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Figure 7 | Molecular Pain

Figure 7

From: Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex

Figure 7

Proposed model for presynaptic Ap oa 1 in the synapse in the ACC from transgenic mice. Diagram showing that activation of presynaptic Ap oa1 leads to the production of cAMP. cAMP-related signaling pathways facilitate the glutamate release from presynaptic terminal. cAMP produced by activation of Ap oa1 in the presynaptic terminal may mimic the effects of cAMP produced by activation of presynaptic calcium-stimulated AC1 [30]. The released glutamate then acts on postsynaptic glutamate receptors, such as AMPA receptors (AMPAR) and NMDA receptors (NMDAR), and trigger the downstream signaling pathways. In the transgenic mice, Ap oa1 is preferentially expressed in the presynaptic terminal in the ACC.

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Molecular Pain

ISSN: 1744-8069

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