Endogenous N-acetylaspartylglutamate (NAAG) inhibits synaptic plasticity/transmission in the amygdala in a mouse inflammatory pain model.

NAAG peptidase inhibition blocked the development of mechanical allodynia in the injected hindpaw while the effect of ZJ43 failed to reach significance (p = 0.13) in the contralateral hindpaws at the 24 hr time point (Figure 1B ).

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In contrast to the control preparations, LY341495 alone appeared to increase eEPSC amplitude as might be expected if the antagonist blocked basal mGluR activation by endogenous NAAG, but this change did not reach statistical significance (Figure 7B and 7D , p = 0.15, n = 7, paired t-test).

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