Natural acoustic stimuli evoke selective responses in the hippocampus of passive listening bats.

A growing body of research details spatial representation in bat hippocampus, and experiments have yet to explore hippocampal neuron responses to sonar signals in animals that rely on echolocation for spatial navigation. To bridge this gap, we investigated bat hippocampal responses to natural echolocation sounds in a non-spatial context. In this experiment, we recorded from CA1 of the hippocampus of three awake bats that listened passively to single echolocation calls, call-echo pairs, or natural echolocation sequences. Our data analysis identified a subset of neurons showing response selectivity to the duration of single echolocation calls. However, the sampled population of CA1 neurons did not respond selectively to call-echo delay, a stimulus dimension posited to simulate target distance in recordings from auditory brain regions of bats. A population analysis revealed ensemble coding of call duration and sequence identity. These findings open the door to many new investigations of auditory coding in the mammalian hippocampus.

Context-dependent coding and gain control in the auditory system of crickets.

Sensory systems process stimuli that greatly vary in intensity and complexity. To maintain efficient information transmission, neural systems need to adjust their properties to these different sensory contexts, yielding adaptive or stimulus-dependent codes. Here, we demonstrated adaptive spectrotemporal tuning in a small neural network, i.e. the peripheral auditory system of the cricket. We found that tuning of cricket auditory neurons was sharper for complex multi-band than for simple single-band stimuli. Information theoretical considerations revealed that this sharpening improved information transmission by separating the neural representations of individual stimulus components. A network model inspired by the structure of the cricket auditory system suggested two putative mechanisms underlying this adaptive tuning: a saturating peripheral nonlinearity could change the spectral tuning, whereas broad feed-forward inhibition was able to reproduce the observed adaptive sharpening of temporal tuning. Our study revealed a surprisingly dynamic code usually found in more complex nervous systems and suggested that stimulus-dependent codes could be implemented using common neural computations.

Coding Deficits in Noise-Induced Hidden Hearing Loss May Stem from Incomplete Repair of Ribbon Synapses in the Cochlea.

Recent evidence has shown that noise-induced damage to the synapse between inner hair cells (IHCs) and type I afferent auditory nerve fibers (ANFs) may occur in the absence of permanent threshold shift (PTS), and that synapses connecting IHCs with low spontaneous rate (SR) ANFs are disproportionately affected. Due to the functional importance of low-SR ANF units for temporal processing and signal coding in noisy backgrounds, deficits in cochlear coding associated with noise-induced damage may result in significant difficulties with temporal processing and hearing in noise (i.e., "hidden hearing loss"). However, significant noise-induced coding deficits have not been reported at the single unit level following the loss of low-SR units. We have found evidence to suggest that some aspects of neural coding are not significantly changed with the initial loss of low-SR ANFs, and that further coding deficits arise in association with the subsequent reestablishment of the synapses. This suggests that synaptopathy in hidden hearing loss may be the result of insufficient repair of disrupted synapses, and not simply due to the loss of low-SR units. These coding deficits include decreases in driven spike rate for intensity coding as well as several aspects of temporal coding: spike latency, peak-to-sustained spike ratio and the recovery of spike rate as a function of click-interval.