title: Feeding-induced decrease in extracellular glutamate level in the rat nucleus accumbens: dependence on glutamate uptake.
abstract: In vivo microdialysis combined with high-performance liquid chromatography and electrochemical detection was used to monitor extracellular glutamate levels in the medial nucleus accumbens of Sprague-Dawley rats during their feeding behaviour. Consumption of a palatable new diet or a diet to which rats were previously exposed caused a decrease in extracellular level of glutamate in the nucleus accumbens during and after feeding. The presentation of an inedible object (a piece of rubber) instead of the expected food caused a marked increase in extracellular glutamate levels. In contrast, if the piece of rubber was presented to rats that did not expect food delivery, the extracellular level of glutamate remained unchanged during the rubber presentation. The feeding-induced decrease in the extracellular glutamate level did not depend on food deprivation and was completely prevented by intraaccumbal infusions through the dialysis probe of 10 mM D,L-threo-beta-hydroxyaspartate (a glutamate uptake inhibitor). Intraaccumbal infusions of 10 microM S-(-)-raclopride L-tartrate (a D2/D3 dopamine receptor antagonist) or 1 microM tetrodotoxin (a voltage-dependent Na(+) channel blocker) also completely reversed the decrease in extracellular glutamate level in response to food intake. The D1/D5 dopamine receptor antagonist SCH-23390 (10 microM) administered into the nucleus accumbens had no significant effect on the feeding-induced decrease in extracellular glutamate level. From the data obtained we suggest that the decrease in the extracellular level of glutamate in the medial nucleus accumbens in response to feeding appears to arise from a temporal increase in glutamate uptake that is probably operated by dopamine inputs to the nucleus accumbens via D2/D3 receptors. Our findings also suggest that the dissociation between the expected biological value of a presented object and the reality might be an important determinant for regulation of glutamate release in this brain area during feeding behaviour.
authors.affiliation: Laboratory of Higher Nervous Activity, I.P. Pavlov Institute of Physiology, Russian Academy of Sciences, 6 Admiral Makarov Embankment, St. Petersburg 199034, Russia. nbs@infran.ru
authors.forename: N B
authors.initials: NB
authors.lastname: Saulskaya
authors.forename: M O
authors.initials: MO
authors.lastname: Mikhailova
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D018492:Dopamine Antagonists / Q000494:pharmacology; D004435:Eating; D005110:Extracellular Space / Q000378:metabolism*; D005247:Feeding Behavior; D018698:Glutamic Acid / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D014179:Neurotransmitter Uptake Inhibitors / Q000494:pharmacology*; D009714:Nucleus Accumbens / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D018492:Dopamine Antagonists; D014179:Neurotransmitter Uptake Inhibitors; C011274:3-hydroxyaspartic acid; D001224:Aspartic Acid; D018698:Glutamic Acid