Rhodopsin, the light-transducing protein that underpins vision, was discovered 65 years ago. Olfactory and gustatory transduction channels have now also been identified and the function of the sensory neurons in which they operate elaborated. In contrast, the identification of mechanosensory ion channels that underpin the senses of touch, hearing and proprioception has proved more problematic. Mechanosensory neurons bear multiple transduction ion channels, whose expression is scarce, and function depends on many other proteins. Stretch-sensitive neurons of insects (so-called chordotonal organs) have emerged as a useful tool to identify candidate mechanotransduction channels and understand cellular mechanotransduction in general (Kernan, 2007). Despite such progress, it is not known how mechanotransduction operates in insect chordotonal organs, and the identity of the mechanotransduction channels is still unclear. At their apical end, insect stretch-sensitive neurons have a mechanosensory cilium, atop a dendrite. At their basal end an axon carries action potentials to synaptic terminals in the thoracic ganglia. We have developed whole-cell patch-clamp recordings in the Muller’s organ of the locust ear to study the mechanotransduction current and its encoding into action potentials. We dissected out the oval-shaped tympanal ear and placed it within a hole of a divided petri dish. The inside of the tympanum was perfused in saline and the outside was stimulated using a loudspeaker. Mechanosensory neurons were visualised for patch-clamp recordings with a water-immersion objective using differential interference contrast optics. We acoustically stimulated the ear and, in conjunction with voltage- and current-clamp protocols and pharmacology, recorded the transduction current and two distinct spike types which, due to their inferred position of generation, are denoted as apical spikes and basal spikes (Hill, 1983). To confirm the sodium-selectivity of both apical and basal spikes we changed from perfusion with normal sodium (213 mM Na+) to low sodium solution (7 mM Na+), which significantly decreased the amplitude of the basal spikes from 3.7 ± 2.2 to 0.9 ± 0.5 nA (mean ± standard deviation, n=10) and apical spikes from 1.3 ± 0.5 to 0.6 ± 0.4 nA (n=9) before abolishing spike generation altogether (spikes recovered after washout: p<0.05, ANOVA) (Figure 1). We blocked both spike types with the sodium channel blocker tetrodotoxin, as found previously by Hill (1983). Current injection into the soma revealed that both spike types were voltage-dependent (Figure 2). This work provides the basis for understanding how mechanotransduction operates in the sensory neurons of chordotonal organs. We are currently using antagonists and agonists of candidate mechanotransduction ion channels to identify their involvement in passing the transduction current.