The involvement of nonspiking cells in long-term potentiation of synaptic transmission in the hippocampus

Sastry, B.R.; Goh, Joanne W.; May, P. B. Y.; Chirwa, S.S.

doi:10.1139/y88-135

Cited by 20 publications

(8 citation statements)

References 13 publications

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“…Thus, the bursting behavior (and concomitant release of glutamate) observed after LTD induction in the presence of cesium might have caused an increased efficacy of synaptic potential generation, masking, or overlapping with the previously developed LTD. This interpretation of our results leads to the conclusion that under impaired glial function, and after even modest elevation in [K ϩ ] out , stimulation paradigms normally used to elicit LTD might result in long-term potentiation of synaptic activity (see also Sastry et al, 1988).…”

Section: Effects Of Cesium On Synaptic Plasticitysupporting

confidence: 72%

Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

et al. 1997

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Extracellular cesium causes synchronous, interictal-like bursting and prevents maintenance of long-term depression (LTD) in the CA1 hippocampal region. We have investigated the cellular mechanisms underlying cesium actions. Whole-cell recordings showed that brief (2 min) bath exposures to cesium caused pyramidal cell hyperpolarization associated with decreased membrane conductance attributable to blockade of an inward h-type current. After prolonged (Ͼ2 min) exposures, a late depolarizing response was observed; this effect was not associated with changes in cell membrane conductance. Recordings from interneurons revealed that I h is expressed in a subpopulation of cells and that cesium effects on interneurons expressing I h are comparable to those observed in pyramidal cells. Consistent with this effect, cesium decreased the early component of the IPSP recorded in pyramidal cells. Interneurons lacking I h were not affected by cesium but developed a depolarizing response when drug applications were paired to orthodromic stimulation. We concluded that cesium actions on LTD and cesium-induced epileptiform activity were not attributable exclusively to its direct effects on neurons. Recordings from hippocampal slice astrocytes revealed that cesium interfered with glial electrical responses during LTD induction. Cesium blocked glial inwardly rectifying potassium channels and increased the amplitude and duration of stimulation-evoked [K ϩ ] out increases. Thus, the effects of cesium on CA1 synchronization and synaptic plasticity appear to be mediated predominantly by blockade of glial voltage-dependent potassium uptake.

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Section: Effects Of Cesium On Synaptic Plasticitysupporting

confidence: 72%

Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

et al. 1997

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“…Previous in vivo and brain slice studies have reported activity in nonspiking cells (Ransom, 1974;Casullo and Kmjevic, 1987;Sastry et al, 1988) that was in synchrony with adjacent neurons. These nonspiking cells were assumed to @.z glia, even though in most of these studies it was not possible to identify them definitively as astrocytes.…”

Section: Discussionmentioning

confidence: 94%

Rapid communication between neurons and astrocytes in primary cortical cultures

et al. 1993

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The identification of neurotransmitter receptors and voltage-sensitive ion channels on astrocytes (reviewed by Barres, 1991) has renewed interest in how these cells respond to neuronal activity. To investigate the physiology of neuron astrocyte signaling, we have employed primary cortical cultures that contain both neuronal and glial cells. As the neurons in these cultures exhibit synchronous spontaneous synaptic activity, we have used both calcium imaging and whole-cell recording techniques to identify physiological activity in astrocytes related to neuronal activity. Whole-cell voltage-clamp records from astrocytes revealed rapid inward currents that coincide with bursts of electrical activity in neighboring neurons. Calcium imaging studies demonstrate that these currents in astrocytes are not always associated with slowly propagating calcium waves. Inclusion of the dye Lucifer yellow within patch pipettes confirmed that astrocytes are extensively coupled to each other but not to adjacent neurons, indicating that the currents observed are not due to gap junction connections between these cell types. These currents do not reflect widespread diffusion of glutamate or potassium released during neuronal activity since a population of small, round, multipolar presumed glial cells that are not dye coupled to adjacent cells did not display electrical currents coincident with neuronal firing, even though they respond to locally applied glutamate and potassium. These findings indicate that, in addition to the relatively slow signaling conveyed by calcium waves, astrocytes also display rapid electrical responses to neuronal activity.

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“…This raises the question of whether stimulation of astrocytic metabotropic glutamate receptors is involved in LTP. Although astrocytic involvement in hippocampal LTP has been reported previously (Sastry et al, 1988(Sastry et al, , 1990) and inhibition of astrocytic metabolism disrupts hippocampal synaptic transmission (Keyser and Pellmar, 1994), more experiments are needed to determine what role if any astrocytes play in LTP. In summary, our results indicate that hippocampal astrocytes in situ respond to the neuronal release of glutamate with increases in [Ca 2ϩ ] i .…”

Section: Are Astrocytes Involved In Long-term Potentiation?mentioning

confidence: 99%

Hippocampal AstrocytesIn SituRespond to Glutamate Released from Synaptic Terminals

1996

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A long-standing question in neurobiology is whether astrocytes respond to the neuronal release of neurotransmitters in vivo. To address this question, acutely isolated hippocampal slices were loaded with the calcium-sensitive dye Calcium Green-1 and the responses of the astrocytes to electrical stimulation of the Schaffer collaterals were monitored by confocal microscopy. To confirm that the responsive cells were astrocytes, the slices were immunostained for the astrocytic marker glial fibrillary acidic protein. Stimulation of the Schaffer collaterals (50 Hz, 2 sec) resulted in increases in the concentration of intracellular calcium ([Ca 2ϩ ] i ) in the astrocytes located in the stratum radiatum of CA1. The astrocytic responses were blocked by the sodium channel blocker tetrodotoxin, the voltage-dependent calcium channel blocker -conotoxin-MVIIC, and the selective metabotropic glutamate receptor antagonist ␣-methyl-4-carboxyphenylglycine (MCPG). These results suggest that the astrocytic responses were induced by stimulation of metabotropic glutamate receptors on the astrocytes by neuronally released glutamate. The astrocytic responses to neuronal stimulation were enhanced in the presence of the K ϩ channel antagonist 4-aminopyridine (4-AP). Inhibition of the astrocytic responses in the presence of 4-AP required the presence of both MCPG and the ionotropic glutamate receptor antagonist kynurenic acid. These results suggest that higher levels of neuronal activity result in stimulation of both metabotropic and ionotropic glutamate receptors on the astrocytes. Overall, the results indicate that hippocampal astrocytes in situ are able to respond to the neuronal release of the neurotransmitter glutamate with increases in [Ca 2ϩ ] i .

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The involvement of nonspiking cells in long-term potentiation of synaptic transmission in the hippocampus

Cited by 20 publications

References 13 publications

Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

Rapid communication between neurons and astrocytes in primary cortical cultures

Hippocampal AstrocytesIn SituRespond to Glutamate Released from Synaptic Terminals

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The involvement of nonspiking cells in long-term potentiation of synaptic transmission in the hippocampus

Cited by 20 publications

References 13 publications

Reduction of K+Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

Reduction of K+Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

Rapid communication between neurons and astrocytes in primary cortical cultures

Hippocampal AstrocytesIn SituRespond to Glutamate Released from Synaptic Terminals

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Product

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Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity

Reduction of K⁺Uptake in Glia Prevents Long-Term Depression Maintenance and Causes Epileptiform Activity