Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DOPA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed2006

Serotonin 2A receptor antagonist treatment reduces dopamine D1 receptor-mediated rotational behavior but not L-DOPA-induced abnormal involuntary movements in the unilateral dopamine-depleted rat.

Previous experiments have demonstrated that serotonin (5-HT) 2A receptor antagonists suppress hyperkinetic behaviors associated with dopamine (DA) D1 receptor supersensitivity in rats with 6-hydroxydopamine (6-OHDA) lesions. Since l-DOPA induced dyskinesia (LID) may be mediated by over-sensitive D1-mediated signaling, the present study examined the effects of the selective 5-HT2A antagonist M100907 on LID behaviors in DA-depleted rats. Adult male Sprague-Dawley rats with unilateral 6-OHDA lesions received daily l-DOPA treatments to produce dyskinetic behaviors as measured by abnormal involuntary movements (AIMs) testing. In these animals, M100907 (0.01, 0.1 or 1.0mg/kg, ip) given 30 min before l-DOPA did not alter the appearance or intensity of AIMs behaviors. Because l-DOPA induced AIMs in rats are dependent upon D1 and D2 receptor activation, a second study was performed to determine if M100907 could suppress D1- or D2-mediated rotational behaviors. Contralateral rotations induced by the D1 agonist SKF82958 were significantly reduced by pre-treatment with M100907. However, M100907 was ineffective in reducing rotations induced by the D2 agonist quinpirole. The finding that M100907 suppresses rotations induced by D1, but not D2, agonists may provide a partial explanation for the lack of effect of a selective 5-HT2A antagonist on l-DOPA-induced AIMs behaviors.

Analysis of Variance↗
PubMed2005

Effects of disease progression and L-dopa therapy on the control of reaching-grasping in Parkinson's disease.

The present study aimed to determine whether the bradykinesia of Parkinson's disease (PD) patients during the execution of reaching-grasping movements (i) is related to an impaired implementation of movement parameters and (ii) selectively involves the control of reach and/or grasp movements. We compared the kinematics of reaching to grasp of differently sized objects placed at different positions, among PD patients in the early stage of disease (ESPD), in the advanced stage of disease (ASPD) without L-dopa medication (off-state), and in healthy controls. In addition, we analysed the effects of L-dopa replacement therapy by comparing the kinematics of the patients in the advanced stage of disease after L-dopa administration with those of the other groups. Bradykinesia increased with disease progression, but only in the initial phases of the reach and grasp components. However at both stages of the disease, the kinematics of reaching and grasping responded to extrinsic and intrinsic object properties just as in controls. L-dopa administration improved the performance of PD patients, though this was more evident for the reach than for the grasp. We suggest that the basal ganglia (BG) are involved in implementing kinematic parameters, but neither (or only marginally) in the initial movement parameterization itself, nor in the on-line control of movement. Specifically, the BG dysfunction in PD induces a slowed implementation of movement parameters. The lack of effect of L-dopa administration on grasp kinematics may be because the motor control of distal effectors is less represented in the motor circuitry formed by the supplementary motor area (SMA), thalamus and BG.

Aged↗
PubMed2005

l-dopa-induced reversal in striatal glutamate following partial depletion of nigrostriatal dopamine with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

