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In Locsta mButria Onratiiides R. and

Intracellular recordings were made from the auditory interneurons ON1, AN1 and AN2 in the prothoracic ganglion of the cricket Gryllus bimaculatus. Their responses to synthesized calling song (carrier frequency 5 kHz, intensity 40-90 dB SPL), presented monaurally and binaurally via legphones (acoustic trachea cut), were recorded (Fig. 2). These data were then analysed to determine the strength of inhibitory coupling of ON1-ON1, ON1-ANI and ON1-AN2 (Fig. 3). Inhibitory coupling of ON1-ON1 and ON1-AN1 are relatively independent of stimulus intensity, ON1-ON1 =-0.25 to -0,4 ap ONla/a p ON1 b ; ON1-AN1 =-0.4 to -0.55 ap AN1/ap ONlcontra. The inhibition of AN2 by ON1 is rather ineffective, maximally -0.13ap AN2/ap ONlcontra. The leftright contrast enhancement or gain, due to lateral inhibition via omega neurons, is 1.6-1.9 for the ON1 pair and 2-3.4 for the AN1 pair, over most of the relevant sound intensity range. For the AN2 pair, there is little contrast enhancement except at sound intensities > 80 dB SPL (Table 1).The above data on auditory information processing in the prothoracic ganglion was incorporated into a simple model of the neural events underlying phonotactic behavior. This model included typical peripheral auditory directionality and simple assumptions about how phonotactic turns are generated. Predictions generated by the model include: a) the enhancement in directional sensitivity of AN1 and AN2 provided by lateral inhibition (Fig. 4). b) The effects on open-and closed-loop phonotactic behavior, of inactivating AN1 or AN2 (Fig 5). c) The effects of inactivating one ON1 on the directional sensitivity of left and right AN1 (Fig. 6), and the consequent effects on phonotactic behavior (Fig. 7) Several of these predictions agree well with currently available ex-G. Horseman ([5~) 1 -E Huber perimental data, others constitute hypotheses for testing in future experiments.

Intracellular recordings were made in the brain of the cricket Gryllus bimaculatus from an ascending auditory interneuron (AN1). Acoustic stimuli with calling song temporal pattern were delivered via earphones in a preparation with the "acoustic" trachea cut (attenuation of crossing sound >30 dB). The input-output function of this cell was then determined by recording its responses to stimulation of the ipsilateral ear alone, of the contralateral ear alone and to stimulation of both ears simultaneously with the same or different carrier frequencies and intensities.This interneuron was excited by the ear ipsilateral to its axon and dendritic field and unresponsive to stimuli presented to the axon-contralateral ear alone. However, in binaural stimulation experiments, the response to a constant ipsilateral stimulus was progressively reduced as the intensity of a simultaneous contralateral stimulus was increased, above a threshold intensity.Tuning curves for threshold of this inhibition, determined in binaural stimulation experiments, indicated significant inhibition in the range 3-20 kHz with lowest threshold at 4-5 kHz. The inhibition was unaffected by sectioning of the contralateral circumoesophageal or neck connective, indicating that the inhibitory influence crosses the midline at the level of the prothoracic ganglion. Intracellular recordings from AN1 in the prothoracic ganglion confirmed that it was indeed neurally inhibited by inputs from the contralateral ear.Tuning curves for excitation of an omega neuron (ON1) by the ear ipsilateral to its soma and also the tuning of inhibition of ONI by its contralateral ON1 part-ner, closely match the tuning of inhibition of AN1 and to a lesser extent, of AN2. This was taken as evidence that each AN1 is inhibited by the 'contralateral' ON1. The significance of this interaction for directional hearing and phonotaxis is discussed.