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Figure 10 | Molecular Pain

Figure 10

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

Figure 10

Model of plasticity, mGluRs and NAAG in an inflammatory pain pathway of the mouse amygdala. In the CeLC region of the amygdala of control mouse brains, ZJ43 inhibits CGPII (glial enzyme) and GCPIII (neuronal and glial enzyme). As a consequence, it effectively elevates the levels of synaptically released NAAG. The peptide acts relatively selectively at the mGluR3 to mediate its inhibition of glutamate release consistent with data on the actions of this peptide in other systems [1].

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