We have reported that 1 month following acute (20mg/kg x 4) or subchronic (30 mg/kg/day x 7d) administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, there is an increase or decrease, respectively, in the extracellular level of striatal glutamate as determined by in vivo microdialysis [Robinson S, Freeman P, Moore C, Touchon JC, Krentz L, Meshul CK (2003) Acute and subchronic MPTP administration differentially affects striatal glutamate synaptic function. Exp Neurol 180:73-86]. The goal of this study was to determine the effects of treatment with l-dopa (15 mg/kg) for 21 days on striatal glutamate starting on day 8 after the first dose of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine was administered to mice. Following acute administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, the increase in extracellular striatal glutamate due to lesion of the nigrostriatal pathway was completely reversed to a level below that found in the vehicle-treated group after l-dopa treatment. Subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment resulted in a decrease in striatal extracellular glutamate that was reversed to the level close to that observed in the vehicle-treated group. There was no change in the density of nerve terminal glutamate immunolabeling associated with the synaptic vesicle pool, suggesting that the alterations in extracellular glutamate most likely originated from the calcium-independent pool. There was a similar decrease in the relative density of tyrosine hydroxylase immunolabeling, a marker for dopamine terminals, within the dorsolateral striatum in both the acute and subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated groups that had been administered l-dopa. There was a decrease in the relative density of immunolabeling within the dorsolateral striatum for the glutamate transporter, GLT-1, following acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment in the groups administered either vehicle or l-dopa. There was no change in GLT-1 immunolabeling following subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. The results demonstrate that the reversal in the extracellular level of striatal glutamate following l-dopa treatment in both the acute and subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated groups is not due to changes in either striatal dopamine nerve terminals or in the density of the glutamate transporter, GLT-1.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2005

The 'magic' of L-dopa: why is it the gold standard Parkinson's disease therapy?

The chronic treatment of Parkinson's disease with L-dopa is often associated with fluctuations of motor response and dyskinesias. Therefore, to overcome the adverse effects of the long-term use of L-dopa, directly acting dopamine receptor agonists have been introduced. However, L-dopa remains the most effective treatment of the slowness of movement, increased muscle tone, and tremor that are typical of Parkinson's disease. Why is this so? In this article, we discuss evidence that suggests that dopamine produced from L-dopa has a larger number of actions compared with dopamine receptor agonists. In addition to stimulating D1- and D2-like dopamine receptors, dopamine might also activate adrenoceptors, novel dopamine sites, the dopamine transporter and trace amine receptors, all of which might contribute to the superior effect of L-dopa in Parkinson's disease.

Antiparkinson Agents↗
PubMed2005

New ideas on the origin of L-dopa-induced dyskinesias: age, genes and neural plasticity.

More than 50% of Parkinson's disease (PD) patients treated with L-dopa develop L-dopa-induced dyskinesias (LIDs) in the long term. Some patients exhibit severe dyskinesias soon after starting low doses of L-dopa, whereas other patients remain free of this disabling complication despite treatment with L-dopa. Avoiding or delaying the appearance of LIDs is one of the main objectives of the management of PD. Plasticity of the brain to adapt to a progressive disease, together with a non-physiological treatment strategy, might be the key physiopathological element that underlies LIDs. Neural plasticity varies among patients according to age and genetics. Thus, I propose that this variation explains the observed differences in the occurrence of LIDs in PD patients. Furthermore, I suggest that denervation and L-dopa treatment act as modulating and triggering factors of LIDs, respectively. In this article, the practical implications of these ideas and the role of pharmacogenetics in PD treatment are discussed. Treatment decisions are likely to rely on this information, challenging the relevance of current 'hot' debates about how to start treatment in PD.

Adult↗
PubMed2002

MK801 suppresses the L-DOPA-induced increase of glutamate in striatum of hemi-Parkinson rats.

In vivo microdialysis in freely moving rats was used to investigate the influence of the indirect dopamine receptor agonist levodopa (L-DOPA), alone and combined with the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK801), on extracellular glutamate levels in the striatum of intact and 6-hydroxydopamine-lesioned rats. L-DOPA (25 mg/kg i.p. after benserazide 10 mg/kg i.p.) increased extracellular glutamate levels in the striatum of both intact and dopamine-depleted rats. A prior injection of MK801 (0.1 and 1.0 mg/kg i.p.) did not alter the L-DOPA-induced glutamate release in the striatum of intact rats. In contrast, the L-DOPA-induced increase in glutamate in the striatum of 6-hydroxydopamine-lesioned rats was suppressed by MK801 (0.1 mg/kg i.p.). The data presented here suggest that NMDA receptors do not play a role in the L-DOPA-induced increase in striatal glutamate in intact rats but are involved in the glutamate release in the dopamine-depleted striatum. The suppression of this increase by prior administration of MK801 could represent a neuroprotective effect.

Animals↗
PubMed2003

Amantadine increases L-DOPA-derived extracellular dopamine in the striatum of 6-hydroxydopamine-lesioned rats.

