fig2

Presynaptic mechanisms at prefrontal synapses involved in persistent pain

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

Neuroimmunology and Neuroinflammation
ISSN 2349-6142 (Online) 2347-8659 (Print)

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