Journal of Neuroscience, Vol 13, 371-386, Copyright © 1993 by Society for Neuroscience
Sound-localization deficits induced by lesions in the barn owl's auditory space map [published erratum appears in J Neurosci 1993 Apr;13(4):following table of contents]
H Wagner
Max-Planck-Institut fur biologische Kybernetik, Tubingen, Germany.
Barn owls possess a two-dimensional map of auditory space. The map appears
in its final form in the external nucleus of the inferior colliculus (ICx)
and is projected from there to the optic tectum (OT). To determine the role
of the map in ICx or its projected version in OT in the localization of
acoustic stimuli, head movements of three adult owls were recorded before
and after lesioning parts of the map either in ICx or in OT. Small
electrolytic lesions caused sound-localization deficits that were
characterized by failures to turn, turns away from the sound source,
increased response latencies, and reduced turning amplitudes. These
deficits occurred at azimuths expected from the physiological data obtained
at the lesion site before passing current. They extended over an azimuthal
range of some 20 degrees. Thus, this is the first unambiguous
demonstration, for sound localization, of a deficit covering a well
circumscribed area within an auditory hemifield. Since the major lesion
deficits were restricted to one hemifield, a second lesion was made in the
space map of the other side of the brain in each animal. The second lesion
resulted in behavioral deficits qualitatively similar to those produced by
the first lesion. In total, the study is based on nine lesions, three in
each owl. Two lesions were sham lesions. These and two further lesions did
not produce a measurable deficit. In four of the five remaining cases, in
which a behavioral deficit was observed initially, the behavioral
performance recovered with time. In two cases, the deficit disappeared
completely. Although improvement occurred also in the remaining two cases,
prelesion response amplitudes were not reached in one case, and response
latency did not reach prelesion values in the other case. Because the
behavioral deficits induced by the second lesions disappeared in the same
way as did the deficits induced by the first lesions, the possibility is
excluded that the animals learned to respond tactically, that is, that they
learned to associate "unlocatable sounds" with the lesioned side. The
deficits were also not due to a generalized motor impairment, because
immediately after the lesion the animals responded as they did before the
lesion to stimulation from outside the well circumscribed affected region
of space. The possibility is discussed that plasticity after small central
(neural) injuries is maintained longer in the lifetime of an animal than
plasticity after peripheral (mechanical) manipulations.
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