Metabolic Coupling and the Role Played By Astrocytes in Energy Distribution and Homeostasis

Medina, José M.; Giaume, Christian; Tabernero, Arantxa

doi:10.1007/978-1-4615-4685-6_28

Cited by 20 publications

(12 citation statements)

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“…(42), while AD patients show an hypometabolism (43). Even in these cases, it is noteworthy that AGJC could play a role since it has been proposed to contribute to the control of glutamate homeostasis, the propagation of intercellular calcium waves and the supply of metabolic substrates (44–46).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, glutamate uptake is impaired by IL-1β and TNF-α (38) and by Aβ (39), intercellular calcium signaling through gap junctions is reduced by IL-1β, while the ATPmediated component is increased (40) by IL-1β and by Aβ (41), and glucose utilization is stimulated by IL-1β and TNF-α (42), while AD patients show an hypometabolism (43). Even in these cases, it is noteworthy that AGJC could play a role since it has been proposed to contribute to the control of glutamate homeostasis, the propagation of intercellular calcium waves and the supply of metabolic substrates (44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

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Proinflammatory cytokines released from microglia inhibit gap junctions in astrocytes: potentiation by β‐amyloid

et al. 2006

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Brain inflammation is characterized by a reactive gliosis involving the activation of astrocytes and microglia. This process, common to many brain injuries and diseases, underlies important phenotypic changes in these two glial cell types. One characteristic feature of astrocytes is their high level of intercellular communication mediated by gap junctions. Previously, we have reported that astrocyte gap junctional communication (AGJC) and the expression of connexin 43 (Cx43), the main constitutive protein of gap junctions, are inhibited in microglia (MG)-astrocyte cocultures. Here, we report that bacterial lipopolysaccharide activation of microglia increases their inhibitory effect on Cx43 expression and AGJC. This inhibition is mimicked by treating astrocyte cultures with conditioned medium harvested from activated microglia. Interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were identified as being the main factors responsible for this conditioned medium-mediated activity. Interestingly, an inflammatory response characterized by MG activation and reactive astrocytes occurs in Alzheimer's disease, at sites of beta-amyloid (Abeta) deposits. We found that this peptide potentiates the inhibitory effect of a conditioned medium diluted at a concentration that is not effective per se. This potentiation is prevented by treating astrocytes with specific blockers of IL-1beta and TNF-alpha activities. Thus, the suppression of communication between astrocytes, induced by activated MG could contribute to the proposed role of reactive gliosis in this neurodegenerative disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Proinflammatory cytokines released from microglia inhibit gap junctions in astrocytes: potentiation by β‐amyloid

et al. 2006

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“…Moreover, inhibition of GJIC in astrocytes by various compounds, including octanol, glyccyrhetinic acid, arachidonic acid, endothelins, increases glucose uptake in astrocytes (Tabernero et al, 1996). Thus, the combination of inhibiting glucose intercellular permeability and increasing its uptake in astrocytes may result in the formation of glial "hotspots" characterized by high concentrations of metabolic substrates in defined astrocyte subpopulations (Medina et al, 1999).…”

Section: Traffıcking and Supply Of Energy-producing Substrates To Neumentioning

confidence: 99%

Gap junctions and connexin expression in the normal and pathological central nervous system

Rouach¹,

Avignone²,

Même³

et al. 2002

Biology of the Cell

308

257

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Gap junctions are widely expressed in the various cell types of the central nervous system. These specialized membrane intercellular junctions provide the morphological support for direct electrical and biochemical communication between adjacent cells. This intercellular coupling is controlled by neurotransmitters and other endogenous compounds produced and released in basal as well as in pathological situations. Changes in the expression and the function of connexins are associated with number of brain pathologies and lesions suggesting that they could contribute to the expansion of brain damages. The purpose of this review is to summarize data presently available concerning gap junctions and the expression and function of connexins in different cell types of the central nervous system and to present their physiopathological relevance in three major brain dysfunctions: inflammation, epilepsy and ischemia.

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“…Astrocytes maintain homeostasis of the neural environment through extensive coupling to other glial cells and neurons to form "functional syncytia" capable of distributing metabolites and propagating signaling molecules and ions (Medina et al, 1999;Verkhratsky and Toescu, 2006). Thus, altered astrocytic function may have pivotal effects on CNS dysfunction in general and neural inflammation in particular.…”

Section: Introductionmentioning

confidence: 99%

Magnetic cell sorting: A fast and effective method of concurrent isolation of high purity viable astrocytes and microglia from neonatal mouse brain tissue

Marek

Caruso

Rostami

et al. 2008

Journal of Neuroscience Methods

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Metabolic Coupling and the Role Played By Astrocytes in Energy Distribution and Homeostasis

Cited by 20 publications

References 54 publications

Proinflammatory cytokines released from microglia inhibit gap junctions in astrocytes: potentiation by β‐amyloid

Proinflammatory cytokines released from microglia inhibit gap junctions in astrocytes: potentiation by β‐amyloid

Gap junctions and connexin expression in the normal and pathological central nervous system

Magnetic cell sorting: A fast and effective method of concurrent isolation of high purity viable astrocytes and microglia from neonatal mouse brain tissue

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