The control of vocalization depends significantly on auditory feedback
in any species of mammals. Echolocating horseshoe bats, however, prov
ide an excellent model system to study audio-vocal (AV) interactions.
These bats can precisely control the frequency of their echolocation c
alls by monitoring the characteristics of the returning echo; they com
pensate for flight-induced Doppler shifts in the echo frequency by low
ering the frequency of the subsequent vocalization calls (Schnitzler,
1968; Schuller et al., 1974,1975). It was the aim of this study to inv
estigate the neuronal mechanisms underlying this Doppler-shift compens
ation (DSC) behavior. For that purpose, the neuronal activity of singl
e units was studied during spontaneous vocalizations of the bats and c
ompared with responses to auditory stimuli such as playback vocalizati
ons and artificially generated acoustic stimuli. The natural echolocat
ion situation was simulated by triggering an acoustic stimulus to the
bat's own vocalization and by varying the time delay of this artificia
l ''echo'' relative to the vocalization onset. Single-unit activity wa
s observed before, during, and/or after the bat's vocalization as well
as in response to auditory stimuli. However, the activity patterns as
sociated with vocalization differed from those triggered by auditory s
timuli even when the auditory stimuli were acoustically identical to t
he bat's vocalization. These neurons were called AV neurons. Their dis
tribution was restricted to an area in the paralemniscal tegmentum of
the midbrain. When the natural echolocation situation was simulated, t
he responses of AV neurons depended on the time delay between the onse
t of vocalization and the beginning of the simulated echo. This delay
sensitivity disappeared completely when the act of vocalization was re
placed by an auditory stimulus that mimicked acoustic self-stimulation
during the emission of an echolocation call. The activity of paralemn
iscal neurons was correlated with all parameters of echolocation calls
and echoes that are relevant in context with DSC. These results sugge
st a model for the regulation of vocalization frequencies by inhibitor
y auditory feedback.