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Title: Imprinted genes, impulsivity and risk-taking
Author: Dent, Claire
ISNI:       0000 0004 5351 1242
Awarding Body: Cardiff University
Current Institution: Cardiff University
Date of Award: 2014
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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 and paternally expressed Grb10, which are expressed in overlapping brain regions, may have a role in mediating risk-taking and/or impulsive behaviours. Impulsivity and risk taking are natural parts of human behaviour; however pathological levels of impulsivity and risk-taking are recognised as clinical traits of many psychiatric disorders. The aim of the current research is to explicitly test whether these two oppositely imprinted genes influence impulsivity and/or risk-taking behaviour in mice by examining mouse models that lack functional copies of paternal Grb10 (Grb10+/p) and maternal Nesp (Nespm/+) in a number of tests of impulsivity and risk-taking. Unlike previous findings in Nespm/+ mice, Grb10+/p mice had the same propensity to explore a novel environment as wild type (WT) controls. However, in a measure of delay-discounting behaviour it was discovered that Grb10+/p mice were less likely to discount delayed rewards. This is in contrast to previous work with Nespm/+ mice, which discounted delayed rewards more steeply. This is the first demonstration that oppositely expressed imprinted genes antagonistically affect behaviour. To further explore these behaviours, a novel test of risk-taking was developed. Using predator odours a perceived ‘risky’ environment was created in order to measure the decision between fear and reward seeking. Using the Predator Odour Risk-Taking (PORT) task it was demonstrated that Nespm/+ and Grb10+/p mice showed comparable levels of risk-taking behaviour to WT littermates. Finally, immunofluorescence was used to discover that Nesp55 and Grb10 are not only expressed in the same brain regions, but are co-expressed in some cells, particularly in serotonergic neurons. This suggests that these imprinted genes may be influencing delay discounting behaviour via the same integral neurotransmitter systems.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: QH426 Genetics ; R Medicine (General)