Neurotransmitter Receptors in Astrocytes

Verkhratsky, Alexei

doi:10.1007/978-0-387-79492-1_3

Cited by 23 publications

(22 citation statements)

References 147 publications

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“…Thus, neither a NMDA-receptor dependent component as described from cortical (Nolte et al, 2001;Lalo et al, 2006) and hippocampal astrocytes (Serrano et al, 2008), nor activation of other receptors expressed by astrocytes (Verkhratsky, 2009) did play an significant role in the generation of calcium transients evoked by our three-pulse stimulation paradigm.…”

Section: Evoked Calcium Signals In Astrocytesmentioning

confidence: 96%

Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

et al. 2010

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Glial cells respond to neuronal activity by transient increases in their intracellular calcium concentration. At hippocampal Schaffer collateral to CA1 pyramidal cell synapses, such activity-induced astrocyte calcium transients modulate neuronal excitability, synaptic activity, and LTP induction threshold by calcium-dependent release of gliotransmitters. Despite a significant role of astrocyte calcium signaling in plasticity of these synapses, little is known about activity-dependent changes of astrocyte calcium signaling itself. In this study, we analyzed calcium transients in identified astrocytes and NG2-cells located in the stratum radiatum in response to different intensities and patterns of Schaffer collateral stimulation. To this end, we employed multiphoton calcium imaging with the low-affinity indicator dye Fluo-5F in glial cells, combined with extracellular field potential recordings to monitor postsynaptic responses to the afferent stimulation. Our results confirm that somata and processes of astrocytes, but not of NG2-cells, exhibit intrinsic calcium signaling independent of evoked neuronal activity. Moderate stimulation of Schaffer collaterals (three pulses at 50 Hz) induced calcium transients in astrocytes and NG2-cells. Astrocyte calcium transients upon this three-pulse stimulation could be evoked repetitively, increased in amplitude with increasing stimulation intensity and were dependent on activation of metabotropic glutamate receptors. Activity-induced transients in NG2-cells, in contrast, showed a rapid run-down upon repeated three-pulse stimulation. Theta burst stimulation and stimulation for 5 min at 1 Hz induced synaptic potentiation and depression, respectively, as revealed by a lasting increase or decrease in population spike amplitudes upon three-pulse stimulation. Synaptic plasticity was, however, not accompanied by corresponding alterations in the amplitude of astrocyte calcium signals. Taken together, our results suggest that the amplitude of astrocyte calcium signals reflects the number of activated synapses but does not correlate with the degree of synaptic potentiation or depression at Schaffer collateral to CA1 pyramidal cell synapses.

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Section: Evoked Calcium Signals In Astrocytesmentioning

confidence: 96%

Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

et al. 2010

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“…Voltage-gated Ca 2+ channels (Parri et al, 2001) might mediate additional entry of Ca 2+ from the extracellular space that is utilized to trigger exocytotic glutamate release from astrocytes of ventrobasal thalamus. The role of the ionotropic transmitter receptors, which represent an additional entry of Ca 2+ in astrocytes [reviewed in [90]], in exocytotic glutamate release from astrocytes is intangible at the moment [reviewed in [75]].…”

Section: Amino Acids As Astrocytic Transmittersmentioning

confidence: 99%

Gliotransmission: Exocytotic release from astrocytes

Parpura

Zorec

2010

Brain Research Reviews

340

277

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Gliotransmitters are chemicals released from glial cells fulfilling a following set of criteria: i) they are synthesized by and/or stored in glia; ii) their regulated release is triggered by physiological and/or pathological stimuli; iii) they activate rapid (milliseconds to seconds) responses in neighboring cells; and iv) they play a role in (patho)physiological processes. Astrocytes can release a variety of gliotransmitters into the extracellular space using several different mechanisms. In this review, we focus on exocytotic mechanism(s) underlying the release of three classes of gliotransmitters: (i) amino acids, such as, glutamate and D-serine; (ii) nucleotides, like adenosine 5'-triphosphate; and (iii) peptides, such as, atrial natriuretic peptide and brain-derived neurotrophic factor. It is becoming clear that astrocytes are endowed with elements that qualify them as cells communicating with neurons and other cells within the central nervous system by employing regulated exocytosis.

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“…These receptors can be activated by synaptically released neurotransmitters, by "glio" transmitters, or by molecules diffusing in the brain extracellular space. 12 Among the receptors expressed on astrocytes are glutamate receptors, and both ionotropic and metabotropic receptors. Ionotropic glutamate receptors of the ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype made up of subunits GluR1 to GluR4 are found on astrocytes.…”

Section: Astrocyte Receptorsmentioning

confidence: 99%

Astrocytes and Epilepsy

2010

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Summary: Astrocytes form a significant constituent of seizure foci in the human brain. For a long time it was believed that astrocytes play a significant role in the causation of seizures. With the increase in our understanding of the unique biology of these cells, their precise role in seizure foci is receiving renewed attention. This article reviews the information now available on the role of astrocytes in the hippocampal seizure focus in patients with temporal lobe epilepsy with hippocampal sclerosis. Our intent is to try to integrate the available data. Astrocytes at seizure foci seem to not be a homogeneous population of cells, and in addition to typical glial fibrillary acidic protein, positive reactive astrocytes also include a population of neuron glia-2-like cells The astrocytes in sclerotic hippocampi differ from those in nonsclerotic hippocampi in their membrane physiology, having elevated Naϩ channels and reduced inwardly rectifying potassium ion channels, and some having the capacity to generate action potentials. They also have reduced glutamine synthetase and increased glutamate dehydrogenase activity. The molecular interface between the astrocyte and microvasculature is also changed. The astrocytes are also associated with increased expression of many molecules normally concerned with immune and inflammatory functions. A speculative mechanism postulates that neuron glia-2-like cells may be involved in creating a high glutamate environment, whereas the function of more typical reactive astrocytes contribute to maintain high extracellular Kϩ levels; both factors contributing to the hyperexcitability of subicular neurons to generate epileptiform activity. The functions of the astrocyte vascular interface may be more critical to the processes involved in epileptogenesis.

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Neurotransmitter Receptors in Astrocytes

Cited by 23 publications

References 147 publications

Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

Gliotransmission: Exocytotic release from astrocytes

Astrocytes and Epilepsy

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