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![Presynaptic mechanisms at prefrontal synapses involved in persistent pain](https://image.oaes.cc/a07577a7-d5bb-4dcd-8f7d-4143dbe4151e/2825.fig.2.png)
Figure 2. Diagram of the potential mechanisms in presynaptic form of long-term potentiation (pre-LTP) in the anterior cingulate cortex (ACC). The presynaptic Ca2+ influx via Gluk1 KAR s leads to activation of the adenylyl cyclase 1 (AC1)-PKA pathway. Then cAMP binds to the HCN channel to increase its sensitivity and activates PKA to enhance the release of glutamate, presumably through activation of extracellular signal-regulated kinase (ERK). The enhanced PKA activity is likely to activate SCRAPPER and RIM1 to regulate vesicle recycling, which is required for pre-LTP in the ACC synapses. KAR: kainate receptor; PKA: protein kinase A; cAMP: cyclic adenosine monophosphate; HCN: hyperpolarization-activated cyclic nucleotide-gated