scholarly journals Potassium activity in photoreceptors, glial cells and extracellular space in the drone retina: changes during photostimulation.

1979 ◽  
Vol 290 (2) ◽  
pp. 525-549 ◽  
Author(s):  
J A Coles ◽  
M Tsacopoulos
Keyword(s):  
Glial Cells ◽  
Extracellular Space

Ultrastructure of region of a low safety factor in inhomogeneous giant axon of the cockroach

1976 ◽  
Vol 39 (4) ◽  
pp. 900-908 ◽  
Author(s):  
M. Castel ◽  
M. E. Spira ◽  
I. Parnas ◽  
Y. Yarom
Keyword(s):  
Electron Microscopy ◽  
Glial Cells ◽  
Extracellular Space ◽  
Light And Electron Microscopy ◽  
Giant Axon ◽  
Serial Sections ◽  
Giant Axons ◽  
Chemical Synapses ◽  
Cytoplasmic Processes ◽  
Periaxonal Space

1. The structure of the ventral giant axons of the cockroach at the level of ganglion T3 was studied by means of light and electron microscopy. 2. From serial sections and cobalt injections, the axons diameter was found to range between 40 and 60 mum at the caudal end of ganglion T3; toward the center of T3 they narrow to 20-40 mum, and again expand to 30-45 mum anteriorly in ganglion T3. 3. Each giant axon sends off several branches, 1-15 mum in diameter, into the neuropil. The giant axons and the bases of their branches are enveloped by cytoplasmic processes of glial cells. The periaxonal space is about 100-200 A. 4. Distally the branches are devoid of glial envelopes and the extracellular space between the branches and other axonal profiles is about 200 A. Terminals with presumptive chemical synapses on the giant axon branches were found. Clear vesicles, 300-400 A in diameter, are seen clustered together. The width of the supposedly synaptic gap is about 100 A. 5. In some areas the branches and other axonal profiles form close appositions.

Effect of osmotic stress on potassium accumulation around glial cells and extracellular space volume in rat spinal cord slices

2001 ◽  
Vol 65 (2) ◽  
pp. 129-138 ◽  
Author(s):  
Lýdia Vargová ◽  
Alexandr Chvátal ◽  
Miroslava Anděrová ◽  
Šárka Kubinová ◽  
Drahomír Žiak ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Osmotic Stress ◽  
Glial Cells ◽  
Extracellular Space ◽  
Rat Spinal Cord ◽  
Potassium Accumulation ◽  
Space Volume

Regulation of Ambient GABA Levels by Neuron-Glia Signaling for Reliable Perception of Multisensory Events

2012 ◽  
Vol 24 (11) ◽  
pp. 2964-2993 ◽  
Author(s):  
Osamu Hoshino
Keyword(s):  
Glial Cells ◽  
Extracellular Space ◽  
Sensory Modality ◽  
Gabaergic Interneuron ◽  
Gain Function ◽  
Principal Cells ◽  
Ambient Gaba ◽  
The Cross ◽  
Multisensory Information ◽  
Stimulation Of

Activities of sensory-specific cortices are known to be suppressed when presented with a different sensory modality stimulus. This is referred to as cross-modal inhibition, for which the conventional synaptic mechanism is unlikely to work. Interestingly, the cross-modal inhibition could be eliminated when presented with multisensory stimuli arising from the same event. To elucidate the underlying neuronal mechanism of cross-modal inhibition and understand its significance for multisensory information processing, we simulated a neural network model. Principal cell to and GABAergic interneuron to glial cell projections were assumed between and within lower-order unimodal networks (X and Y), respectively. Cross-modality stimulation of Y network activated its principal cells, which then depolarized glial cells of X network. This let transporters on the glial cells export GABA molecules into the extracellular space and increased a level of ambient (extrasynaptic) GABA. The ambient GABA molecules were accepted by extrasynaptic GABAa receptors and tonically inhibited principal cells of the X network. Cross-modal inhibition took place in a nonsynaptic manner. Identical modality stimulation of X network activated its principal cells, which then activated interneurons and hyperpolarized glial cells of the X network. This let their transporters import (remove) GABA molecules from the extracellular space and reduced tonic inhibitory current in principal cells, thereby improving their gain function. Top-down signals from a higher-order multimodal network (M) contributed to elimination of the cross-modal inhibition when presented with multisensory stimuli that arose from the same event. Tuning into the multisensory event deteriorated if the cross-modal inhibitory mechanism did not work. We suggest that neuron-glia signaling may regulate local ambient GABA levels in order to coordinate cross-modal inhibition and improve neuronal gain function, thereby achieving reliable perception of multisensory events.

