Echolocating bats use the time from biosonar pulse emission to the arrival of echo (defined as echo delay) to calculate the space depth of targets. In the dorsal auditory cortex of several species, neurons that encode increasing echo delays are organized rostrocaudally in a topographic arrangement defined as chronotopy. Precise chronotopy could be important for precise target-distance computations. Here we show that in the cortex of three echolocating bat species (Pteronotus quadridens, Pteronotus parnellii and Carollia perspicillata), chronotopy is not precise but blurry. In all three species, neurons throughout the chronotopic map are driven by short echo delays that indicate the presence of close targets and the robustness of map organization depends on the parameter of the receptive field used to characterize neuronal tuning. The timing of cortical responses (latency and duration) provides a binding code that could be important for assembling acoustic scenes using echo delay information from objects with different space depths.

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neuronal computation of object distance from echo delay is an essential task that echolocating bats must master for spatial orientation and the capture of prey. In the dorsal auditory cortex of bats, neurons specifically respond to combinations of short frequency-modulated components of emitted call and delayed echo. These delay-tuned neurons are thought to serve in target range calculation. It is unknown whether neuronal correlates of active space perception are established by experience-dependent plasticity or by innate mechanisms. Here we demonstrate that in the first postnatal week, before onset of echolocation and flight, dorsal auditory cortex already contains functional circuits that calculate distance from the temporal separation of a simulated pulse and echo. This innate cortical implementation of a purely computational processing mechanism for sonar ranging should enhance survival of juvenile bats when they first engage in active echolocation behaviour and flight.

Audition in bats serves passive orientation, alerting functions and communication as it does in other vertebrates. In addition, bats have evolved echolocation for orientation and prey detection and capture. This put a selective pressure on the auditory system in regard to echolocation-relevant temporal computation and frequency analysis. The present review attempts to evaluate in which respect the processing modules of bat auditory cortex (AC) are a model for typical mammalian AC function or are designed for echolocation-unique purposes. We conclude that, while cortical area arrangement and cortical frequency processing does not deviate greatly from that of other mammals, the echo delay time-sensitive dorsal cortex regions contain special designs for very powerful time perception. Different bat species have either a unique chronotopic cortex topography or a distributed salt-and-pepper representation of echo delay. The two designs seem to enable similar behavioural performance.

Ketamine is a dissociative anaesthetic, analgesic drug as well as an N-methyl-D-aspartate receptor antagonist and has been reported to influence otoacoustic emission amplitudes. In the present study, we assess the effect of ketamine-xylazine on high-frequency distortion-product otoacoustic emissions (DPOAE) in the bat species Carollia perspicillata, which serves as model for sensitive high-frequency hearing. Cubic DPOAE provide information about the nonlinear gain of the cochlear amplifier, whereas quadratic DPOAE are used to assess the symmetry of cochlear amplification and potential efferent influence on the operating state of the cochlear amplifier. During anaesthesia, maximum cubic DPOAE levels can increase by up to 35 dB within a medium stimulus level range from 35 to 60 dB SPL. Close to the -10 dB SPL threshold, at stimulus levels below about 20-30 dB SPL, anaesthesia reduces cubic DPOAE amplitudes and raises cubic DPOAE thresholds. This makes DPOAE growth functions steeper. Additionally, ketamine increases the optimum stimulus frequency ratio which is indicative of a reduction of cochlear tuning sharpness. The effect of ketamine on cubic DPOAE thresholds becomes stronger at higher stimulus frequencies and is highly significant for f2 frequencies above 40 kHz. Quadratic DPOAE levels are increased by up to 25 dB by ketamine at medium stimulus levels. In contrast to cubic DPOAEs, quadratic DPOAE threshold changes are variable and there is no significant loss of sensitivity during anaesthesia. We discuss that ketamine effects could be caused by modulation of middle ear function or a release from ipsilateral efferent modulation that mainly affects the gain of cochlear amplification.