Glia: The many ways to modulate synaptic plasticity

Achour, Sarrah Ben; Pascual, Olivier

doi:10.1016/j.neuint.2010.02.013

Cited by 193 publications

(156 citation statements)

References 101 publications

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“…Upon activation, astrocytes are capable of expressing the full array of immune signaling and detection systems, such as cytokines and chemokines (Ben Achour and Pascual, 2010). However, the manner in which this pattern of expression changes from basal homeostasis to a fully reactive state remains to be fully described.…”

Section: A What Do Immunocompetent Cells Contribute Tomentioning

confidence: 99%

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

338

315

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Section: A What Do Immunocompetent Cells Contribute Tomentioning

confidence: 99%

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

338

315

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“…Glial cells, including astrocytes and microglia, are in charge of maintaining brain homeostasis, neuronal survival, and synaptic plasticity (Ben Achour and Pascual, 2010;Nave, 2010;Prinz and Mildner, 2011;Verkhratsky, 2010). Astrocytes are essential to neuronal survival as they: (i) provide nutrients and structural support for synapses, (ii) contribute to the integrity of the bloodbrain barrier, (iii) release molecules involved in neuronal survival and neurite formation, and by (iv) buffer excess potassium and neurotransmitters (Wang and Bordey, 2008).…”

Section: Introductionmentioning

confidence: 99%

The ribotoxin deoxynivalenol affects the viability and functions of glial cells

Razafimanjato

Benzaria

Taïeb

et al. 2011

Glia

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Glial cells are responsible for maintaining brain homeostasis. Modification of the viability and functions of glial cells, including astrocytes and microglia, are associated with neuronal death and neurological diseases. Many toxins (heavy metals, pesticides, bacterial or viral toxins) are known to impact on brain cell viability and functions. Although recent publications suggest a potential link between environmental exposure of humans to mycotoxins and neurological diseases, data regarding the effects of fungal toxins on brain cells are scarce. In the present study, we looked at the impact of deoxynivalenol (DON), a fungal ribotoxin, on glial cells from animal and human origin. We found that DON decreased the viability of glial cells with a higher toxicity against microglial cells compared with astrocytes. In addition to cellular toxicity, DON affected key functions of glial cells. Thus, DON caused a biphasic effect on the neuroinflammatory response of microglia to lipopolysaccharide (LPS), while sublethal doses of DON increased the LPS-induced secretion of TNF-α and nitric oxide, toxic doses inhibited it. In addition to affecting microglial functions, sublethal doses of DON also suppressed the uptake of L-glutamate by astrocytes. This inhibition was associated with a modification of the expression of the glutamate transporters at the plasma membrane. Our results suggest that environmental ribotoxins such as DON could, at low doses, cause modifications of brain homeostasis and possibly participate in the etiology of neurological diseases in which alterations of the glia are involved.

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“…Cortical astrocytes express norepinephrine transporters similar to those expressed by neurons (Inazu et al 2003;Takeda et al 2002), which contribute to terminate norepinephrine actions, influencing the efficacy (Gordon et al 2005) and plasticity (Achour and Pascual 2010;Inoue et al 2007) of synaptic transmission. Several psychoactive drugs exert their effects by blocking norepinephrine transporters (Axelrod et al 1961;Perry 1996), but the role of P2Y receptors in the regulation of glial norepinephrine transporters and its implication in the regulation of noradrenergic transmission has never been investigated.…”

mentioning

confidence: 99%

Purinergic modulation of norepinephrine release and uptake in rat brain cortex: contribution of glial cells

Pinho

Quintas

Sardo

et al. 2013

Journal of Neurophysiology

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Pinho D, Quintas C, Sardo F, Cardoso TM, Queiroz G. Purinergic modulation of norepinephrine release and uptake in rat brain cortex: contribution of glial cells. J Neurophysiol 110: 2580 -2591, 2013. First published September 11, 2013 doi:10.1152/jn.00708.2012.-The pathogenesis of psychiatric and neurodegenerative diseases is often associated with a deregulation of noradrenergic transmission. Considering the potential involvement of purinergic signaling in the modulation of noradrenergic transmission in the brain cortex, this study aimed to identify the P2Y receptor subtypes involved in the modulation of neuronal release and neuronal/glial uptake of norepinephrine. Electrical stimulation (100 pulses at 5 Hz) of rat cortical slices induced norepinephrine release that was inhibited by ATP and ADP (0.01-1 mM), adenosine 5=-O-(2-thiodiphosphate) (ADP␤S, 0.03-0.3 mM), and UDP (0.1-1 mM). The effect of ADP␤S was mediated by P2Y 1 receptors and possibly by A 1 /P2Y 1 heterodimers since it was attenuated by the A 1 receptor antagonist DPCPX and by the P2Y 1 receptor antagonist MRS 2500 but was resistant to the effect of adenosine deaminase (ADA). UDP inhibited norepinephrine release through activation of P2Y 6 receptors, an effect that was abolished by the P2Y 6 receptor antagonist MRS 2578 and by DPCPX, indicating that it depends on the formation and/or release of adenosine and activation of A 1 receptors. Supporting this hypothesis, the inhibitory effect of UDP was also prevented by inhibition of ectonucleotidases, by ADA and was attenuated by the inhibitor of nucleoside transporter 6-[(4-nitrobenzyl)thio]-9-␤-D-ribofuranosylpurine (NBTI). Additionally, the inhibitory effect of UDP was attenuated when norepinephrine uptake 1 or 2 was inhibited. In astroglial cultures, ADP␤S and UDP increased norepinephrine uptake mainly by activation of P2Y 1 and P2Y 6 receptors, respectively. The results indicate that neuronal and glial P2Y 1 and P2Y 6 receptors may represent new targets of intervention to regulate noradrenergic transmission in CNS diseases. adenosine receptors; P2Y receptors; glial norepinephrine uptake; glia-neuron communication

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Glia: The many ways to modulate synaptic plasticity

Cited by 193 publications

References 101 publications

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

The ribotoxin deoxynivalenol affects the viability and functions of glial cells

Purinergic modulation of norepinephrine release and uptake in rat brain cortex: contribution of glial cells

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