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At least 883 records · Page 49Linked to original sources
PubMed1999

Striatal biopterin and tyrosine hydroxylase protein reduction in dopa-responsive dystonia.

OBJECTIVE: To determine the mechanism leading to striatal dopamine (DA) loss in dopa-responsive dystonia (DRD). BACKGROUND: Although mutations in the gene GCH1, coding for the tetrahydrobiopterin (BH4) biosynthetic enzyme guanosine triphosphate-cyclohydrolase I, have been identified in some patients with DRD, the actual status of brain BH4 (the cofactor for tyrosine hydroxylase [TH]) is unknown. METHODS: The authors sequenced GCH1 and measured levels of total biopterin (BP) and total neopterin (NP), TH, and dopa decarboxylase (DDC) proteins, and the DA and vesicular monoamine transporters (DAT, VMAT2) in autopsied brain of two patients with typical DRD. RESULTS: Patient 1 had two GCH1 mutations but Patient 2 had no mutation in the coding region of this gene. Striatal BP levels were markedly reduced (<20% of control subjects) in both patients and were also low in two conditions characterized by degeneration of nigrostriatal DA neurons (PD and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treated primate), whereas brain NP concentrations were selectively decreased (<45%) in the DRD patients. In the putamen, both DRD patients had severely reduced (<3%) TH protein levels but had normal concentrations of DDC protein, DAT, and VMAT2. CONCLUSIONS: The data suggest that 1) brain BH4 is decreased substantially in dopa-responsive dystonia, 2) dopa-responsive dystonia can be distinguished from degenerative nigrostriatal dopamine deficiency disorders by the presence of reduced brain neopterin, and 3) the striatal dopamine reduction in dopa-responsive dystonia is caused by decreased TH activity due to low cofactor concentration and to actual loss of TH protein. This reduction of TH protein, which might be explained by reduced enzyme stability/expression consequent to congenital BH4 deficiency, can be expected to limit the efficacy of acute BH4 administration on dopamine biosynthesis in dopa-responsive dystonia.

Adult↗
PubMed1999

Time course of frontal somatosensory evoked potentials. Relation to L-dopa plasma levels and motor performance in PD.

OBJECTIVE: To verify whether the change in L-dopa plasma levels after a single dose of carbidopa/L-dopa 50/200 (controlled-release) transiently modifies frontal components of somatosensory evoked potentials (SEPs) in patients with PD in parallel with improvement of motor performance. BACKGROUND: Apomorphine, a potent dopamine-agonist drug, transiently increases frontal SEP components, which may be depressed in PD; however, relationships between clinical status, frontal SEPs, and therapy are still unclear. METHODS: Nineteen PD patients (mean age 65.9 years, range 52 to 77, responders to L-dopa therapy, were studied in the same day at times T0 (baseline predose level), T1 (presumed L-dopa peak time), and T2 (end of dose-induced motor response). The following were monitored: L-dopa plasma concentration, tapping test, reaction times, peak latency (with central conduction times), and amplitude of cervical, subcortical, as well as cortical parietal and frontal SEP components elicited by median nerve stimulation of the more clinically affected arm. RESULTS: The average amplitude of frontal components of PD patients was significantly reduced at T0 with respect to control subjects. A significant and transient amplitude increase of frontal SEPs was found at T1, in parallel with the L-dopa peak concentration and improvement in motor performance (tapping and reaction times), without significant changes in amplitude of parietal SEP waves. No latency shifts were observed in brain and spinal waves. CONCLUSIONS: L-Dopa may influence the responsiveness of the parkinsonian brain as assessed by frontal somatosensory evoked potentials. The time course of these modifications coincides with that of the clinical response in the motor performance.

Aged↗
PubMed2000

The long-duration response to L-dopa in the treatment of early PD.

