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Behavior and memory evaluation in Wistar rats with hypothalamus arcuate nucleus lesion
Author(s) -
Guimarães Ernesto da Silveira Goulart,
Caires Luiz Carlos,
Musso Camila Manso,
Vasconcellos Rebecca,
Assis Diego,
Andreazzi Ana Eliza,
Mourão-Júnior Carlos Alberto,
Garcia Raúl Marcel González
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.709.3
Subject(s) - monosodium glutamate , arcuate nucleus , hypothalamus , hippocampus , lesion , open field , endocrinology , medicine , nucleus , amygdala , psychology , neuroscience , surgery
The administration of L‐monosodium glutamate (MSG) in neonatal rats causes lesions in the arcuate nucleus of the hypothalamus leading to obesity development. Because of the many connections between these regions with important neuronal regulating centers, the aim of this study was to evaluate the behavioral and memory patterns of these animals. At the first 5 days of life, male Wistar rats received subcutaneous doses of MSG. At 90 days of life the animals was submit to the open field arena test regarding episodes of rearing, freezing, number of traversed squares and the time spent in the arena's center. We evaluated the animals’ memory using the object recognition test regarding the working memory (WM) and the long‐term memory (LTM). The Lee Index (LI) was calculated and the perigonadal fat pad was weighed to check the obesity and hypertrophy of adipocytes. The MSG rats showed a significant increase in the episodes of rearing, freezing and decrease in the number of squares traversed and in the time spent in the arena's center. In the LTM test MSG animals showed a reduced discrimination index, the WM test showed no significant difference. The MSG group had an increased LI and perigonadal fat pad mass. MSG obese rats showed a behavior that indicates a stress and anxiety profile, which may be due to the arcuate nucleus lesion. The impaired LTM can be explained by the some neural connections between the hypothalamus and hippocampus. Financial Support: Capes, CNPq, Fapemig and UFJF