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1. Membrane potential and input resistance measurements were made from acinar cells of cat and rabbit submaxillary glands in vivo, using intracellular glass micro-electrodes.

2. The mean resting cell membrane potential was higher than previously reported, but ranged widely from -15 to -80 mV.

3. Single shock electrical stimulation of the parasympathetic nerve fibres evoked characteristic potential changes. In some cases monophasic hyperpolarizations, in others biphasic responses (depolarization — hyperpolarization) were observed.

4. The latency of the hyperpolarizing response was considerably longer (300-550 msec) than the latency of the biphasic response (about 150 msec).

5. Hyperpolarizing and biphasic responses could be observed in the same cell at different levels of membrane potential. The initial depolarization of the biphasic response was dependent on the magnitude of the resting potential in such a manner that it was very small or absent at the lowest potentials and increased gradually with increasing level of the resting potential.

6. Single-shock stimulation of the sympathetic nerve fibres to the gland did not evoke any response. In the cat, repetitive stimulation evoked hyperpolarizing or biphasic responses similar to those seen after repetitive stimulation of the parasympathetic nerve fibres. In the rabbit small hyperpolarizations were seen in a few cells only; mostly there was no response. Repetitive stimulation of the parasympathetic nerve fibres to the rabbit submaxillary gland evoked complex potential changes mostly of the depolarization—hyperpolarization type.

7. Both single shock and repetitive stimulation of the parasympathetic nerve fibres evoked marked reductions in cell input resistance. In the hyperpolarizing cell type the conductance change sometimes preceded the potential change whereas they always occurred simultaneously in the biphasic cell type.

8. It is concluded that both the hyperpolarizing and the biphasic secretory potentials are derived from the same type of acinar cells. The neurotransmitter released by the parasympathetic nerve endings (ACh) acts on the acinar cell membrane by increasing the ion permeability.