We investigated the effect of amantadine on L-DOPA-derived extracellular dopamine (DA) levels and aromatic L-amino acid decarboxylase (AADC) activity in the striatum of rats with nigrostriatal dopaminergic denervation by 6-hydroxydopamine (6-OHDA). Pretreatment with 30 mg/kg amantadine increased the cumulative amount of extracellular DA in the striatum of 6-OHDA-lesioned rats treated with 10 mg/kg benserazide and 50 mg/kg L-DOPA to 250% of that without amantadine (P<0.01). Under pretreatment with 10 mg/kg benserazide, AADC activity after 30 mg/kg amantadine administration was reduced to 43% of controls (P<0.01). Amantadine-induced increase in L-DOPA-derived extracellular DA provides the basis for the clinical usefulness of amantadine in combination with L-DOPA. However, the effect of amantadine on L-DOPA-derived extracellular DA may not be caused by changes in AADC activity.

Adrenergic Agents↗
PubMed2003

Monoamine neuron innervation of the normal human brain: an 18F-DOPA PET study.

18F-DOPA positron emission tomography (PET) has been used for two decades to study the organization and pathology of the striatal dopamine system in the human brain, particularly in Parkinson's disease. High resolution 3D PET allows a more detailed analysis than previously available and was employed in this study to determine the regional uptake of 18F-DOPA in control brain. Eleven healthy volunteers underwent 18F-DOPA PET with a region of interest (ROI) study performed using individual volumetric MRI's coregistered to the PET ADD image. A Patlak linear graphical analysis was undertaken to obtain influx constant (Ki) values. The highest Ki values were from neostriatal areas, with a rostrocaudal gradient of increasing Ki values from head of caudate nucleus to rostral putamen to caudal putamen. However, Ki values for transaxial slices from dorsal to ventral through the caudate and putamen were uniform. Ventral striatum Ki was 81% with red nucleus and globus pallidus Ki values of approximately 40% of neostriatum. In limbic areas, highest values were obtained from amygdala (35% neostriatal Ki). Neocortical Ki values varied from 22% in temporal pole to 6% in occipital cortex of neostriatal values. Hypothalamic Ki was high (45%) in comparison to thalamus (17%) and retina (17%). 18F-DOPA is taken up by serotonin (raphe, 51%), and noradrenaline (locus coeruleus, 37%) as well as dopamine neurons. These data indicate that 18F-DOPA PET can be used with detailed, anatomically based ROIs as a tool for in vivo analysis of regional changes in monoamine neuron systems throughout the brain in Parkinson's disease and other disorders.

Adult↗
PubMed1999

Loss of regulation by presynaptic dopamine D2 receptors of exogenous L-DOPA-derived dopamine release in the dopaminergic denervated striatum.

To determine whether dopamine release derived from exogenous l-DOPA is under inhibitory control of presynaptic dopamine D2 receptors in the dopaminergic denervated striatum, extracellular dopamine levels were measured in the striatum of 6-hydroxydopamine-lesioned rats using in vivo brain microdialysis. Quinpirole, a D2 agonist, dose-dependently (0.01-3 mg/kg s.c.) inhibited endogenous dopamine release both in the intact and dopaminergic denervated striatum. The dose-response curve obtained from the denervated striatum showed a shift to the right. Administration of l-DOPA (30 mg/kg i.p.) with carbidopa (25 mg/kg i.p.) increased dopamine release to 130% of basal levels in the intact striatum and 770% of basal levels in the denervated striatum. In the intact striatum, dopamine release was continuously inhibited by quinpirole pretreatment (1 mg/kg s.c.) even after l-DOPA administration. In the denervated striatum, l-DOPA-derived dopamine release was not affected by quinpirole pretreatment. These results suggest that, in the striatum with dopaminergic denervation, regulation by presynaptic D2 receptors is still operative on endogenous dopamine release but it does not work on dopamine release derived from exogenously administered l-DOPA.

Animals↗
PubMed2001

Tonic function of nicotinic receptors in stress-induced release of L-DOPA from the nucleus accumbens in freely moving rats.

