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                  <mods:namePart>García-García, David</mods:namePart>
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                  <mods:namePart>Fundación Tatiana Pérez de Guzmán el Bueno</mods:namePart>
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                  <mods:dateAccessioned encoding="iso8601">2018-10-26T07:59:25Z</mods:dateAccessioned>
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                  <mods:dateIssued encoding="iso8601">2018</mods:dateIssued>
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               <mods:identifier type="none"/>
               <mods:identifier type="citation">PLoS One. 2018; 13(9):e0204740</mods:identifier>
               <mods:identifier type="doi">10.1371/journal.pone.0204740</mods:identifier>
               <mods:identifier type="issn">1932-6203</mods:identifier>
               <mods:identifier type="journal">PLoS ONE</mods:identifier>
               <mods:identifier type="pubmedID">30261068</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/6531</mods:identifier>
               <mods:abstract>Purpose The nucleus accumbens (NAcc) has been suggested as a possible target for deep brain stimulation (DBS) in the treatment of obesity. Our hypothesis was that NAcc-DBS would modulate brain regions related to reward and food intake regulation, consequently reducing the food intake and, finally, the weight gain. Therefore, we examined changes in brain glucose metabolism, weight gain and food intake after NAcc-DBS in a rat model of obesity. Procedures Electrodes were bilaterally implanted in 2 groups of obese Zucker rats targeting the NAcc. One group received stimulation one hour daily during 15 days, while the other remained as control. Weight and daily consumption of food and water were everyday registered the days of stimulation, and twice per week during the following month. Positron emission tomography (PET) studies with 2-deoxy-2-[F-18] fluoro-D-glucose (FDG) were performed 1 day after the end of DBS. PET data was assessed by statistical parametric mapping (SPM12) software and region of interest (ROI) analyses. Results NAcc-DBS lead to increased metabolism in the cingulate-retrosplenial-parietal association cortices, and decreased metabolism in the NAcc, thalamic and pretectal nuclei. Furthermore, ROIs analyses confirmed these results by showing a significant striatal and thalamic hypometabolism, and a cortical hypermetabolic region. However, NAcc-DBS did not induce a decrease in either weight gain or food intake. Conclusions NAcc-DBS led to changes in the metabolism of regions associated with cognitive and reward systems, whose impairment has been described in obesity.</mods:abstract>
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                  <mods:topic>MESOLIMBIC DOPAMINE SYSTEM</mods:topic>
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               <mods:subject>
                  <mods:topic>SPRAGUE-DAWLEY RATS</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>SMALL-ANIMAL PET</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>RETROSPLENIAL CORTEX</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>CLINICAL ARTICLE</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>REWARD CIRCUITRY</mods:topic>
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               <mods:subject>
                  <mods:topic>NETWORK ACTIVITY</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>ZUCKER RATS</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>LEPTIN</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>MEMORY</mods:topic>
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                  <mods:title>Stimulating the nucleus accumbens in obesity: A positron emission tomography study after deep brain stimulation in a rodent model</mods:title>
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