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Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
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MPTP-induced executive dysfunction is associated with altered prefrontal serotonergic function.

Panchanan Maiti1, Laura C Gregg1, Michael P McDonald1

  • 1Departments of Neurology and Anatomy & Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, United States.

Behavioural Brain Research
|September 23, 2015
PubMed
Summary

Parkinson's disease impairs executive functions like attention and impulse control. MPTP-induced dopamine depletion in mice led to executive deficits, particularly linked to prefrontal serotonin turnover.

Keywords:
Executive functionImpulse controlMPTPMiceParkinson’s diseaseSustained attention

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Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Cognitive Science

Background:

  • Parkinson's disease (PD) is characterized by cognitive deficits, specifically fronto-striatally mediated executive dysfunction.
  • Executive functions include attention, planning, judgment, and impulse control, which are crucial for daily activities.

Purpose of the Study:

  • To investigate the impact of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) -induced neurodegeneration on executive function in mice.
  • To explore the relationship between neurochemical changes, particularly dopamine and serotonin pathways, and executive impairments in a PD mouse model.

Main Methods:

  • Utilized a 3-choice serial reaction-time (SRT) task to assess sustained attention and impulse control in MPTP-lesioned and control mice.
  • Measured striatal dopamine, tyrosine-hydroxylase-positive neurons in the substantia nigra, and serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the prefrontal cortex (PFC) and striatum.
  • Correlated neurochemical data with behavioral performance on the SRT task.

Main Results:

  • MPTP-lesioning acutely impaired all measures of impulsive behavior, which normalized with training, but deficits reappeared with shorter cue durations or longer pre-cue times.
  • MPTP-lesioned mice exhibited significantly slower reaction times and a loss of impulse control at longer pre-cue durations.
  • Striatal dopamine was reduced by 54%, and substantia nigra neurons by 75% in MPTP-lesioned mice.
  • Prefrontal 5-hydroxyindoleacetic acid/serotonin ratio was significantly reduced and correlated with executive impairments, while striatal norepinephrine correlated with slower reaction times.

Conclusions:

  • Prefrontal serotonin turnover, indicated by the 5-HIAA/5-HT ratio, plays a critical role in MPTP-induced executive dysfunction.
  • The study highlights the complex interplay between neurochemical changes and cognitive deficits in Parkinson's disease models.
  • Behavioral deficits in MPTP-treated mice are linked to specific neurochemical alterations in dopaminergic and serotonergic systems.