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Within the brain, glycogen and glycogen phosphorylase activity are each confined to astrocytes (Pfeiffer-Guglielmi et al.PMID:32695810 , 2003). Although astrocytes usually are not excitable cells, they may be critically involved in the uptake from the excess K+ released inside the extracellular space by neurons through action and synaptic potentials (Hertz et al., 2007). These astrocytic competences, namely glycogenolysis and K+ uptake, happen to be recently shown to become functionally linked. In cultured and tissue slice astrocytes, glycogen was found to fuel particularly K+ uptake (Choi et al., 2012; Xu et al., 2013). Importantly, the astrocytic uptake of K+ was abolished by inhibiting glycogenolysis employing the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-d-arabinitol (DAB) (Xu et al., 2013). Here we describe the regulatory mechanisms which are anticipated to couple K+ uptake with glycogen mobilization inCorrespondence to: Mauro DiNuzzo, Ph.D., Magnetic Resonance for Brain Investigation Laboratory, Fondazione Santa Lucia IRCCS, By way of.
