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Research article summary (published 2 Mar 2009):

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

Full 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.

 

Author information

Author/s: Kazama, Andy (A); Bachevalier, Jocelyne (J);

Affiliation: Department of Neurobiology and Anatomy, University of Texas Health Science Center, Houston, Texas 77030, USA.

Grants: HD-35471 (Agency:NICHD NIH HHS) ; MH-58846 (Agency:NIMH NIH HHS) ; RR00165 (Agency:NCRR NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Mar; vol 29 (issue 9) : pp 2794-804

Dates: Created 2009/03/05; Completed 2009/04/10; Revised 2009/06/25;

PMID: 19261875, status: MEDLINE (last retrieval date: 6/26/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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Associated Chemicals: Neurotoxins (0)

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