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. 2019 Jan 21;12:117. doi: 10.3389/fncir.2018.00117

Figure 3.

Figure 3

Co-transmission in the regulation of ingestion and egestion in the Aplysia feeding circuit. (A) Repeated stimulation of the cerebral buccal interneuron 2 (CBI-2) progressively induces the ingestive motor programs in Aplysia. The command neuron CBI-2 uses acetylcholine (Ach) as its fast-excitatory neurotransmitter onto the motor neurons B61/62. CBI-2 also co-localize the two neuropeptides feeding circuitry activating peptide (FCAP) and cerebral peptide 2 (CP-2). Both peptides are released by high frequency stimulation of CBI-2 and contributes to post-tetanic potentiation (PTP) of the fast-cholinergic transmission at the CBI-2 to B61/62 synapses, however by different mechanisms. CP-2 is acting presynaptically and FCAP postsynaptically. (A1) Recording traces showing the potentiation of the cholinergic EPSP by FCAP and CP-2 in B8. (B) Repeated stimulation of the esophageal nerve and high frequency stimulation of the interneuron B20 that co-localizes dopamine and γ-aminobutyric acid (GABA) induces egestion and a short-term potentiation of the fast dopaminergic EPSPs between B20 and the motor neuron B8. Dopamine acts on a 5-HT3-like receptor and GABA contributes to the potentiation of the B20 to B8 EPSP by a postsynaptic mechanism that involves activation a GABAB receptor of protein kinase C (PKC). (B1) High frequency stimulation of B20 potentiates the dopaminergic EPSPs in B8. GABA potentiated fast dopaminergic responses in B8 and the effect is blocked by the GABAB receptor antagonist phaclofen. Adapted from Koh et al. (2003), Koh and Weiss (2005) and Svensson et al. (2014).