Translational neuroscience of basolateral amygdala lesions: Studies of Urbach-Wiethe disease.

Détails

ID Serval
serval:BIB_1C134FD1623A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Translational neuroscience of basolateral amygdala lesions: Studies of Urbach-Wiethe disease.
Périodique
Journal of neuroscience research
Auteur(s)
Koen N., Fourie J., Terburg D., Stoop R., Morgan B., Stein D.J., van Honk J.
ISSN
1097-4547 (Electronic)
ISSN-L
0360-4012
Statut éditorial
Publié
Date de publication
06/2016
Peer-reviewed
Oui
Volume
94
Numéro
6
Pages
504-512
Langue
anglais
Notes
Publication types: Journal Article ; Review Publication Status: ppublish
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review

Résumé
Urbach-Wiethe disease (UWD) is an extremely rare autosomal recessive disorder characterized by mutations in the extracellular matrix protein 1 gene on chromosome 1. Typical clinical manifestations include voice hoarseness in early infancy and neuropsychiatric, laryngeal, and dermatological pathologies later in life. Neuroimaging studies have revealed a pattern of brain calcification often but not exclusively leading to selective bilateral amygdala damage. A large body of work on amygdala lesions in rodents exists, generally employing a subregion model focused on the basolateral amygdala (BLA) and the central-medial amygdala. However, human work usually considers the amygdala as a unified structure, not only complicating the translation of animal findings to humans but also providing a unique opportunity for further research. To compare data from rodent models with human cases and to complement existing data from Europe and North America, a series of investigations was undertaken on UWD subjects with selective BLA damage in the Namaqualand region, South Africa. This review presents key findings from this work, including fear processing, social-economic behavior, and emotional conflict processing. Our findings are broadly consistent with and support rodent models of selective BLA lesions and show that the BLA is integral to processing sensory stimuli and exhibits inhibitory regulation of responses to unconditioned innate fear stimuli. Furthermore, our findings suggest that the human BLA mediates calculative-instrumental economic behaviors and may compromise working memory via competition for attentional resources between the BLA salience detection system and the dorsolateral prefrontal cortex working memory system.

Mots-clé
Animals, Basolateral Nuclear Complex/injuries, Brain Injuries/complications, Brain Injuries/pathology, Disease Models, Animal, Humans, Lipoid Proteinosis of Urbach and Wiethe/etiology, Lipoid Proteinosis of Urbach and Wiethe/pathology, Translational Medical Research
Pubmed
Création de la notice
03/05/2016 16:40
Dernière modification de la notice
20/08/2019 12:52
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