Abstract:Glial-neuronal communication was studied by monitoring the effect of intercellular glial Ca 2ϩ waves on the electrical activity of neighboring neurons in the eyecup preparation of the rat. Calcium waves in astrocytes and Mü ller cells were initiated with a mechanical stimulus applied to the retinal surface. Changes in the light-evoked spike activity of neurons within the ganglion cell layer occurred when, and only when, these Ca 2ϩ waves reached the neurons. Inhibition of activity was observed in 25 of 53 neur… Show more
“…The effect of these activated glial cells on neurons has been assessed by recording the light-evoked spike activity of a nearby ganglion cell with an extracellular microelectrode (Newman and Zahs, 1998). We found that stimulated glial cells either enhance or depress light-evoked neuronal activity (Fig.…”
Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron-glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca 2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A 1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.
“…The effect of these activated glial cells on neurons has been assessed by recording the light-evoked spike activity of a nearby ganglion cell with an extracellular microelectrode (Newman and Zahs, 1998). We found that stimulated glial cells either enhance or depress light-evoked neuronal activity (Fig.…”
Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron-glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca 2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A 1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.
“…The bar at the bottom shows the repetitive light stimulus that evoked neuronal spiking. Reproduced with modification from Newman and Zahs (1998). Glial modulation of synaptic transmission by glutamate transport and release of D-serine.…”
Section: Future Directions and Implicationsmentioning
Glial modulation of synaptic transmission and neuronal excitability in the mammalian retina is mediated by several mechanisms. Stimulation of glial cells evokes Ca 2+ waves, which propagate through the network of retinal astrocytes and Müller cells and result in the modulation of the activity of neighboring ganglion cells. Light-evoked spiking is enhanced in some ganglion cells and depressed in others. A facilitation or depression of light-evoked excitatory postsynaptic currents is also seen in ganglion cells following glial stimulation. In addition, stimulation of glial cells evokes a sustained hyperpolarizing current in ganglion cells which is mediated by ATP release from Müller cells and activation of neuronal A 1 adenosine receptors. Recent studies reveal that light-evoked activity in retinal neurons results in an increase in the frequency of Ca 2+ transients in Müller cells. Thus, there is two-way communication between neurons and glial cells, suggesting that glia contribute to information processing in the retina.
“…Interestingly, mechanical stimulation of a single astrocyte leads to a propagating calcium wave involving both astrocytes and Muller cells in the intact adult retina. These glial waves modulate the firing rate of retinal neurons, presumably by release of glutamate from the glial cells (Newman and Zahs, 1998). …”
Section: Possible Physiologic Roles For Nachrs On Nonexcitable Cellsmentioning
ABSTRACT:The finding that neuronal nicotinic acetylcholine receptors (nAChRs) are present in nonneuronal cells both within and outside the nervous system raises some interesting issues. The mechanisms underlying receptor signaling and its downstream consequences in these cells remain to be elucidated. Factors controlling the release of acetylcholine and the extent of its diffusion are likely to be different for these cells than for traditional neuronal synapses. Recent advances on the physiologic functions of some of these cell types have provided a better insight into possible functional roles for nAChRs in nonexcitable cells. The presence of nAChRs on these cells also implies a broader scope for the actions of nicotine that needs to be considered from a clinical viewpoint. Revealing the potential physiologic roles for nAChRs on nonexcitable cells is likely to provide a more complete understanding of cholinergic signaling.
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