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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Copper signalling: causes and consequences

Fig. 4

Copper signaling via neuro-glia coupling. Astroglia, a previously neglected cell type of the brain [340], operate a variety of copper-dependent metabolic functions [6, 80, 240, 341, 342]. For this reason, in addition to synaptic and extrasynaptic copper signalling by way of excitatory/inhibitory receptors and ionic channels [22, 234, 235, 237,238,239,240,241,242,243,244, 246, 255, 336, 345,346,347,348,349,350,351,352,353,354,355,355], we place copper-dependent production of pAs in astrocytes [338] and correlated gap-junction modulation in the centre of this option. The proposed scheme conjectures activity-dependent changes of copper pools [179, 180] and polyamines (pAs), produced by CuAOs in astrocytes. First, an enhanced gap junction communication can be achieved by pAs [356,357,358], possibly promoting activity-dependent synchronization [339, 359]. Second, major inhibitory neurotransmitter gamma-aminobutyric acid (GABA) formed from pAs is released by astrocyte-specific GABA transporter [360]. Acting on its extrasynaptic receptor, GABA elevates tonic inhibition and enhances the fast (gamma band) neural oscillations [360]. These ways, the steady-state pA level in astrocytes determined by copper-dependent forming and consuming can be associated with neural circuit activity [244, 255, 362]

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