We investigated whether stress induces the release of L-3,4-dihydroxyphenylalanine (DOPA) and dopamine from the nucleus accumbens in conscious rats and characterized the stress-induced response. Electrical foot-shock stress induced both DOPA and dopamine release, measured by microdialysis, from the nucleus accumbens in freely moving rats. Pretreatment of rats with mecamylamine completely blocked stress-induced DOPA release, but only partially blocked dopamine release. Diazepam did not affect the foot-shock-induced release of DOPA, while the same dose of diazepam partially blocked the stress-induced release of dopamine. These findings suggest a tonic function of central nicotinic receptors in stress-induced DOPA release from the nucleus accumbens in conscious rats.

Animals↗
PubMed2003

Atipamezole, an alpha2-adrenoceptor antagonist, augments the effects of L-DOPA on evoked dopamine release in rat striatum.

The effects of atipamezole, an alpha(2)-adrenoceptor antagonist, L-3,4-dihydroxyphenylalanine (L-DOPA) and the combination of these drugs on dopamine overflow were studied in dopaminergic presynaptic terminals of rat caudate and nucleus accumbens. Dopamine overflow evoked by 100 pulses of electrical stimulation of the medial forebrain bundle at a low (20 Hz) and high (50 Hz) frequency was measured by in vivo voltammetry. L-DOPA (15 mg/kg) increased dopamine overflow in the caudate nucleus, but this dose had no effects in the nucleus accumbens. Atipamezole (300 microg/kg) had no effects on its own on dopamine overflow, but it did increase the size of the readily releasable storage pool and the effects of L-DOPA treatment in both structures. The combination of the drugs increased dopamine overflow to a larger extent at high compared to low stimulation frequencies. We conclude that the rat caudate nucleus is more sensitive than the nucleus accumbens to the effects of L-DOPA, and the effects of L-DOPA treatment might be effectively enhanced by antagonism of alpha(2)-adrenoceptors.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1997

Adenosine A2A receptor antagonism potentiates L-DOPA-induced turning behaviour and c-fos expression in 6-hydroxydopamine-lesioned rats.

In order to investigate the role of adenosine A2A receptor blockade on dopamine-mediated motor responses, contralateral turning behaviour and expression of the early-gene c-fos was evaluated in rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigrostriatal pathway. SCH 58261, (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1 , 5-c]pyrimidine) a potent and selective antagonist of adenosine A2A receptors (5 mg/kg i.p.), induced a 70-fold increase in the contralateral turning behaviour induced by a low dose (2 mg/kg i.p.) of the dopamine precursor L-DOPA (L-3, 4-dihydroxyphenylalanine). Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain. SCH 58261 induced a less marked potentiation (7-fold) of turning behaviour induced by dopamine D2 receptor stimulation with quinpirole, while Fos-like immunoreactivity in the striatum and globus pallidus was not affected. Previous studies have shown that SCH 58261 strongly potentiated dopamine D1 receptor-mediated responses. The results of the present study therefore indicate that the positive interaction between SCH 58261 and L-DOPA, in 6-hydroxydopamine-lesioned rats, is mainly due to an interaction with dopamine D1 receptors. The data also suggest that adenosine A2A receptor antagonists might be useful for potentiating the effects of L-DOPA in Parkinson's disease.

Animals↗
PubMed1998

Effect of trihexyphenidyl, a non-selective antimuscarinic drug, on decarboxylation of L-dopa in hemi-Parkinson rats.

