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Notes: Summary 1. From intracellular recordings from auditory receptors in locusts, confirmed by dye injection (Fig. 1), five distinct types of sustained or transient membrane potentials are identified that are associated with sensory function. 2. Receptor cell membranes are at resting potentials of 50–65 mV, inside negative, relative to a presumed potassium ion equilibrium potential of about -70 mV (Fig. 2). 3. Spontaneous and stimulus-evoked, discrete subthreshold depolarizations of up to about 5 mV are recorded (as described in the preceding paper) (Figs. 3, 9, 12). 4. Stimulus-evoked receptor potentials of up to about 20 mV and graded with stimulus intensity, result from the superposition of discrete depolarizations (as indicated in the preceding paper). In some of the cells recorded, there is pronounced adaptation in the receptor potential (Figs. 3, 4). 5. Regenerative (transient), depolarizing potentials of consistent, small amplitude (from 10 mV to 30 mV in any particular cell) occur spontaneously and/or in response to acoustic stimuli. Based on the inferred site of the generation of this class of spike, they are termed apical spikes (Figs. 5, 6, 7, 8). 6. The generation of apical spikes is membrane voltage-dependent. Their occurrence is reduced by hyperpolarization of the cell and increased by depolarization (Figs. 5, 6). 7. The apical spike potentials seem to be restricted to a region of the cell membrane. The conduction of the apical spike potential along the dendrite appears to be electrotonic. 8. Regenerative (transient) depolarizations of consistent, large amplitude (from 50 mV to 65 mV in any cell) occur spontaneously and/or in response to acoustic stimuli. Based on the inferred site of the generation of this class of spike, they are termed basal spikes (Fig. 9). 9. The generation of basal spikes is also membrane voltage-dependent. They are suppressed by hyperpolarization and are initiated by depolarization of the cell. Basal spike frequency is directly proportional to membrane depolarization (Figs. 2, 3). 10. Apical spikes appear normally to initiate basal spikes, with one to one correspondence. On occasions, the basal spike fails, evidently due to insufficient depolarization of the membrane by the apical spike (Figs. 7, 8). 11. Basal spikes appear to depend on conventional sodium ion (inward) and potassium ion (outward) currents via voltage-dependent conductance channels. The spiking mechanism is disabled by excessive depolarization of the cell. Spike potentials are abolished by extracellular application of the sodium conductance blocker, tetrodotoxin (TTX) (Fig. 4). Intracellular application of the potassium conductance blockers, tetraethylammonium ion (TEA) or caesium ion rapidly abolishes the hyperpolarizing undershoot on the action potentials (Fig. 10). 12. Within 1–2 min of injection of either TEA or caesium ion into receptor cells, all voltage-dependent and stimulus-dependent conductance mechanisms are disabled and the cell becomes unexcitable. In one case, this effect was reversed by about one hour after drug injection. 13. Intracellular recordings from some unidentified, unexcitable cells in M/:uller's organ reveal small amplitude (1–4 mV), transient and sustained potentials. The sustained potentials are negative going and adapting. The transient potentials are biphasic with the negative phase leading. In most cases, the relative amplitude of each phase of the transient potentials systematically varies with the amplitude of the sustained potential (Fig. 11). 14. By analogy with recordings from identified attachment cells in the crista acustica of tettigoniids and with transepithelial recordings from insect epidermal sensilla, the recordings of sensory events from unexcitable cells in Müller's organ are attributed to penetrations of attachment cells. 15. Based on these initial intracellular recordings from receptor cells, a proposal for the functional organization of the locust auditory sensillum is presented.