Determination of extracellular glutamate after local K+ stimulation in the striatum of non-anaesthetised rats after treatment with dopaminergic drugs--studies using microdialysis.
The present experiments were performed in order to investigate the effects of dopamine(DA)ergic drugs on the concentrations of extracellular glutamate (GLU) in the striatum of non-anaesthetised, freely moving rats by using microdialysis and to get further information about the interactions between glutamatergic and dopaminergic pathways. GLU was determined after pre-column derivatisation with o-phthaldialdehyde by HPLC and fluorescence detection. For increasing the fraction of extracellular GLU which is of neuronal origin, an enhanced release of this neurotransmitter was evoked by 100 mM K+ administered via the dialysis probe. This stimulation was applied twice in each experiment, at the second time after administration of a subcutaneously (s.c.) given DAergic drug. For basal conditions, a perfusion fluid containing 148.2 mM Na+, 4mM K+, 1.2 mM Ca2+ was used, for conditions of stimulation with 100 mM K+ the Na+ concentration was reduced correspondingly. Activation of the D1 receptor with the selective D1 sector agonist SKF 38393 ((+/-) 1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol) 15 mg/kg) failed to influence the stimulated release of GLU, and neither a combination of the selective D2 antagonist (-)sulpiride (150 mg/kg) with the mixed D1/D2 agonist apomorphine (1 mg/kg), nor a combination of sulpiride (150 mg/kg) with SKF 38393 (15 mg/kg) were effective. Also the two selective D2 agonists quinpirole (0.5 mg/kg) or talipexole (50 micrograms/kg) had no significant influence on the release of GLU. The results suggest that DA receptor agonists have less effect on the K(+)-stimulated GLU-release than might be expected from in vitro studies or behavioral experiments (Kornhuber and Kornhuber, 1986).
Dietze
S
S
Institute for Pharmacology and Toxicology, Faculty of Pharmacy, University of Marburg, Federal Republic of Germany.
Kuschinsky
K
K
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001381:Azepines / Q000494:pharmacology; D002851:Chromatography, High Pressure Liquid; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D003956:Dialysis; D015259:Dopamine Agents / Q000494:pharmacology*; D004873:Ergolines / Q000494:pharmacology; D005971:Glutamates / Q000032:analysis / Q000378:metabolism*; D018698:Glutamic Acid; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D019257:Quinpirole; D051381:Rats; D017208:Rats, Wistar; D013050:Spectrometry, Fluorescence; D013268:Stimulation, Chemical; D013469:Sulpiride / Q000494:pharmacology
D001381:Azepines; D015259:Dopamine Agents; D004873:Ergolines; D005971:Glutamates; D019257:Quinpirole; D018698:Glutamic Acid; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; C024763:talipexole; D013469:Sulpiride; D001058:Apomorphine; D011188:Potassium