studies of such models, it has become clear that the effects of the initial mechanical destruction of tissue are exacerbated by physiological and biochemical alterations that produce "secondary injury" (Young, 1993;Tator and Fehlings, 1991).One important component of secondary injury is the elevation of extracellular excitatory amino acids (Panter, et al., 1990;Liu et al., 1991) to levels known to be toxic to neurons (Choi et al., 1987;Choi and Rothman, 1990). Antagonists of both the NMDA and AMPA / kainate subclasses of glutamate receptors, administered after experimental SCI, have been shown to reduce chronic neurological impairment (Faden et al., 1988;Gom...

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“…November 2014 1763 (Bernstein et al, 1996;Kriegler and Chiu, 1993). In addition, electrophysiological criteria have been used to distinguish glial cell types, allowing the first descriptions of functional glutamate, GABA-A and glycine receptors in identified astrocytes, oligodendrocytes, glioblasts and OPCs in situ (Berger et al, 1992;Butt and Jennings 1994;Pastor et al, 1995 ] does not duplicate the effects of GABA upon excitability leading to the conclusion that receptor expression is axonal (Sakatani et al, 1994).…”

Section: Butt Et Al: Neurotransmitter Signaling In White Mattermentioning

confidence: 99%

Neurotransmitter signaling in white matter

Butt

Fern

Matute

2014

Glia

113

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White matter (WM) tracts are bundles of myelinated axons that provide for rapid communication throughout the CNS and integration in grey matter (GM). The main cells in myelinated tracts are oligodendrocytes and astrocytes, with small populations of microglia and oligodendrocyte precursor cells. The prominence of neurotransmitter signaling in WM, which largely exclude neuronal cell bodies, indicates it must have physiological functions other than neuron-to-neuron communication. A surprising aspect is the diversity of neurotransmitter signaling in WM, with evidence for glutamatergic, purinergic (ATP and adenosine), GABAergic, glycinergic, adrenergic, cholinergic, dopaminergic and serotonergic signaling, acting via a wide range of ionotropic and metabotropic receptors. Both axons and glia are potential sources of neurotransmitters and may express the respective receptors. The physiological functions of neurotransmitter signaling in WM are subject to debate, but glutamate and ATP-mediated signaling have been shown to evoke Ca 21 signals in glia and modulate axonal conduction. Experimental findings support a model of neurotransmitters being released from axons during action potential propagation acting on glial receptors to regulate the homeostatic functions of astrocytes and myelination by oligodendrocytes. Astrocytes also release neurotransmitters, which act on axonal receptors to strengthen action potential propagation, maintaining signaling along potentially long axon tracts. The co-existence of multiple neurotransmitters in WM tracts suggests they may have diverse functions that are important for information processing. Furthermore, the neurotransmitter signaling phenomena described in WM most likely apply to myelinated axons of the cerebral cortex and GM areas, where they are doubtless important for higher cognitive function. GLIA 2014;62:1762-1779 Key words: glia, axon, astrocyte, oligodendrocyte, glutamate, ATP Introduction W hite matter (WM) is defined as a tract of myelinated axons-WM appears opaque or dense due to the fatty myelin in anatomical sections and in brain scans. Notwithstanding this, myelination is not restricted to WM and is also critical to rapid communication and integration in grey matter (GM) areas, such as in axons in the cortical GM and hippocampus. Hence, many aspects of neurotransmitter signaling to be covered in this review have resonance in GM and higher cognitive function. Indeed, in the human brain WM is a prominent feature of the cerebral cortex, the seat of higher intelligence. Myelination of GM is also evident in rodents, but discrete WM tracts are not pronounced in the cerebral cortex. As a general concept, WM are simply concentrations of myelinated axons bundled together into tracts that interconnect areas of GM. The molecular physiology of myelinated axons will be very similar in WM and GM, and they will be subject to the same neurotransmitter signaling phenomena that is the subject of this review. The main cells associated with myelinated axons are the myelinating oligodendro...

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Receptor-mediated calcium signalling in glial cells from mouse corpus callosum slices

Cited by 72 publications

References 45 publications

ATP Released from Astrocytes Mediates Glial Calcium Waves

ATP Released from Astrocytes Mediates Glial Calcium Waves

2,3-Dihydroxy-6-Nitro-7-Sulfamoyl-Benzo(f)Quinoxaline Reduces Glial Loss and Acute White Matter Pathology after Experimental Spinal Cord Contusion

Neurotransmitter signaling in white matter

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