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Impulsive choices in mice lacking imprinted Nesp55.

C L Dent1, T Humby2, K Lewis1

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Genes, Brain, and Behavior
|August 11, 2016
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Summary
This summary is machine-generated.

Loss of the imprinted gene Nesp55 in mice leads to increased impulsive choices, particularly a preference for immediate rewards over delayed ones. This suggests a role for genomic imprinting in regulating decision-making behavior.

Keywords:
Action impulsivityNesp55choice impulsivitydelayed reinforcementepigeneticsgenomic imprintingimprinted genesmouseserotoninstop-signal reactiontime

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Area of Science:

  • Neuroscience
  • Genetics
  • Epigenetics

Background:

  • Genomic imprinting regulates parent-of-origin specific gene expression.
  • The imprinted gene Nesp encodes Nesp55 protein, found in brain regions like the hypothalamus and midbrain.
  • Previous studies linked Nesp55 loss to altered novelty-related behavior.

Purpose of the Study:

  • To investigate the role of Nesp55 in impulsive behavior using a mouse model.
  • To explore the neurochemical underpinnings of Nesp55-associated behavioral changes.

Main Methods:

  • Utilized the Nespm/+ mouse model (loss of Nesp55).
  • Assessed impulsive choices using a delayed-reinforcement task.
  • Evaluated response inhibition with a stop-signal reaction time task.
  • Analyzed serotonin system gene expression (Tph2, Slc6a4) and dopamine gene expression (Th) via mRNA levels.

Main Results:

  • Nespm/+ mice exhibited increased preference for immediate, smaller rewards over delayed, larger rewards.
  • Response inhibition, measured by the stop-signal reaction time task, remained unaffected.
  • Nesp55 co-localized with serotonin, and midbrain Tph2 and Slc6a4 mRNA expression were reduced in Nespm/+ mice.
  • Th mRNA expression was not significantly altered.

Conclusions:

  • Loss of Nesp55 in mice promotes impulsive decision-making, specifically a reduced willingness to delay gratification.
  • Altered serotonergic system activity in midbrain regions may contribute to Nesp55-related impulsive behavior.
  • Genomic imprinting of Nesp offers a novel mechanism influencing brain function and potentially implicated in disorders of response control.