OBJECTIVE: To investigate the long-duration response (LDR) to L-dopa resulting from different regimens of L-dopa. BACKGROUND: In clinical practice, L-dopa is usually administered without considering the LDR due to the drug. Moreover, it has not been established whether in early PD a multiple daily intake of small doses of L-dopa may induce a sustained LDR. METHODS: Twenty-four patients with early PD underwent a double-blind, crossover trial, comparing three different 15-day treatment periods with L-dopa: treatment A (250 mg every 24 hours); treatment B (250 mg every 8 hours); and treatment C (125 mg every 8 hours). After completion, 20 patients underwent a subsequent open-label randomized trial with prolonged treatments (250 mg every 24 hours or 125 mg every 8 hours) up to 3 months. LDR was measured at the end of each treatment. RESULTS: All patients achieved a sustained LDR after treatments A and B, whereas only 17% of patients reached a sustained LDR after treatment C. Overall, the LDRs resulting from treatments A and B had similar magnitude and were larger than the LDR deriving from treatment C. After 3 months of prolonged treatments, only three of 10 patients treated with 125 mg every 8 hours increased their LDR, whereas all 10 patients treated with 250 mg every 24 hours had a maximal and stable LDR. CONCLUSIONS: Sustained LDR to L-dopa is dependent on the amount of the single doses of the drug. A regimen scheduling small, divided doses during the day, as done in clinical practice, is a questionable therapy for the achievement of a sustained LDR.

Aged↗
PubMed1988

Positive regulation of melanin pigmentation by two key substrates of the melanogenic pathway, L-tyrosine and L-dopa.

We describe results demonstrating the positive regulation of melanogenesis by two substrates of the melanogenic pathway. We have found that L-tyrosine and L-dihydroxyphenylalanine (L-dopa), whose metabolic fates are affected by the activity of that pathway, can also act as its regulators. In living pigment cells, tyrosinase (EC 1.14.18.1), a crucial and rate-limiting enzyme of melanogenesis, acts in subcellular organelles known as melanosomes. Melanin is laid down only in these organelles. We demonstrate that supplementing Ham's F-10 medium with additional L-tyrosine or L-dopa during the culture of amelanotic Bomirski hamster melanoma cells results in a rapid increase in melanin formation, which is not simply due to greater availability of substrate. There is a rapid increase in tyrosinase activity and a large scale synthesis of melanosomes. The effects of L-tyrosine and L-dopa are prevented by the addition of cycloheximide. The actions of L-tyrosine and L-dopa are specific in that under similar conditions D-tyrosine, D-dopa, N-acetyl-L-tyrosine, L-phenylalanine, L-tryptophan and L-valine have little or no effect. The two substrates, L-tyrosine and L-dopa, appear to act through related but distinct mechanisms. Our findings provide an example of a little-known phenomenon: regulation of a differentiated eukaryotic phenotype through positive control by substrates in the pathway.

Animals↗
PubMed1995

Effects of L-dopa on cholecystokinin octapeptide tissue levels in normal and 6-hydroxydopamine-treated rat brain.

We investigated the changes in cholecystokinin octapeptide (CCK8) tissue levels after the intraperitoneal administration of L-3,4-dihydroxyphenylalanine (L-dopa) in normal and 6-hydroxydopamine (6-OHDA) treated rat brains to clarify the interaction between CCK8 and dopamine (DA). The administration of L-DOPA to the normal rats elevated the regional CCK8-like immunoreactivity (CCK8LI) tissue levels in a dose dependent manner in the frontal cortex, striatum, and nucleus accumbens where CCK neurons were closely associated with DA neurons but not in the hippocampus where CCK neurons were identified as local circuit neurons. Moreover, coadministration of D2-selective antagonist, L-sulpiride, with L-dopa inhibited the elevation of CCK8LI levels in several brain regions. This evidence indicates that CCK8 release was inhibited by exogenous DA converted from L-dopa via D2 receptor stimulation. In the 6-OHDA treated rats on the 3rd day after the treatment, the L-dopa administration elevated the CCK8 levels in several regions. However, the elevation of CCK8LI levels was not observed on the 7th day after the 6-OHDA treatment. These results suggest that there would be a great difference in the effect of L-DOPA on CCK8LI levels between the 3rd day and 7th day after 6-OHDA treatment. It was concluded that the changes in CCK8LI levels would be due to changes in CCK8 release, and that the CCK8 release would be regulated by extracellular DA via D2 receptor.

Animals↗
PubMed1980

Antagonism of KW-5338 (domperidone) against emesis and depression of intestinal motility induced by L-DOPA.

