. Astrocytes regulate GluR2 expression in motor neurons and their vulnerability to excitotoxicity. Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14825-30. PubMed.

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  1. Astrocytes are three times more abundant in brain than are neurons. They control the synaptic boutons of the neurons by controlling the amount of receptor in there (see Perea and Araque, 2007). Now these researchers discovered that astrocytes can control the number of GluR2. Taken together, the research suggests that in brain, astrocytes probably are doing some of the work that the cell matrix performs in other parts of the body. Now we need to study how astrocytes are doing that.

    SOD1 is an enzyme involved in oxidative stress. I suspect that astrocytes are controlling the oxidative stress in brain to save neurons from oxidative damage. Also, astrocytes probably perform some immune functions in brain. We published that astrocytes control the number of IL-1 receptors and the number of LPS receptors (TLR4). So I agree with this paper looking for astrocyte functions. I personally think astrocytes are even more important cells than are neurons. Neurons communicate with other cells, but astrocytes are also crucial to memory.

    References:

    . Involvement of TLR4/type I IL-1 receptor signaling in the induction of inflammatory mediators and cell death induced by ethanol in cultured astrocytes. J Immunol. 2005 Nov 15;175(10):6893-9. PubMed.

    . Chronic ethanol treatment enhances inflammatory mediators and cell death in the brain and in astrocytes. Brain Pathol. 2004 Oct;14(4):365-71. PubMed.

    . Ethanol-induced iNOS and COX-2 expression in cultured astrocytes via NF-kappa B. Neuroreport. 2004 Mar 22;15(4):681-5. PubMed.

    . Ceramide pathways modulate ethanol-induced cell death in astrocytes. J Neurochem. 2003 Dec;87(6):1535-45. PubMed.

    . Ethanol exposure affects glial fibrillary acidic protein gene expression and transcription during rat brain development. J Neurochem. 1997 Dec;69(6):2484-93. PubMed.

    . Oestradiol or genistein rescues neurons from amyloid beta-induced cell death by inhibiting activation of p38. Aging Cell. 2008 Jan;7(1):112-8. Epub 2007 Nov 21 PubMed.

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