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Fig. 10. Blocking extracellular peptidase-mediated degradation of CabTRP Ia prolongs the actions of the POC neurons. (A) Before, during and after superfusion of the endopeptidase inhibitor phosphoramidon (10^–5 mol l^–1) to the CoGs, CPN2 was weakly active before poc stimulation and LG was silent (left panel: top, middle, bottom). CPN2 activity was monitored with an intra-axonal recording near the entrance to the STG (Beenhakker and Nusbaum, 2004). 30 s after poc stimulation (15 Hz, 15 s), the gastric mill rhythm was triggered (as indicated by the rhythmic LG bursting) and CPN2 activity was strengthened (middle panel: top, middle, bottom). 90 s after poc stimulation, the gastric mill rhythm had terminated and CPN2 activity had subsided during saline superfusion, both before and after phosphoramidon application (right panel: top, bottom). By contrast, 90 s after poc stimulation during phosphoramidon superfusion, CPN2 activity remained strong and the gastric mill rhythm persisted. (B) (Left) There was a significant increase in the duration of LG bursting after poc stimulation in the presence of phoshoramidon (Phos., 10^–5 mol l^–1; P<0.05, N=5), compared with its bursting duration in saline before phosphoramidon application (Ctl.). (Right) By contrast, phosphoramidon (10^–5 mol l^–1) did not alter the duration of LG bursting after stimulation of the proprioceptor sensory GPR neuron. Most hyperpolarized membrane potentials: CPN2_stn, –73 mV; LG, –63 mV.

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