KW-5338 (domperidone), a new dopamine antagonist, is considered to be an agent to cross the blood-brain barrier with difficulty. The antagonistic activities of KW-5338 against L-DOPA were investigated, KW-5338 showed a strong anti-emetic action against L-DOPA induced emesis in beagle dogs (ED50=0.056 mg/kg (p.o.)) and restored the L-DOPA induced depression of intestinal motility to some extent, while it did not antagonize anti-tremorine activities of L-DOPA and trihexyphenidyl in mice. These results suggest that KW-5338 prevents side effects of L-DOPA such as nausea, vomiting and constipation, without reduction in therapeutic effects of L-DOPA in Parkinson's disease.

Animals↗
PubMed1976

Prolactin inhibition test with L-dopa: decrease and restoration of plasma prolactin levels in the rat by a peripheral process.

L-DOPA, within 30 min after administration, induced a highly significant decrease of plasma prolactin levels (phase 1) in a number of groups of rats, differing in age and/or endocrine status, apparently by direct inhibition of prolactin release from the pituitary. Three hours after administration of L-DOPA these low plasma prolactin concentrations in treated animals had increased (phase 2) and did not differ significantly from levels in control animals, indicating that the effect of L-DOPA on plasma prolactin levels is only of short duration. During this process some interesting phenomena were observed, especially in the animals treated with oestrone. The elimination rate of prolactin from plasma was very high (t 1/2 = 2.8 min), as indicated by decreasing concentrations of the hormone during phase 1. Pituitary prolactin content did not change during phase 1, suggesting that prolactin synthesis was also stopped. Notwithstanding the high elimination rate, plasma prolactin regained initial concentrations in phase 2, suggesting release of a substantial part of the pituitary prolactin content. The latter,however, remained constant during the whole experiment (i.e. before L-DOPA administration and during phase 1 as well as phase 2). The results suggested another working mechanism of L-DOPA in decreasing plasma prolactin levels, namely by stimulating the uptake of this hormone in the periphery. After the effect of L-DOPA had ceased, most of the prolactin from the periphery returned into the bloodstream, causing a rapid restoration of plasma prolactin levels without substantial release from the pituitary. The nature of the processes responsible for the peripheral uptake of prolactin is discussed.

Animals↗
PubMed1991

Effects of L-dopa or dopamine on human decidual prostaglandin synthesis.

L-Dopa and three catecholamines in the amniotic fluid before and after labor were measured to confirm the amniotic fluid catecholamine levels at the end of gestation. L-Dopa values were higher than those of three catecholamines, and dopamine which was the predominant catecholamine, rose significantly after the onset of labor. Then, to evaluate the effects of L-dopa or dopamine on prostaglandin synthesis, strips of human decidua vera obtained from fetal membranes at the time of elective cesarean sections before the onset of labor were incubated in Krebs-Ringer buffer in the presence of L-dopa or dopamine. When L-dopa was added, the net production of prostaglandin(PG)F was significantly greater than that of the control at each incubation time. On the other hand, the significant rise was observed only after 10 min of incubation for PGE2 production. Dopamine had a stimulatory effect on PGF synthesis only after 15 and 30 min of incubation, and it also stimulated the release of PGE2 at each incubation time. These results suggest that dopamine and L-dopa in amniotic fluid stimulate the production of prostaglandin by the decidua in humans.

Amniotic Fluid↗
PubMed1978

Effect of glucose on the glucagon response to L-dopa in normal and diabetic subjects.

The effect of an oral dose of 1 gm. L-dopa either without or after a concomitant oral administration of 100 gm. glucose on the plasma level of pancreatic glucagon, plasma immunoreactive insulin (IRI), and plasma growth hormone (GH) was assessed in eight normal and 10 insulin-treated diabetic subjects. In the normal group the stimulatory effect o L-dopa on pancreatic glucagon release was reconfirmed. Moreover, in the diabetics essentially the same plasma glucagon increase after drug administration was found, such a response being inhibited in both groups by glucose. The increase of plasma GH after L-dopa in both healthy persons and diabetics and the inhibition of this response by glucose in healthy subjects was reconfirmed. Furthermore, the same effect of exogenous glucose on the L-dopa induced GH release was observed in diabetics. It may be concluded that glucagon may play a pathogenetic role in the worsening of parkinsonian diabetic patients during the treatment with L-dopa and that diabetic hyperglycemia per se seems to be insufficient for an inhibition of the release of both glucagon and GH AFTer L-dopa.

