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Involvement of glutamate receptors in the striatal enkephalin-induced dopamine release
Affiliation:1. King''s College London, Institute of Psychiatry, Psychology & Neuroscience, London SE5 8AF, UK;2. King''s College London, Institute of Pharmaceutical Science, London SE1 9NH, UK;3. Kiel University, Department of Pharmaceutics and Biopharmaceutics, 24118 Kiel, Germany;4. Intertek-Melbourn, Melbourn SG8 6DN, UK;5. Nemera, La Verpillière 38292, France;6. Unilever R&D, Colworth Science Park, Sharnbrook, Bedford MK44 1LQ, UK;7. Diabetes Research Group, King''s College London, King''s College Hospital Campus, Weston Education Central, London, UK;8. Institute of Diabetes and Obesity, King''s Health Partners, London, UK
Abstract:
In anesthetized rats, the intrastriatal infusion of the δ-opioid receptor agonist, [d-Pen2,d-Pen5]enkephalin, increased the extracellular concentration of dopamine. This effect was abolished by the NMDA receptor antagonist, 3-[(±)-2-carboxypiperazine-4-yl] propyl-1-phosphonate, but was unchanged by the AMPA (d,l-α-amino-3-hydroxy-5-methyl-4-isoxazole propionate) and kainate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione. This suggests that the dopamine release induced by the δ-opioid agonist depends critically on the involvement of glutamatergic transmission via NMDA receptors.
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