Figure 1.

(A) IJPs recorded in smooth muscle of the atropinized guinea pig taenia coli in response to transmural stimulation of the intramural nerves remaining following degeneration of the adrenergic nerves by treatment of the animal with 6-hydroxydopamine (250 mg·kg⁻¹ i.p. for 2 successive days) 7 days previously. Upper trace, mechanical record. Lower trace, changes in membrane potential recorded with a sucrose-gap method. The junction potentials recorded with this method are qualitatively, but not quantitatively, similar to those recorded with intracellular microelectrodes. Top left-hand panel: responses to low-frequency stimulation (l s⁻¹). Note the long latency and slow time course of individual IJPs, and rebound excitation (spike and contraction) following cessation of stimulation. Top right-hand panel: response to a stimulation frequency of 3 s⁻¹. Note of the summation of individual IJPs and rebound contraction. Bottom panel: response of a spontaneously active preparation to stimulation at 4 s. Note that the hyperpolarization maintained during repetitive stimulation raises the membrane potential beyond the zone of spontaneous initiation of action potentials and leads to relaxation. Rebound contraction follows cessation of stimulation. [Reproduced from Burnstock (1972), with permission from ASEPT.] (B) Sucrose gap recording of membrane potential changes in smooth muscle of guinea pig taenia coli in the presence of atropine (0.3 µM) and guanethidine (4 µM). Transmural field stimulation (0.5 ms, 0.033 Hz, 8 V) evoked transient hyperpolarizations, which were followed by rebound depolarizations. Tetrodotoxin (TTX, 3 µM) added to the superfusing Kreb's solution (applied at arrow) rapidly abolished the response to transmural field stimulation establishing these as inhibitory junction potentials in response to non-adrenergic, non-cholinergic neurotransmission. [Reproduced from Burnstock (1986), reproduced with kind permission of Blackwell Publishing.]