Neurotransmitters and Neurohormones

The Neuron ◽  
2015 ◽  
pp. 213-238
Author(s):  
Irwin B. Levitan ◽  
Leonard K. Kaczmarek
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Target Cell ◽  
Calcium Ions ◽  
Intercellular Communication ◽  
Extracellular Space ◽  
Presynaptic Terminal ◽  
Nerve Terminals ◽  
Transporter Proteins

A multitude of chemicals called neurotransmitters mediate intercellular communication in the nervous system. These include acetylcholine, the catecholamines, serotonin, glutamate, GABA, glycine, and a wide variety of neuropeptides. Although they exhibit great diversity in many of their properties, all are stored in vesicles in nerve terminals and are released to the extracellular space via a process requiring calcium ions. Their actions are terminated by reuptake into the presynaptic terminal or nearby glial cells by specific transporter proteins or by their destruction in the extracellular space. The role of neurotransmitters is to alter the properties—chemical, electrical, or both—of some target cell. With the arrival on the scene of the neuropeptides, it has become evident that signaling in the nervous system occurs through the use of rich and varied forms of chemical currency, and that some neurons use more than one type of currency simultaneously.

Preferential uptake of rubidium from extracellular space by glial cells compared to neurons in leech ganglia

1992 ◽  
Vol 577 (1) ◽  
pp. 64-72 ◽  
Author(s):  
Albert J. Saubermann ◽  
Carolyn M. Castiglia ◽  
Margaret C. Foster
Keyword(s):  
Glial Cells ◽  
Extracellular Space ◽  
Preferential Uptake

scholarly journals Neuronal activity drives pathway-specific depolarization of astrocyte distal processes

2021 ◽  
Author(s):  
Moritz Armbruster ◽  
Saptarnab Naskar ◽  
Jacqueline Garcia ◽  
Mary Sommer ◽  
Elliot Kim ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Glial Cells ◽  
Neuronal Activity ◽  
Extracellular Space ◽  
Membrane Dynamics ◽  
Neuronal Synapses ◽  
Neuron Interaction ◽  
Voltage Dependent ◽  
New Form ◽  
Activity Dependent

Astrocytes are glial cells that interact with neuronal synapses via their distal processes, where they remove glutamate and potassium (K+) from the extracellular space following neuronal activity. Astrocyte clearance of both glutamate and K+ is voltage-dependent, but astrocyte membrane potential (Vm) has been thought to be largely invariant. As a result, these voltage-dependencies have not been considered relevant to astrocyte function. Using genetically encoded voltage indicators enabling the measurement of Vm at distal astrocyte processes (DAPs), we report large, rapid, focal, and pathway-specific depolarizations in DAPs during neuronal activity. These activity-dependent astrocyte depolarizations are driven by action potential-mediated presynaptic K+ efflux and electrogenic glutamate transporters. We find that DAP depolarization inhibits astrocyte glutamate clearance during neuronal activity, enhancing neuronal activation by glutamate. This represents a novel class of sub-cellular astrocyte membrane dynamics and a new form of astrocyte-neuron interaction.

Deficient GABAergic Gliotransmission May Cause Broader Sensory Tuning in Schizophrenia

2013 ◽  
Vol 25 (12) ◽  
pp. 3235-3262 ◽  
Author(s):  
Osamu Hoshino
Keyword(s):  
Glial Cell ◽  
Glial Cells ◽  
Extracellular Space ◽  
Regulatory Mechanism ◽  
Intracortical Inhibition ◽  
Gaba Concentration ◽  
Principal Cells ◽  
Dynamic Cell ◽  
Ambient Gaba ◽  
Feature Stimulus

