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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Neurogastroenterol Motil. 2013 Jan 2;25(2):e101–e113. doi: 10.1111/nmo.12059

Figure 5.

Figure 5

In the presence of L-NNA and apamin, stretch-dependent excitatory responses are revealed. (A) Shows electric, mechanical and length ramp, respectively in the presence of L-NNA (100 μM) and apamin (0.3 μM), application of length ramps produced membrane depolarization and increase in phasic motor activity. The depolarization (dashed line in A) and increase in phasic mechanical activity in response to stretch was partially inhibited by atropine (B), suggesting that cholinergic motor input contributed to part of the excitatory response observed in the presence of L-NNA and apamin. Neurokinin release from enteric motor nerves contributes to depolarization response. (C) Shows depolarization in membrane potential (dashed line) and increase in electrical activity in response to an active stretch ramp, observed in the presence of L-NNA (100 μM), apamin (0.1 μM) and atropine (1 μM). (D) Shows membrane depolarization (dashed line) in response to stretch was significantly attenuated by the NK1 and NK2 receptor antagonists GR 82334 (1 μM) and SR 48968 (1 μM).