In vivo microdialysis was used to study the effect of the non-selective muscarinic antagonist, trihexyphenidyl, on the decarboxylation of levodopa (L-dopa) in the striatum of hemi-Parkinson rats. In normal rats, continuous perfusion of trihexyphenidyl (1 mM) via the microdialysis probe induced a significant increase in striatal dopamine release, followed by a decrease to below baseline values. A similar effect was observed, though less pronounced, in denervated striatum of rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway. In these hemi-Parkinson rats, continuous striatal perfusion of trihexyphenidyl had no effect on the biotransformation of locally applied L-dopa (2 microM for 20 min) to dopamine in either intact or denervated striatum. However, systemic administration of trihexyphenidyl (1.5 mg/kg i.p.) produced an attenuation of the L- dopa-induced dopamine release in the intact striatum (contralateral to the lesion) of hemi-Parkinson rats. This effect was absent in the denervated striatum of these animals. We confirmed that L-dopa induces an increase in striatal dopamine output which is influenced by the severity of the dopaminergic denervation. The absence of an effect of trihexyphenidyl locally applied in the striatum, on biotransformation of L-dopa suggests that the site of action of antimuscarinic drugs may not be in the striatum and, therefore, remains unclear. The mechanism of action of these drugs is not well understood but appears more complicated than previously thought.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Effect of renal interstitial infusion of L-dopa on sodium and phosphate excretions.

It has been hypothesized that dopamine synthesized by the proximal tubule can act as a paracrine substance that regulates reabsorption by the proximal tubule. The present study was performed to study the effects of the stimulation of endogenous synthesis of dopamine by infusion of L-DOPA directly into the renal interstitium on sodium and phosphate excretions and to determine the roles of D1 and D2 receptors in the response. The infusion of L-DOPA (50 microg/kg/min) into the renal interstitium through an implanted matrix significantly increased the fractional excretion of sodium (FENa) from 1.0%+/-0.2% to 3.1%+/-0.6% and the fractional excretion of phosphate (FEPi) from 23%+/-3% to 36%+/-3%, P < .05, n = 10. The infusion of D1 receptor antagonist SCH23390 or SKF83566 (5 microg/kg/min) into the renal interstitium blocked the natriuretic (FENa 1.5%+/-0.2% to 1.9%+/-0.4%) and phosphaturic (FEPi 41%+/-3% to 41%+/-4%) effects of L-DOPA infusion. The infusion of the D2 receptor antagonist sulpiride at a rate of 4 microg/kg/min into the renal interstitium also attenuated the natriuretic (FENa 1.3%+/-0.3% to 1.6%+/-0.5%) and phosphaturic effects of L-DOPA infusion (FEPi 36%+/-5% to 39%+/-5%). We conclude that the renal interstitial infusion of L-DOPA increases sodium and phosphate excretions and that these responses are mediated by D1 and D2 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1975

Evaluation of growth hormone release in children using arginine and L-dopa in combination.

L-Dopa in a dose ranging from 125-500 mg and arginine monochloride in a dose of 0.5 gm/kg were given simultaneously to 56 children with short stature (height less than third percentile). Sixteen of these children were subsequently diagnosed as having growth hormone deficiency. The diagnosis of hyposomatotropism was based on clinical findings and on responses to the combination test and to arginine and L-dopa administered as separate tests. All of the remaining 40 children had a normal GH response of greater than 6 ng/ml to the combination test. However, in this group, nine children were identified who responded to the combination test but who failed to respond to arginine and L-dopa in individual tests. The data suggest that a positive response to arginine and L-dopa in combination in children, who do not respond to the usual provocative tests when administered individually, may fail to identify children with partial GH deficiency who would benefit from treatment. The integrated stimulated GH response in the 31 children in whom a normal GH response to all three tests occurred suggests that the effects of L-dopa and arginine are additive.

Adolescent↗
PubMed2003

Hypertrophy of IMC of carotid artery in Parkinson's disease is associated with L-DOPA, homocysteine, and MTHFR genotype.

In recent years, an intense interest has developed in the association between Parkinson's disease (PD) and hyperhomocysteinemia. Homocysteine (Hcy) is a neuronal excitotoxic amino acid, and is well known as a risk factor for vascular diseases. Some reports suggest that the administration of L-DOPA may promote hyperhomocysteinemia and idiopathic atherosclerosis. In this study, we report that a mild hypertrophy of the intima-media complex (IMC) of the carotid artery, which has been established as a marker for systemic atherosclerosis, is observed in PD patients compared with normal subjects. PD patients that were treated with L-DOPA for long durations showed a hypertrophic IMC, while the patients that were not treated with L-DOPA did not show any hypertrophic changes in the IMC. These hypertrophic changes were observed primarily in patients with a Hoehn-Yahr stage of 3-5. PD patients with hypertrophic IMC of the carotid artery also exhibited elevated plasma levels of Hcy associated with the C677T genotype of 5,10-methylenetetrahydrofolate reductase (MTHFR). Moreover, a prolonged duration of treatment with L-DOPA in patients with MTHFR T/T genotype enhanced the hypertrophy of IMC, compared with patients with the C/C or C/T genotype. These results suggest that hyperhomocysteinemia promoted by the C677T genotype of MTHFR and prolonged treatment with L-DOPA enhances atherosclerosis in PD patients and affects their general condition.

