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. Author manuscript; available in PMC: 2020 Aug 7.
Published in final edited form as: Neuron. 2019 Jun 17;103(3):432–444.e3. doi: 10.1016/j.neuron.2019.05.031

Figure 8. Model of Disynaptic Substance P Action in the NAcC.

Figure 8.

High-frequency activation with sustained depolarization of NAcC D1-MSNs causes release of substance P, activation of NK1Rs on ChAT neurons, and increased ChAT activity. Acetylcholine release is enhanced by increased ChAT activity activating M1Rs and a Gq-protein signaling cascade. G-protein activation of PLC putatively activates PIP2-IP3-IP3 receptor signaling, releasing calcium from internal stores promoting calcium-mediated insertion of calcium-permeable, GluR2-lacking AMPARs.