Loss of mGluR5 receptors on dopamine D1-expressing neurons abolishes novelty-seeking behaviours

• Autorzy: Sikora M. , Rodriguez J. , Przewlocki R.
• Języki publikacji: EN

Abstrakty

EN

High novelty seeking behaviour has been suggested to be related to altered dopaminergic activity, however the underlying mechanisms are still poorly understood. Here we investigate how glutamatergic modulation of dopaminoceptive neurons affects novelty seeking in a mouse model with selective knock down of metabotropic glutamate receptor 5 (mGluR5) in neurons expressing D1 receptors. Mutant mice (mGluR5KD-D1) displayed normal habituation to a novel environment (time F3.84=11.33; p<0.0001, genotype F4.86=1.29; p=0.2661). When a novel object was placed in the middle of the open field apparatus mGluR5KD-D1 mice spent significantly less time interacting with it compared to wild-type controls (t=28.39; p=0.0095). Moreover, mGluR5KD-D1 mice showed no operant sensation seeking behaviour. While over subsequent training sessions wild-type animals gradually increased the number of operant responses associated with presentation of a light and noise, mutant mice showed no such behaviour (two-way ANOVA for active lever: genotype F1.90=22.06; p=0.001; session F10.90=4.5; p<0.0001; genotype × session F10.90=1.963; p=0.04). Decreased operant sensation seeking was not assosiated with higher anxiety as assessed by the elevated plus maze. Finally, mGluR5KD-D1 mice exhibited normal operant responding for food as a reinforcer (two-way ANOVA for active lever: genotype F1.45=0.93; p=0.359; session F5.45=19.09; p<0.0001; genotype × session F5.45=0.13; p=0.985). In conclusion, these results indicate mGluR5 receptors located on dopamine D1 receptor-expressing neurons are essential in novelty-seeking behaviour.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: S
• Opis fizyczny: p.89

Twórcy

autor

Sikora M.

• Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland

autor

Rodriguez J.

• Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland

autor

Przewlocki R.

• Department of Molecular Neuropharmacology, Institute of Pharmacology PAS, Krakow, Poland

Uwagi

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