Aged↗
PubMed2003

The L-DOPA-sparing effect of R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane hydrochloride [(-)-BPAP] in reserpine-pretreated rats.

R-(-)-1-(Benzofuran-2-yl)-2-propylaminopentane hydrochloride [(-)-BPAP], a highly potent enhancer of impulse propagation-mediated release of catecholamines and serotonin in the brain, and significantly increased the locomotor activity of normal rats at the doses of 0.3 and 1 mg/kg s.c. (P < 0.05), while L-DOPA (200 and 400 mg/kg i.p.) had no significant effect. The locomotor activity of rats simultaneously administered L-DOPA and (-)-BPAP was significantly higher than with (-)-BPAP alone (P < 0.05). In rats pretreated with reserpine (1 mg/kg i.v.), the hypolocomotion was significantly reversed by 400 mg/kg i.p. L-DOPA, or 1 or 3 mg/kg s.c. (-)-BPAP (P < 0.05). Furthermore, the combined administration of subthreshold doses of 200 mg/kg i.p. L-DOPA and 0.3 mg/kg s.c. (-)-BPAP highly potentiated the locomotor activity in the reserpine-pretreated rats. However, (-)-BPAP failed to reverse the hypolocomotion in rats pretreated with reserpine + alpha-methyl-DL-p-tyrosine. Thus, (-)-BPAP was demonstrated to possess the L-DOPA-sparing effect in normal and reserpine-pretreated rats.

Animals↗
PubMed2001

Interruption of the MnO2 oxidative process on dopamine and L-dopa by the action of S2O3(2-).

The oxidation effects of Mn2+, Mn3+ or MnO2 on dopamine can be studied in vitro and, therefore, this offers a model of the auto-oxidation process that appears naturally in neurons causing Parkinson's disease. The use of MnO, as an oxidizer in aqueous solution at pH 7 causes the oxidation of catecholamines (L-dopa, dopamine, noradrenaline and adrenaline) to melanin. However, this work shows that, in water at pH 6-7, the oxidation of catecholamines by MnO2 in the presence of sodium thiosulphate (Na2S2O3) occurs by other mechanisms. For dopamine and L-dopa, MLCT complexes were formed with bands at 312, 350 (sh), 554 (sh) nm, and an intense band at 597 nm (epsilon approximately/= 4 x 10(3) M(-1) cm(-1)) and at ca. 336, 557 (sh) nm, and an intense band at 597 nm (epsilon approximately 6 x 10(3) M(-1) cm(-1)), respectively. The latter transitions were assigned to d(pi)-->pi*-SQ. Noradrenaline and adrenaline do not form this blue complex in solution, but generate soluble oxidized compounds. The resonance Raman spectra of these complexes in solution showed bands at 950, 1006, 1258, 1378, 1508 and 1603 cm(-1) for the complex derivation of L-dopa and at 948, 1010, 1255, 1373, 1510 and 1603 cm(-1) for the dopamine-derived compound. The most intense Raman band at ca. 1378 cm(-1) was assigned to C-O stretching with major C1-C2 characteristics and indicated that dopamine and L-dopa do not occur complexed with manganese in the catecholate or quinone form, but suggests an intermediate compound such as an anionic o-semiquinone (SQ-), forming a complex such as [Mn(II)(SQ-)3]-. All enhanced Raman frequencies are characteristic of the benzenic ring without the participation of the aminic nitrogen. A mechanism is proposed for the formation of the dopamine and L-dopa complexes and a computational simulation was performed to support it.

Dopamine↗