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. 2016 Aug 24;36(34):8783–8789. doi: 10.1523/JNEUROSCI.1181-16.2016

Figure 2.

Figure 2.

GCPII antagonist slows synapse elimination. A, Model of glutamate production and induction of calcium level influx at the NMJ. The motor neuron terminal (gray) releases ACh and NAAG. GCPII on the Schwann cell (cyan) cleaves NAAG into NAA and glutamate. Glutamate then activates AMPA and NMDA receptors on the muscle (orange), leading to further calcium influx. B, Presynaptic expression of the enzyme GCPII during the period of synapse elimination. Whole mount of a P11 EDL muscle immunolabeled for GCPII, AChR, and terminal Schwann cells using the antibody GCP-04 against GCPII (green), rhodamine-α-bungarotoxin (red), and S100 against Schwann cells (blue). Scale bar, 25 μm. C, GCPII antagonist slows synapse elimination by reducing glutamate at the NMJ. Muscles treated with 2-PMPA-infused Elvax contained higher proportions of multiply innervated fibers than internal control muscles (EDL: 4 ± 1% control limb vs 15 ± 2% treated limb, p = 0.0004, n = 9, 10; soleus: 9 ± 2% control limb vs 26 ± 3% treated limb, p = 0.004, n = 11, 11). Scale bar, 50 μm.