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J Neurophysiol 97: 557-562, 2007. First published September 13, 2006; doi:10.1152/jn.00591.2006
0022-3077/07 $8.00
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Multisensory Orientation Behavior Is Disrupted by Neonatal Cortical Ablation

Wan Jiang, Huai Jiang, Benjamin A. Rowland and Barry E. Stein

Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, North Carolina

Submitted 6 June 2006; accepted in final form 5 September 2006

The integration of visual and auditory information can significantly amplify the sensory responses of superior colliculus (SC) neurons and the behaviors that depend on them. This response amplification depends on the development of SC inputs that are derived from two regions of cortex: the anterior ectosylvian sulcus (AES) and the rostral lateral suprasylvian sulcus (rLS). Neonatal ablation of these cortico-collicular areas has been shown to disrupt the development of the multisensory enhancement capabilities of SC neurons and the present results demonstrate that it also precludes the development of the normal multisensory enhancements in orientation behavior. Animals with neonatal ablation of AES and rLS were tested at maturity and found unable to benefit from the combination of visual and auditory cues in their efforts to localize targets in contralesional space. In contrast, their ipsilesional multisensory orientation capabilities were indistinguishable from those of normal animals. However, when only one of these cortical areas was removed during early life, later behavioral consequences were negligible. Whether similar compensatory processes would occur in adult animals remains to be determined. These observations, coupled with those from previous studies, also suggest that a surprisingly high proportion of SC neurons capable of multisensory integration must be present for orientation behavior benefits to be realized. Compensatory mechanisms can achieve this if early lesions spare either AES or rLS, but even the impressive plasticity of the neonatal brain cannot compensate for the early loss of both of them.


Address for reprint requests and other correspondence: B. E. Stein, Dept. of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1010 (E-mail: bestein{at}wfubmc.edu)




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