Mesolimbic dopaminergic mechanisms underlying individual differences in sugar consumption and amphetamine hyperlocomotion in Wistar rats

Authors

  • Terrence L. Sills,

    1. Section on Behavioural Neuropharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, MD 20892-1380, USA
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  • Ava O. Onalaja,

    1. Section on Behavioural Neuropharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, MD 20892-1380, USA
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  • Jacqueline N. Crawley

    1. Section on Behavioural Neuropharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, MD 20892-1380, USA
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Abstract

Individual differences within strains of rats have been demonstrated for dopamine-mediated behaviours and responses to dopaminergic drugs. Differences in mesolimbic dopamine function may underlie individual differences in some of these behaviours, including sugar consumption and amphetamine hyperlocomotion. The present study addressed two potential mechanisms for these differences in dopamine-mediated behaviours. The possibility of functional differences in dopamine receptor subtypes was tested in LOW and HIGH sugar feeders. LOW and HIGH feeders did not differ in their response to the partial D1 agonist SKF-38393. The highest dose (2.5 mg/kg) of the D2 agonist quinpirole stimulated locomotor activity to a greater degree in a subset of HIGH sugar feeders as compared with LOW feeders. All doses of amphetamine induced a greater locomotor response in HIGH feeders as compared with LOW feeders, and HIGH feeders exhibited higher levels of extracellular dopamine in the nucleus accumbens than LOW feeders following exposure to sugar and treatment with amphetamine. These results support the interpretation that LOW and HIGH feeders exhibit differences in presynaptic nucleus accumbens dopamine function that account for the expression of individual differences in sugar consumption and response to amphetamine treatments. A subset of HIGH feeders may also exhibit greater D2 receptor function.

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