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Journal of Cerebral Blood Flow & Metabolism (2006) 26, 301–309. doi:10.1038/sj.jcbfm.9600203; published online 14 September 2005
Imaging visual recognition memory network by PET in the baboon: perirhinal cortex heterogeneity and plasticity after perirhinal lesion
GR was supported by the France Alzheimer association, XB by the Junta de Comunidades de Castilla-la Mancha (Spain), and RI by grants BFI-2000-0418 of the Ministry of Science and Technology, and GC02-022 of the Science and Technology (Spain).
Géraldine Rauchs1, Xavier Blaizot2, Cyrille Giffard1, Jean-Claude Baron3, Ricardo Insausti2 and Chantal Chavoix1,4
- 1INSERM, U320, Caen, France
- 2Laboratory of Human Neuroanatomy, School of Medicine, University of Castilla-La Mancha, Albacete, Spain
- 3Department of Neurology, University of Cambridge, Cambridge, UK
- 4University of Caen, UPRES-EA 3917, Caen, France
Correspondence: Dr C Chavoix, UPRES-EA 3917, UFR de Médecine, Avenue de la Côte de Nacre, 14032 Caen Cedex, France. E-mail: chantal.chavoix@wanadoo.fr
Received 27 April 2005; Accepted 1 July 2005; Published online 14 September 2005.
Abstract
We recently mapped the visual recognition memory network in the behaving baboon using a positron emission tomography (PET) activation paradigm with 18F-fluoro-deoxyglucose during a visual delayed matching-to-sample task. This study confirmed the key role of the perirhinal cortex and documented an unexpected left-sided advantage. Specific contribution of each subdivision of the perirhinal cortex has, however, never been investigated. Furthermore, although alteration to the perirhinal cortex has been implicated in several brain disorders, putative plasticity within the entire brain network after perirhinal damage remains largely unknown. To confirm our previous data and to investigate these latter issues, we used our PET activation paradigm on a second healthy baboon before and after 16 months after bilateral excitotoxic lesions of the perirhinal cortex. Activation common to our two healthy baboons occurred only in the left rostroventral perirhinal cortex (i.e., areas 36pm and rostral 36r) and insular cortex. Although histologic analysis disclosed that the perirhinal lesions achieved in the present baboon were essentially caudal to this preoperatively activated area, memory performance was severely impaired. Concomitant with this long-lasting cognitive deficit, changes in the neural network implicated in the task were observed, involving disappearance of the preoperative activations and appearance of a significant activation of the frontal and occipital cortices. However, different activation patterns were found in the first and last eight postoperative months. These findings highlight the functional heterogeneity of the perirhinal cortex and evidence progressive plasticity after perirhinal cortex damage.
Keywords:
excitotoxic lesion, functional imaging, nonhuman primate, perirhinal cortex, plasticity, visual recognition memory
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