We examined how the depression of intracortical inhibition due to a reduction in ambient GABA concentration impairs perceptual information processing in schizophrenia. A neural network model with a gliotransmission-mediated ambient GABA regulatory mechanism was simulated. In the network, interneuron-to-glial-cell and principal-cell-to-glial-cell synaptic contacts were made. The former hyperpolarized glial cells and let their transporters import (remove) GABA from the extracellular space, thereby lowering ambient GABA concentration, reducing extrasynaptic GABAa receptor-mediated tonic inhibitory current, and thus exciting principal cells. In contrast, the latter depolarized the glial cells and let the transporters export GABA into the extracellular space, thereby elevating the ambient GABA concentration and thus inhibiting the principal cells. A reduction in ambient GABA concentration was assumed for a schizophrenia network. Multiple dynamic cell assemblies were organized as sensory feature columns. Each cell assembly responded to one specific feature stimulus. The tuning performance of the network to an applied feature stimulus was evaluated in relation to the level of ambient GABA. Transporter-deficient glial cells caused a deficit in GABAergic gliotransmission and reduced ambient GABA concentration, which markedly deteriorated the tuning performance of the network, broadening the sensory tuning. Interestingly, the GABAergic gliotransmission mechanism could regulate local ambient GABA levels: it augmented ambient GABA around stimulus-irrelevant principal cells, while reducing ambient GABA around stimulus-relevant principal cells, thereby ensuring their selective responsiveness to the applied stimulus. We suggest that a deficit in GABAergic gliotransmission may cause a reduction in ambient GABA concentration, leading to a broadening of sensory tuning in schizophrenia. The GABAergic gliotransmission mechanism proposed here may have an important role in the regulation of local ambient GABA levels, thereby improving the sensory tuning performance of the cortex.

Potential role of the glial water channel aquaporin-4 in epilepsy

2007 ◽  
Vol 3 (4) ◽  
pp. 287-297 ◽  
Author(s):  
Mike S. Hsu ◽  
Darrin J. Lee ◽  
Devin K. Binder
Keyword(s):  
Synaptic Transmission ◽  
Glial Cells ◽  
Extracellular Space ◽  
Functional Role ◽  
Potential Role ◽  
Water Channel ◽  
Aquaporin 4 ◽  
Membrane Channels ◽  
Human Epilepsy

AbstractRecent studies have implicated glial cells in novel physiological roles in the CNS, such as modulation of synaptic transmission, so it is possible that glial cells might have a functional role in the hyperexcitability that is characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors and transporters have all been associated with the epileptic state. This paper focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulating brain excitability and in epilepsy. We review studies of seizure phenotypes, K+ homeostasis and extracellular space physiology of mice that lack AQP4 (AQP4−/− mice) and discuss the human studies demonstrating alterations of AQP4 in specimens of human epilepsy tissue. We conclude with new studies of AQP4 regulation by seizures and discuss its potential role in the development of epilepsy (epileptogenesis). Although many questions remain unanswered, the available data indicate that AQP4 and its molecular partners might represent important new therapeutic targets.

Reduced glutamate uptake by retinal glial cells under ischemic/hypoxic conditions

1999 ◽  
Vol 16 (1) ◽  
pp. 149-158 ◽  
Author(s):  
GENEVIEVE A. NAPPER ◽  
MICHAEL J. PIANTA ◽  
MICHAEL KALLONIATIS
Keyword(s):  
Glial Cells ◽  
Extracellular Space ◽  
Glutamate Uptake ◽  
Müller Cells ◽  
Uptake System ◽  
Muller Cells ◽  
Rat Retina ◽  
Glutamate Neurotoxicity ◽  
High K ◽  
Isolated Rat

The high-affinity uptake of glutamate by glial cells and neurons of the central nervous system, including the retina, serves to inactivate synaptically released glutamate and maintains glutamate at low concentrations in the extracellular space. This uptake prevents accumulation of glutamate extracellularly and thus minimizes the possibility of glutamate neurotoxicity secondary to ischemic insult. One mechanism whereby glutamate neurotoxicity may occur in ischemic/hypoxic insult is through increased extracellular K+ reversing the electrogenic glutamate uptake into retinal glial (Müller) cells. We investigated glial uptake of the amino acids glutamate, GABA, and D-aspartate in the intact isolated rat retina under high extracellular K+ conditions and under conditions simulating ischemia. Immunocytochemical findings showed that uptake of glutamate and GABA by Müller cells in the intact isolated rat retina continues under conditions simulating ischemia and high extracellular K+ conditions, and uptake of D-aspartate also continues under high K+ conditions. However, under high K+ conditions, the glutamate uptake system saturates at a lower concentration of exogenous glutamate than in the normal K+ condition. These findings provide evidence that disruption of glutamate uptake by Müller cells is likely to be a significant contributing factor to excess glutamate accumulation in the extracellular space which can lead to neurotoxicity.

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