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1 Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas, United States; Physiology and Pharmacology, University of Western Ontario, London, Canada
2 Physiology and Pharmacology, University of Western Ontario, London, Canada; Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas, United States
* To whom correspondence should be addressed. E-mail: steve.lomber{at}uwo.ca.
While the contributions of primary auditory cortex to sound localization have been extensively studied in a large number of mammals, little is known of the contributions of non-primary auditory cortex to sound localization. Therefore, the purpose of this study was to examine the contributions of both primary and all the recognized regions of acoustically-responsive non-primary auditory cortex to sound localization during both bilateral and unilateral reversible deactivation. The cats learned to make an orienting response (head movement and approach) to a 100ms broad-band noise stimulus emitted from a central speaker or one of 12 peripheral sites (located in front of the animal, from left 90° to right 90°, at 15° intervals) along the horizontal plane after attending to a central visual stimulus. Twenty-one cats had one or two bilateral pairs of cryoloops chronically implanted over one of ten regions of auditory cortex. We examined AI (which included the dorsal zone (DZ)), the three other tonotopic fields (anterior auditory field-AAF, posterior auditory field-PAF, ventral posterior auditory field-VPAF), as well as six non-tonotopic regions that included, second auditory cortex (AII), the anterior ectosylvian sulcus (AES), the insular (IN) region, the temporal (T) region (which included the ventral auditory field (VAF)), the dorsal posterior ectosylvian (dPE) gyrus (which included the intermediate posterior ectosylvian (iPE) gyrus), and the ventral posterior ectosylvian (vPE) gyrus. In accord with earlier studies, unilateral deactivation of AI/DZ caused sound localization deficits in the contralateral field. Bilateral deactivation of AI/DZ resulted in bilateral sound localization deficits throughout the 180° field examined. Of the three other tonotopically organized fields, only deactivation of PAF resulted in sound localization deficits. These deficits were virtually identical to the unilateral and bilateral deactivation results obtained during AI/DZ deactivation. Of the six non-tonotopic regions examined, only deactivation of AES resulted in sound localization deficits in the contralateral hemifield during unilateral deactivation. While bilateral deactivation of AI/DZ, PAF, or AES resulted in profound sound localization deficits throughout the entire field, the cats were generally able to orient towards the hemifield that contained the acoustic stimulus, but not accurately identify the location of the stimulus. Neither unilateral nor bilateral deactivation of areas AAF, VPAF, AII, IN, T, dPE, nor vPE had any effect on the sound localization task. Finally, bilateral heterotopic deactivations of AI/DZ, PAF, or AES yielded deficits that were as profound as bilateral homotopic cooling of any of these sites. The fact that deactivation of any one region (AI/DZ, PAF, or AES) was sufficient to produce a deficit indicated that normal function of all three regions was necessary for normal sound localization. Neither unilateral nor bilateral deactivation of AI/DZ, PAF, or AES affected the accurate localization of a visual target. The results suggest that hemispheric deactivations contribute independently to sound localization deficits. ______________________________________________________________________________
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