Adult↗
PubMed1996

Evaluation of the pro-oxidant and antioxidant actions of L-DOPA and dopamine in vitro: implications for Parkinson's disease.

The antioxidant and pro-oxidant properties of L-DOPA and dopamine were investigated in vitro. Both compounds inhibited the peroxidation of ox-brain phospholipids, with IC50 values of 8.5 microM for dopamine and 450 microM for L-DOPA. Dopamine and L-DOPA reacted with trichloromethyl peroxyl radicals (CCl3O2.) with rate constants of 2.1 x 10(7)M-1s-1 and 1.3 x 10(7)M-1s-1 respectively. The effects of dopamine and L-DOPA on iron ion-dependent hydroxyl radical generation from H2O2 were complex. In general, low concentrations stimulated OH. formation in the presence of ferric-EDTA and, in the case of L-DOPA, ferric-ADP and ferric citrate chelates. Both compounds also reacted with superoxide radical and hypochlorous acid. The products of the reaction with HOCl could still inhibit alpha 1-antiproteinase and appear to be 'long lived' chloramine-type oxidizing species. Our results suggest that L-DOPA and dopamine might have a complex mixture of pro- and anti- oxidant effects, which could contribute to tissue damage due to oxidative stress in Parkinson's disease and other neurological disorders.

Animals↗
PubMed2001

Changes of gastric lipase activity after ethanol and indomethacin administration: influence of pretreatment with allopurinol, pentoxifylline and L-DOPA.

Gastric lipase (GL) plays an important role in emulsification and digestion of food fat. Lipids are components of the hydrophobic mucus and mucosa barrier. Damage of the gastric mucosa may therefore be related to changes in the lipid content and GL activity. In the present paper, we studied the effect of administration of a single dose of 96 % ethanol (E) and indomethacin 20 mg x kg(-1) (IND) on the activity of GL and on the concentrations of nonesterified fatty acids (NEFA) and triacylglycerols (TG) in the gastric mucosa of rats. Furthermore, we studied how these changes are affected by allopurinol (ALO), pentoxifylline (PX) and L-DOPA pretreatment 30 min before administration of E or IND. The effect of sialoadenectomy (SA) on these parameters was also evaluated. We found: 1) significant (p < 0.01) inhibition of GL activity after administration of E and IND and also ALO, as well as after pretreatment with ALO before E and PX before IND. L-DOPA administered alone stimulated GL activity, but its administration before IND significantly (p < 0.01) inhibited this enzymatic activity. GL activity was decreased to the threshold values in SA rats and after administration of E to SA animals. 2) NEFA concentrations were decreased after E and increased significantly (p < 0.01) after IND administration. A marked significant (p < 0.01) decrease in NEFA was found after PX and L-DOPA administration. The administration of ALO also lowered the concentration of NEFA. Pretreatment by drugs before E and IND resulted in a significant increase of NEFA in comparison with the drugs given alone (p < 0.05 for ALO + E; p < 0.01 for PX + IND). 3) TG were also decreased in all experimental groups in comparison with the control group, i.e. after E and IND, after ALO and SA and also after pretreatment by ALO before E. The concentration of TG decreased after PX, significantly (p < 0.05) after L-DOPA and after pretreatment by PX before IND. Pretreatment by ALO before E and L-DOPA before IND resulted in the increase of TG in comparison with drugs alone. Thus, these results suggest certain protective effect of pretreatment with ALO, PX and L-DOPA against the E- and IND-induced decrease in NEFA and TG during injury of the gastric mucosa. On the other hand, inhibition of GL activity was also apparent after administration of these drugs before E and IND, which suggest presence of a persisting impairment of lipid digestion in the stomach.

Allopurinol↗
PubMed1975

Intestinal decarboxylation of orally administered L-dopa. Influence of pharmacological preparations, dose magnitude, dose sequence and food intake.

