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Chunk #16 — RESULTS — Neither adenosine nor D-serine accounted for the enhancement of LTP by human glia

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Forebrain engraftment by human glial progenitor cells enhances synaptic plasticity and learning in adult mice.
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Astrocytes can also modulate excitatory transmission via their release of D-serine (Panatier et al., 2006; Yang et al., 2003). D-serine acts as an endogenous co-agonist of NMDA receptors and facilitates NMDA receptor activation, thereby potentiating the insertion of additional AMPA receptors into the post-synaptic membrane (Panatier et al., 2006; Yang et al., 2003). We tested the effect of adding D-serine to the bath of slices prepared from control mice. D-serine had no effects on the fEPSP slopes in accordance with previous reports (p=0.216, n=6) (Panatier et al., 2006; Yang et al., 2003). Moreover, neither D-serine nor immunolabeling for its synthetic enzyme, serine racemase, differed between human glial chimeric and uninjected control mice (Fig. S3D-E). These observations suggest that the lower threshold for induction of LTP in human glial chimerics was not a consequence of altered adenosine tone or increased glial release of D-serine.