کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2494615 | 1115572 | 2008 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: 6-OHDA-induced hemiparkinsonism and chronic l-DOPA treatment increase dopamine D1-stimulated [3H]-GABA release and [3H]-cAMP production in substantia nigra pars reticulata of the rat 6-OHDA-induced hemiparkinsonism and chronic l-DOPA treatment increase dopamine D1-stimulated [3H]-GABA release and [3H]-cAMP production in substantia nigra pars reticulata of the rat](/preview/png/2494615.png)
It has been proposed that striatonigral GABAergic transmission in the substantia nigra reticulata (SNr) is enhanced during Parkinson's disease and subsequent l-DOPA treatment. To evaluate this proposal we determined the effects of activating dopamine D1 receptors on depolarization induced [3H]-GABA release and on [3H]-cAMP accumulation in slices of SNr of rats with unilateral 6-OHDA lesions with and without l-DOPA treatment. Denervation increased depolarization induced D1-stimulated [3H]-GABA release, while repeated l-DOPA treatment further enhanced this response. Both also enhanced the effects of forskolin on [3H]-cAMP production and [3H]-GABA release, while neither modified the stimulating effects of 8-Br-cAMP on the release. These results shown that, after 6-OHDA lesions and l-DOPA treatment, cAMP signaling is enhanced. Furthermore, the results suggest that activation of sites in the signaling cascade downstream of cAMP synthesis is not required to increase release.
Journal: Neuropharmacology - Volume 55, Issue 5, October 2008, Pages 704–711