The intestinal decarboxylation and the absorption of orally administered L-dopa have been studied in 20 parkinsonian patients in different conditions. The decarboxylation generally amounted to 50-70% of the dose given, i.e. only 30-50% of orally administered L-dopa reached the general circulation. The shape of the plasma concentration curve varied individually and with the resolvation time of the type of pharmacological preparation given. No obvious difference in the degree of intestinal decarboxylation was observed when tablets with different resolvation times were given but the net absorption of L-dopa was somewhat greater when it was given as a solution. The decarboxylation in the intestinal organs was found to be rather constant at different times of the day. Isocaloric meals, whether rich in protein or carbohydrate, caused a delay in absorption of L-dopa, but did not change the degree of decarboxylation. Diurnal variations in the clinical response to L-dopa, could, thus, not be related to diurnal variations in the decarboxylation in the intestinal organs. The delay in L-dopa absorption after meals may be misinterpreted as lack of response. At dosage with short intervals, the delay may cause an additive effect of two doses.

Administration, Oral↗
PubMed1993

Effect of L-dopa on human muscle sympathetic nerve activity.

This study was undertaken to clarify the mechanism of orthostatic hypotension, one of the side effects frequently encountered after administration of levodopa (L-dopa). Muscle sympathetic nerve activity (MSNA) was measured concomitantly with blood pressure (BP), heart rate (HR) and calf blood flow (calf BF). The responses of these variables to head-up tilting (HUT) were analyzed before and after intravenous administration of L-dopa (50 mg) in eight healthy subjects. L-dopa induced significant increases in MSNA, with concomitant decreases in BP and no changes in calf BF in the supine position. At each angle of HUT, both MSNA and the calf BF increased, following administration of L-dopa. The pattern of MSNA changes was dissociated from that of the calf BF under the influence of L-dopa. These results suggest that peripheral, rather than central, mechanisms are involved in L-dopa-induced orthostatic hypotension.

Adult↗
PubMed1976

[The effect of L-tryptophan on L-dopa absorption (author's transl)].

Dopa blood levels were measured in healthy subjects after oral intake of 0.5 g L-dopa (seven subjects) as well as of 0.5 g L-dopa and 1.0 g L-tryptophan (six subjects). Combined L-dopa and L-tryptophan administration produced significantly less of a rise in dopa blood levels than L-dopa alone.

Dihydroxyphenylalanine↗
PubMedDate not supplied

Synergistic effect of SCH 58261, an adenosine A2A receptor antagonist, and L-DOPA on the reserpine-induced muscle rigidity in rats.

The aim of the present study was to find out whether a blockade of adenosine A2A receptors by the selective antagonist, SCH 58261, potentiates the attenuating effect of L-DOPA, the well-known antiparkinsonian drug, on parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic method, which simultaneously measured muscle resistance of a rat hindfoot to passive extension and flexion in the ankle joint and the electromyographic (EMG) activity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was produced by reserpine (5 mg/kg ip) injected in combination with alpha-methyl-p-tyrosine (alpha-MT, 250 mg/kg ip). L-DOPA (25 mg/kg ip) or SCH 58261 (0.1 mg/kg ip) administered separately, slightly influenced the reserpine + alpha-MT-induced muscle rigidity. However, only ankle joint extension was affected significantly while the effect on flexion of the rat hindfoot was not significant. Neither L-DOPA nor SCH 58261 given separately modified the reserpine-enhanced tonic or reflex EMG activities in both muscles examined. However, when L-DOPA (25 mg/kg) was given together with SCH 58261 (0.1 mg/kg), a clear synergistic effect was seen on both examined movements and muscles. The present results show that the blockade of adenosine A2A receptors potentiates the antiparkinsonian effect of L-DOPA. Since such an effect was seen in different animal models of Parkinson's disease (PD), it seems that co-administration of SCH 58261 may allow for the lowering of the doses of L-DOPA in clinical practice, which indicates a potential therapeutic value of this compound in the treatment of PD.

Adenosine A2 Receptor Antagonists↗
PubMed1992

L-dopa induces opposing effects on pain in intact rats: (-)-sulpiride, SCH 23390 or alpha-methyl-DL-p-tyrosine methylester hydrochloride reveals profound hyperalgesia in large antinociceptive doses.

