Glial potassium channels activated by neuronal firing or intracellular cyclic AMP in Helix.

Gommerat, I; Gola, Maurice

doi:10.1113/jphysiol.1996.sp021623

Cited by 14 publications

(10 citation statements)

References 39 publications

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“…6 A3,A4 ). This result is consistent with the facts that K ϩ channels are abundant on astrocytes in the SON (Armstrong et al, 2005), and burst firing can activate membrane K ϩ channels on neighboring astrocytes (Gommerat and Gola, 1996). K ϩ channel activity is closely associated with water transportation.…”

Section: Suckling-evoked Gfap Reexpansion By Transiently Increasing Esupporting

confidence: 79%

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Wang¹,

Hatton²

2009

J. Neurosci.

123

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Astroglial-neuronal interactions are important in brain functions. However, roles of glial fibrillary acidic protein (GFAP) in this interaction remain unclear in acute physiological processes. We explored this issue using the supraoptic nucleus (SON) in lactating rats. At first, we identified the essential role of astrocytes in the milk-ejection reflex (MER) by disabling astrocytic functions via intracerebroventricular application of L-aminoadipic acid (L-AAA). L-AAA blocked the MER and reduced GFAP levels in the SON. In brain slices, L-AAA suppressed oxytocin (OT) neuronal activity and EPSCs. Suckling reduced GFAP in immunocytochemical images and in Western blots, reductions that were partially reversed after the MER. OT, the dominant hormone mediating the MER, reduced GFAP expression in brain slices. Tetanus toxin suppressed EPSCs but did not influence OT-reduced GFAP. Protease inhibitors did not influence OT-reduced GFAP images but blocked the degradation of GFAP molecules. In the presence of OT, transient 12 mM K ϩ exposure, simulating effects of synchronized bursts before the MER, reversed OT-reduced GFAP expression. Consistently, suckling first reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K ϩ channels. Moreover, GFAP molecules were associated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine racemase. GFAP-aquaporin 4 association decreased during initial suckling and increased after the MER, whereas opposite changes occurred between GFAP and actin. MER also decreased the association between GFAP and glutamine synthetase. These results indicate that suckling elicits dynamic glial neuronal interactions in the SON; GFAP plasticity dynamically reflects OT neuronal activity.

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Section: Suckling-evoked Gfap Reexpansion By Transiently Increasing Esupporting

confidence: 79%

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Wang¹,

Hatton²

2009

J. Neurosci.

123

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“…However, when we applied IBMX (100 M) to control for this effect, we observed no change in the extent of EP cell migration (data not shown). Because IBMX and caffeine have generally been found to have similar membrane permeabilities (Kehoe, 1990;Usachev et al, 1995;Gommerat and Gola, 1996), this observation supports our conclusion that the effect of caffeine on EP cell migration resulted from the release of intracellular Ca 2ϩ . causes a concentrationdependent inhibition of migration.…”

Section: Effects Of Calcium Manipulations On Migrationsupporting

confidence: 78%

G Protein-Mediated Inhibition of Neuronal Migration Requires Calcium Influx

Horgan

Copenhaver

1998

J. Neurosci.

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Neuronal migration is an essential feature of the developing nervous system, but the intracellular signaling mechanisms that regulate this process are poorly understood. During the formation of the enteric nervous system (ENS) in the moth Manduca sexta, the migration of an identified set of neurons (the EP cells) is regulated in part by the heterotrimeric guanyl-nucleotide binding protein (G protein

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“…These authors reported that thrombin, which is likely to enter the retina during a breakdown of the blood-brain barrier, inhibited K IR through a rise in intracellular [Ca 2ϩ ]. Gommerat and Gola (1996; Fig. 4) succeeded in demonstrating activation of K IR channels in satellite glial cells in Helix pomatia when the underlying neuron was depolarized.…”

Section: Modulation Of K E Muffling Modulation Of K ؉ Conductancementioning

confidence: 89%

“…The inset diagram of the cells shows the experimental design. (Taken with permission from Gommerat and Gola, 1996). homeostasis requires very little energy, its requirements might be comfortably met by glycolysis alone (Fig.…”

Section: Implications For Glial Cell Energy Metabolismmentioning

confidence: 99%

Potassium homeostasis and glial energy metabolism

Amédée

Robert²,

Coles

1997

Glia

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Since capillaries appear not to contribute significantly to rapid removal of K+ from brain tissue, the K+ released into extracellular clefts by neurons at the onset of electrical activity is presumably removed either by redistribution in the clefts or by uptake into cells. What appear to be the three major processes require no energy from the glial cells. These are diffusion through the extracellular clefts, spatial buffering by glial cells, and net uptake of K+ into glial cells through glial K+ channels associated with uptake of Cl−through an independent Cl‐ conductance. There is a relatively slow uptake by the Na+/K+‐ATPase, which directly consumes ATP. In addition, some glial cells take up K+ on the Na+/K+/2Cl‐ cotransporter, which leads indirectly to energy consumption when the Na+ is subsequently pumped out. Currently available data suggest that the glial energy metabolism devoted to K+ homeostasis is less than a tenth of the total tissue energy metabolism, even under conditions of pathologically high extracellular [K+]. Hence, in situ, it is possible that glial cells could function with much less ATP than neurons do. All the various routes of muffling of changes in extracellular [K+] can be modulated, directly or indirectly, by transmitters liberated by neurons. A consequence of this could be regulation of the entry of Na+ into glial cells such that the Na+/K+‐ATPase is activated. The degree of activation might be adjusted so that the resulting activation of the glial glycolytic pathway is appropriate to the provision of the quantity of metabolic substrates required by the neurons. GLIA 21:46–55, 1997. © 1997 Wiley‐Liss, Inc.

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Glial potassium channels activated by neuronal firing or intracellular cyclic AMP in Helix.

Cited by 14 publications

References 39 publications

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

Astrocytic Plasticity and Patterned Oxytocin Neuronal Activity: Dynamic Interactions

G Protein-Mediated Inhibition of Neuronal Migration Requires Calcium Influx

Potassium homeostasis and glial energy metabolism

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