Role of striatal acetylcholine on dopamine D-1 receptor agonist-induced turning behavior in 6-hydroxydopamine lesioned rats: a microdialysis-behavioral study

Citation
S. Fenu et al., Role of striatal acetylcholine on dopamine D-1 receptor agonist-induced turning behavior in 6-hydroxydopamine lesioned rats: a microdialysis-behavioral study, NEUROL SCI, 22(1), 2001, pp. 63-64
Citations number
8
Categorie Soggetti
Neurology
Journal title
NEUROLOGICAL SCIENCES
ISSN journal
15901874 → ACNP
Volume
22
Issue
1
Year of publication
2001
Pages
63 - 64
Database
ISI
SICI code
1590-1874(200102)22:1<63:ROSAOD>2.0.ZU;2-J
Abstract
The effects of MK-801, a non-competitive N-methyl D-aspartate (NMDA) recept or antagonist, of quinpirole, a dopamine (DA) D-2 receptor agonist, and of SCH 58261, an A(2A) adenosine antagonist, were studied on acetyl choline (A Ch) release in the striatum of B-hydroxydopamine (60HDA) lesioned rats and on turning behavior induced by the administration of the DA D-1 agonist CY 208-243. Administration of CY 208-243 to 60HDA lesioned rats induced turnin g behavior and dose-dependently stimulated ACh release. At the dose of 50 m ug/kg, MK-801 failed to affect basal ACh, while at 100 mug/kg MK-801 reduce d it; however, MK-801 (50 and 100 mug/kg) potentiated the turning behavior elicited by CY 208-243, but failed to affect the CY 208-243-induced increas e of striatal ACh release. The administration of quinpirole induced low-int ensity turning behavior and decreased basal ACh release; on the other hand, quinpirole potentiated the turning behavior induced by CY 208-243, but fai led to affect the eY 208-243-elicited increase of ACh release. Finally, int ravenous administration of SCH 58261 stimulated basal ACh release but not t urning behavior; SCH 58261, however, potentiated turning behavior induced b y CY 208-243, while failing to affect the DI-elicited increase of ACh relea se. These results indicate that potentiation of D-1-dependent turning behav ior by MK-801, quinpirole and SCH 58261 is not mediated by a reduced abilit y of D-1-agonists to stimulate ACh release from the denervated striatum.