The present study shows that during the time course of the action of single doses, L-dopa induces multiphasic opposing effects on pain, recorded as vocalization during the presentation of electrical stimulation applied to the tail of normal rats. This indicates that two or more functional systems contribute to produce the net response. A small dose (15 mg/kg) of L-dopa facilitates pain slightly, whereas larger doses (100-200 mg/kg) can produce an antinociceptive effect following an initial hyperalgesia. Moreover, profound hyperalgesia is revealed by either dopamine (DA) D1 and D2 receptor blockade by means of SCH 23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetra-hydro-1H- 3-benzazepine hydrochloride] or (-)-sulpiride, respectively, as well as after a reduction of the presynaptic synthesis of catecholamines after pretreatment of the animals with the tyrosine hydroxylase inhibitor alpha-methyl-DL-p-tyrosine (alpha-MPT). The enhancement of L-dopa's hyperalgesic effect after SCH 23390 treatment is maximal already at the onset of the effects, whereas (-)-sulpiride or alpha-methyl-DL-p-tyrosine precipitates the hyperalgesia after a certain temporal delay during defined phases of the time course of the effects of large L-dopa doses. The D1 receptor agonist (+)-SKF 38393 potentiates both the hyperalgesic and antinociceptive effects of 100 mg/kg of L-dopa. It is suggested that L-dopa's net effect on pain is modulated from concentration-dependent, opposing effector systems involving both DA stimulatory and inhibitory receptor mechanisms. At high dosing, activation of D2 receptors enhancing DA functional activity produces an antinociceptive response that normally outweighs the hyperalgesia, but this effect becomes dissociable with inhibition of central DA activity.

Analgesics↗
PubMed1990

Role of opiates in striatal D-1 dopamine receptor supersensitivity induced by chronic L-dopa treatment.

Repeated administration of L-dihydroxyphenylalanine (L-dopa) to rats lesioned with monolateral intranigral injections of 6-hydroxydopamine counteracted the increased density of striatal [3H]spiroperidol binding sites induced by the lesion. On the contrary, the treatment with L-DOPA further enhanced the hypersensitivity of adenylate cyclase to dopamine stimulation that follows striatal denervation. In addition, the apomorphine-induced rotations were strongly potentiated. The latter effect was antagonized by morphine given acutely shortly before the dopamine agonist. On the other hand, the efficacy of [D-Ala2]-methionine enkephalinamide to inhibit striatal adenylate cyclase was decreased in 6-hydroxydopamine-lesioned rats chronically treated with L-dopa. Moreover, in these animals, when naltrexone was given chronically together with L-dopa, the supersensitivity of the enzyme to dopamine stimulation did not develop. Finally, in 6-hydroxydopamine-lesioned rats, chronic morphine, similarly to L-dopa, further enhanced the responses of adenylate cyclase to dopamine stimulation. These data suggest that prolonged indirect activation of striatal opiate receptors and their consequent desensitization could be among the causes of the hyperactivity of D-1 dopamine receptors that follows chronic L-dopa treatment.

Adenylyl Cyclases↗
PubMed1989

Quality control procedure for 6-[18F]fluoro-L-DOPA: a presynaptic PET imaging ligand for brain dopamine neurons.

The goal of the current study was to establish a quality control procedure for clinical use of 6-[18F]fluoro-L-DOPA (6-[18F]-DOPA) as a selective presynaptic positron emission tomographic (PET) imaging ligand for brain dopamine neurons. A high performance liquid chromatographic procedure using a 5-mu C-18 reverse phase column and ion-pairing mobile phase was used for the quantification of 6-[18F]-DOPA. The radiochemical purity of 6-[18F]-DOPA was measured by 18F radioactivity in HPLC fractions while the chemical purity was determined by an amperometric electrochemical detector with a sensitivity of 25 pg. Quality control of eight consecutive batches of highly purified 6-[18F]-DOPA sample used in a pre-clinical trial revealed that the chemical and/or radiochemical purity of the PET imaging ligand, 6-[18F]-DOPA was greater than 97 +/- 0.5% with a specific activity of 365 +/- 31 mCi/mmol. The knowledge and assurance of radiochemical purity of PET ligands are essential for the interpretation of clinical PET imaging results. The assurance of such quality control would enable comparisons of 6-[18F]-DOPA/PET data obtained from various medical centers using different radiopharmaceutical procedures.

Brain↗