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Sound Localization Deficits During Reversible Deactivation of Primary Auditory Cortex and/or the Dorsal Zone

¹Departments of Physiology and Pharmacology, and Psychology, University of Western Ontario, London, Ontario, Canada; ²School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas; ³Department of Speech and Hearing Sciences, University of Washington, Seattle, Washington; and ⁴Kresge Hearing Research Institute, University of Michigan, Ann Arbor, Michigan

Submitted 6 November 2007; accepted in final form 15 January 2008

We examined the contributions of primary auditory cortex (A1) and the dorsal zone of auditory cortex (DZ) to sound localization behavior during separate and combined unilateral and bilateral deactivation. From a central visual fixation point, cats learned to make an orienting response (head movement and approach) to a 100-ms broadband noise burst 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. Following training, each cat was implanted with separate cryoloops over A1 and DZ bilaterally. Unilateral deactivation of A1 or DZ or simultaneous unilateral deactivation of A1 and DZ (A1/DZ) resulted in spatial localization deficits confined to the contralateral hemifield, whereas sound localization to positions in the ipsilateral hemifield remained unaffected. Simultaneous bilateral deactivation of both A1 and DZ resulted in sound localization performance dropping from near-perfect to chance (7.7% correct) across the entire field. Errors made during bilateral deactivation of A1/DZ tended to be confined to the same hemifield as the target. However, unlike the profound sound localization deficit that occurs when A1 and DZ are deactivated together, deactivation of either A1 or DZ alone produced partial and field-specific deficits. For A1, bilateral deactivation resulted in higher error rates (performance dropping to 45%) but relatively small errors (mostly within 30° of the target). In contrast, bilateral deactivation of DZ produced somewhat fewer errors (performance dropping to only 60% correct), but the errors tended to be larger, often into the incorrect hemifield. Therefore individual deactivation of either A1 or DZ produced specific and unique sound localization deficits. The results of the present study reveal that DZ plays a role in sound localization. Along with previous anatomical and physiological data, these behavioral data support the view that A1 and DZ are distinct cortical areas. Finally, the findings that deactivation of either A1 or DZ alone produces partial sound localization deficits, whereas deactivation of either posterior auditory field (PAF) or anterior ectosylvian sulcus (AES) produces profound sound localization deficits, suggests that PAF and AES make more significant contributions to sound localization than either A1 or DZ.