作者: Claire Dent
DOI:
关键词: GRB10 、 Psychology 、 Gene 、 Affect (psychology) 、 Pathological 、 Genomic imprinting 、 Genetics 、 Wild type 、 Impulsivity 、 Developmental psychology 、 Serotonergic
摘要: genes show monoallelic parent-of-origin specific expression and have an important role in mediating adult behaviour. Previous research has indicated that maternally expressed Nesp paternally Grb10, which are overlapping brain regions, may a risk-taking and/or impulsive behaviours. Impulsivity risk taking natural parts of human behaviour; however pathological levels impulsivity recognised as clinical traits many psychiatric disorders. The aim the current is to explicitly test whether these two oppositely imprinted influence behaviour mice by examining mouse models lack functional copies paternal Grb10 (Grb10+/p) maternal (Nespm/+) number tests risk-taking. Unlike previous findings Nespm/+ mice, Grb10+/p had same propensity explore novel environment wild type (WT) controls. However, measure delay-discounting it was discovered were less likely discount delayed rewards. This contrast work with discounted rewards more steeply. first demonstration antagonistically affect behaviour. To further behaviours, developed. Using predator odours perceived ‘risky’ created order decision between fear reward seeking. Predator Odour Risk-Taking (PORT) task demonstrated showed comparable WT littermates. Finally, immunofluorescence used discover Nesp55 not only but co-expressed some cells, particularly serotonergic neurons. suggests be influencing delay discounting via integral neurotransmitter systems.