Role of striatal acetylcholine on dopamine D1 receptor agonist-induced turning behavior in 6-hydroxydopamine lesioned rats: a microdialysis-behavioral study.
The effects of MK-801, a non-competitive N-methyl D-aspartate (NMDA) receptor antagonist, of quinpirole, a dopamine (DA) D2 receptor agonist, and of SCH 58261, an A2A adenosine antagonist, were studied on acetylcholine (ACh) release in the striatum of 6-hydroxydopamine (60HDA) lesioned rats and on turning behavior induced by the administration of the DA D1 agonist CY 208-243. Administration of CY 208-243 to 6OHDA lesioned rats induced turning behavior and dose-dependently stimulated ACh release. At the dose of 50 microg/kg, MK-801 failed to affect basal ACh, while at 100 microg/kg MK-801 reduced it; however, MK-801 (50 and 100 microg/kg) potentiated the turning behavior elicited by CY 208-243, but failed to affect the CY 208-243-induced increase of striatal ACh release. The administration of quinpirole induced low-intensity turning behavior and decreased basal ACh release; on the other hand, quinpirole potentiated the turning behavior induced by CY 208-243, but failed to affect the CY 208-243-elicited increase of ACh release. Finally, intravenous administration of SCH 58261 stimulated basal ACh release but not turning behavior; SCH 58261, however, potentiated turning behavior induced by CY 208-243, while failing to affect the D1-elicited increase of ACh release. These results indicate that potentiation of D1-dependent turning behavior by MK-801, quinpirole and SCH 58261 is not mediated by a reduced ability of D1-agonists to stimulate ACh release from the denervated striatum.
Fenu
S
S
Department of Toxicology, University of Cagliari, Italy.
Acquas
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E
Di Chiara
G
G
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D017551:Microdialysis; D009043:Motor Activity / Q000187:drug effects* / Q000502:physiology; D017072:Neostriatum / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D016627:Oxidopamine / Q000494:pharmacology; D020734:Parkinsonian Disorders / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D058915:Purinergic P1 Receptor Antagonists; D051381:Rats; D043705:Receptor, Adenosine A2A; D017447:Receptors, Dopamine D1 / Q000819:agonists* / Q000378:metabolism; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000378:metabolism; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000378:metabolism; D018047:Receptors, Purinergic P1 / Q000378:metabolism; D013565:Sympatholytics / Q000494:pharmacology
D018491:Dopamine Agonists; D018691:Excitatory Amino Acid Antagonists; D058915:Purinergic P1 Receptor Antagonists; D043705:Receptor, Adenosine A2A; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D011976:Receptors, Muscarinic; D016194:Receptors, N-Methyl-D-Aspartate; D018047:Receptors, Purinergic P1; D013565:Sympatholytics; D016627:Oxidopamine; D000109:Acetylcholine