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Details

Autor(en) / Beteiligte
Titel
Endocannabinoid Modulation of Orbitostriatal Circuits Gates Habit Formation
Ist Teil von
  • Neuron (Cambridge, Mass.), 2016-06, Vol.90 (6), p.1312-1324
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2016
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • Everyday function demands efficient and flexible decision-making that allows for habitual and goal-directed action control. An inability to shift has been implicated in disorders with impaired decision-making, including obsessive-compulsive disorder and addiction. Despite this, our understanding of the specific molecular mechanisms and circuitry involved in shifting action control remains limited. Here we identify an endogenous molecular mechanism in a specific cortical-striatal pathway that mediates the transition between goal-directed and habitual action strategies. Deletion of cannabinoid type 1 (CB1) receptors from cortical projections originating in the orbital frontal cortex (OFC) prevents mice from shifting from goal-directed to habitual instrumental lever pressing. Activity of OFC neurons projecting to dorsal striatum (OFC-DS) and, specifically, activity of OFC-DS terminals is necessary for goal-directed action control. Lastly, CB1 deletion from OFC-DS neurons prevents the shift from goal-directed to habitual action control. These data suggest that the emergence of habits depends on endocannabinoid-mediated attenuation of a competing circuit controlling goal-directed behaviors. •OFC-DS circuit mediates goal-directed control of actions•Inhibition of OFC-DS transmission is necessary for habitual action control•Selective deletion of CB1 receptors in OFC-DS neurons prevents habit formation•Endocannabinoid-mediated weakening of goal-directed circuits allows for habit formation Gremel et al. show an endogenous molecular mechanism in an identified corticostriatal circuit that controls shifts in behavioral control between goal-directed and habitual strategies. Habitual action control necessitates the endocannabinoid-mediated weakening of an orbitostriatal circuit that sustains goal-directed control.

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