Selective aspiration or neurotoxic lesions of orbital frontal areas 11 and 13 spared monkeys' performance on the object discrimination reversal task

• Type of Material: Article
• Authors: Andrew Kazama, Emory University; Jocelyne Bachevalier, Emory University
• Language: English
• Date: 2009-03-04
• Publisher: Lippincott, Williams & Wilkins
• Publication Version: Final Published Version
• Copyright Statement: © 2009 Society for Neuroscience.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1523/JNEUROSCI.4655-08.2009
• Title of Journal or Parent Work: Journal of Neuroscience Nursing
• ISSN: 0888-0395
• Volume: 29
• Issue: 9
• Start Page: 2794
• End Page: 2804
• Grant/Funding Information: his work was supported by grants from the National Institute of Mental Health (MH-58846), the National Institute of Child Health and Human Development (HD-35471), Autism Speaks Mentor-Based Predoctoral Fellowship, Yerkes Base Grant NIH RR00165, and Center for Behavioral Neuroscience Grant NSF IBN-9876754.
• Keywords: Male; Neurotoxicity Syndromes; Orbit; Form Perception; Nerve Net; Frontal Lobe; Reversal Learning; Psychomotor Performance; Suction; Animals; Macaca mulatta; Discrimination (Psychology); Neurotoxins; Hippocampus; Brain Injuries; Magnetic Resonance Imaging
• Research Categories: Health Sciences, Toxicology; Psychology, Behavioral; Biology, Neuroscience

Abstract

Damage to the orbital frontal cortex (OFC) has long been associated with reversal learning deficits in several species. In monkeys, this impairment follows lesions that include several OFC subfields. However, the different connectional patterns of OFC subfields together with neuroimaging data in humans have suggested that specific OFC areas play distinctive roles in processing information necessary to guide behavior (Kringelbach and Rolls, 2004; Barbas, 2007; Price, 2007). More specifically, areas 11 and 13 contribute to a sensory network, whereas medial areas 10, 14, and 25 are heavily connected to a visceromotor network. To examine the contribution of areas 11 and 13 to reversal learning, we tested monkeys with selective damage to these two OFC areas on two versions of the ODR task using either one or five discrimination problems. We compared their performance with that of sham-operated controls and of animals with neurotoxic amygdala lesions, which served as operated controls. Neither damage to areas 11 and 13 nor damage to the amygdala affected performance on the ODR tasks. The results indicate that areas 11 and 13 do not critically contribute to reversal learning and that adjacent damage to OFC subfields (10, 12, 14, and 25) could account for the ODR deficits found in earlier lesion studies. This sparing of reversal learning will be discussed in relation to deficits found in the same animals on tasks that measure behavioral modulation when relative value of affective (positive and negative) stimuli was manipulated.