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. 2016 Feb 24;115(5):2434–2445. doi: 10.1152/jn.00737.2015

Fig. 1.

Fig. 1.

Postinhibitory rebound (PIR) in the pyloric dilator (PD), medial gastric (MG), lateral pyloric (LP), gastric mill (GM), and lateral posterior gastric (LPG) neurons was blocked by 30 mM CsCl. Arrowheads show PIR after releasing from injecting 10-nA hyperpolarizing current. A1: the PIR was present in the PD neurons in the control condition. A2: the PIR was present in the PD neurons after application of 5 mM CsCl. A3: the PIR was blocked in the PD neurons after application of 30 mM CsCl. B1′ and B2′ are magnified images to show PIR in B1 and B2, respectively. B1 and B1′: the PIR was present in the MG neuron in the control condition and caused the temporary increase in burst duration and inraburst spike frequency. B2 and B2′: the PIR was present in the MG neuron after application of 5 mM CsCl and caused the temporary increase in burst duration and intraburst spike frequency. B3: the PIR was blocked in the MG neuron after application of 30 mM CsCl. C1: PIR was present in the control condition in the GM neurons. C2: PIR was present in the GM neurons after application of 5 mM CsCl. C3: the PIR was blocked in the GM neurons after application of 30 mM CsCl. D1: the PIR was present in the LPG neurons in the control condition. D2: the PIR was present in the LPG neurons after application of 5 mM CsCl. D3: the PIR was blocked in the LPG neurons after application of 30 mM CsCl. E1: the PIR was present in the LP neuron in the control condition. E2: PIR was blocked in the LP neuron after application of 30 mM CsCl. The number of trials (n) is indicated.