CNS AND ADRENAL GLAND TYROSINE HYDROXYLASE AND THE INFLUENCE OF DRUG TREATMENT ON cAMP - ACTIVITY IN PARKINSON'S DISEASE - HUMAN POST MORTEM STUDIES

Riederer, Peter; Eirkmayer, Walther; Wolf-Dieter, Rausch; Jellinger, K. A.; Danielczyk, W

doi:10.1016/b978-1-4832-8363-0.50499-7

Cited by 3 publications

(2 citation statements)

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“…The explanation for the discrepancy is not clear but might relate to the selection in the two studies of patients with different extent of dopamine neuronal loss or exposure to dopaminergic drugs. A direct comparison of our results (and those of Pifl and colleagues15) with several earlier reports of either sensitized16 or desensitized17, 18 dopamine stimulation of striatal AC in PD is not possible because the earlier studies were conducted without addition of GTP, the substrate of G‐protein required for mediating receptor–AC coupling.…”

Section: Discussionmentioning

confidence: 42%

Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy

Tong

Fitzmaurice

Ang³

et al. 2003

Annals of Neurology

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The dopamine D(1) receptor is considered to participate in levodopa's antiparkinsonian action and levodopa-induced dyskinesias. We examined the functional status of the D(1) receptor in brain of patients with Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Dopamine-stimulated adenylyl cyclase activity was significantly increased in putamen (+43%) and frontal cortex (+52%) in PD, normal in PSP, but decreased by 47% in putamen in MSA. The supersensitive dopamine D(1) receptors in both striatum and cerebral cortex in PD might compensate for dopamine deficiency, but could also contribute to long-term complications of levodopa therapy.

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Section: Discussionmentioning

confidence: 42%

Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy

Tong

Fitzmaurice

Ang³

et al. 2003

Annals of Neurology

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“…1 1 (Parkinson). adenylyl cyclase activity in brains of monkeys rendered parkinsonian by MPTP, contradictory results have been reported for the brain of human subjects with Parkinson's disease, showing a disease-related sensitization (Nagatsu et al, 1978), as well as desensitization (Riederer et al, 1979;Shibuya, 1979), of the striatal DA-sensitive adenylyl cyclase; in these studies, however, low NaCl concentrations or no NaCl was used.…”

Section: Discussionmentioning

confidence: 91%

Sensitization of Dopamine‐Stimulated Adenylyl Cyclase in the Striatum of 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine‐Treated Rhesus Monkeys and Patients with Idiopathic Parkinson's Disease

Pifl¹,

Nanoff

Schingnitz

et al. 1992

Journal of Neurochemistry

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Dopamine-stimulated adenylyl cyclase activity was measured in striatal homogenates of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated rhesus monkeys and humans with idiopathic Parkinson's disease and compared with the activity in control tissue. No differences between parkinsonian and control tissue were found in the presence of 20 mM NaCl. However, when 120 mM NaCl was included in the assay medium, a significantly higher increase in the Vmax of dopamine-stimulated adenylyl cyclase activity was observed in the caudate of MPTP-parkinsonian rhesus monkeys and the putamen of patients with idiopathic Parkinson's disease. No such sensitization was seen in the MPTP-treated rhesus putamen or human Parkinson's disease caudate tissue. A role of D2 receptors in this sensitization could be ruled out by the concomitant use of the D2 antagonist l-sulpiride and by [3H]spiperone saturation analysis of the D2 receptor density, which was found at control level in the caudate tissue of MPTP-treated rhesus monkeys. Similarly, on the basis of saturation binding with the D1 selective ligand 125I-SCH 23982, there was no difference in caudate nucleus D1 receptor densities between control and MPTP-treated monkeys. Our results point to a region-specific functional sensitization of D1 receptors as a consequence of severe dopaminergic denervation of the striatum and suggest the possibility of a therapeutic potential of a D1 agonist with full intrinsic activity in Parkinson's disease.

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Hypothalamic-Locus Coeruleus Mechanisms in the Pathophysiology of “On-Off” in L-Dopa Treated Parkinson's Disease: A Hypothesis

Sandyk

1989

International Journal of Neuroscience

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Fluctuations in motor performance remain a major problem in the longterm management of Parkinson's disease (PD) patients. Although alterations in striatal dopaminergic activity have been initially thought to induce these complications, recent studies failed to support a major role for impaired dopaminergic neuronal or receptor functions in the pathogenesis of the on-off phenomenon. In the following I discuss the possibility that alterations in the activity of norepinephrinergic neurons at the level of the locus coeruleus (LC) associated with dysregulation of descending endorphinergic projections from the arcuate nucleus of the hypothalamus may be intimately involved in the pathogenesis of motor fluctuations in L-dopa treated PD.

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CNS AND ADRENAL GLAND TYROSINE HYDROXYLASE AND THE INFLUENCE OF DRUG TREATMENT ON cAMP - ACTIVITY IN PARKINSON'S DISEASE - HUMAN POST MORTEM STUDIES

Cited by 3 publications

References 3 publications

Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy

Brain dopamine‐stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy

Sensitization of Dopamine‐Stimulated Adenylyl Cyclase in the Striatum of 1‐Methyl‐4‐Phenyl‐1,2,3,6‐Tetrahydropyridine‐Treated Rhesus Monkeys and Patients with Idiopathic Parkinson's Disease

Hypothalamic-Locus Coeruleus Mechanisms in the Pathophysiology of “On-Off” in L-Dopa Treated Parkinson's Disease: A Hypothesis

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