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PubMed1994

Acute effects of perinatal hypoxic insult on concentrations of dopamine, serotonin, and metabolites in fetal monkey brain.

Seven monkeys (Macaca mulatta) were laparotomized under general anesthesia (halothane, nitrous oxide, oxygen). Fetal hypoxia was induced in four monkeys by occlusion of the umbilical cord with a hydraulic occluder for 5-6 min. Three sham-operated fetuses served as controls. After unclamping, the fetuses were allowed to reperfuse for 20-30 min. To monitor hypoxia, the fetal electrocardiogram was recorded continuously. Hypoxic insult was associated with a decrease in fetal heart rate during the occlusion. After reperfusion, fetuses were immediately sacrificed and neocortex regions dissected on ice, frozen on dry ice and stored at -70 degrees C. Dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, and 5-hydroxyindoleacetic acid were assayed by high performance liquid chromatography with electrochemical detection (HPLC/EC) in hippocampus, caudate nucleus and cortical regions. In the hippocampus, there was a significant increase in 5-hydroxyindoleacetic acid concentration. In prefrontal cortex, there was a trend toward an increase in serotonin but no effects on dopamine and homovanillic acid concentrations. Dopamine, serotonin and metabolites were not altered in the caudate nucleus. These data demonstrate that fetal hypoxia followed by reperfusion produced an increase in serotonin concentration measured within the hippocampus and selected cortical areas known to be targets of hypoxic injury.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1984

Negative feedback control of serotonin release in vivo: comparison of 5-hydroxyindolacetic acid levels measured by voltammetry in conscious rats and by biochemical techniques.

All evidence that serotonin release from central neurones is controlled by a negative feedback mechanism comes from in vitro studies. To study this problem in vivo we performed differential pulse voltammetry in conscious rats, in which carbon fibre electrodes had been implanted 2-15 weeks previously. The effects of monoamine oxidase inhibition (which decreases the amount of 5-hydroxyindoleacetic acid), as well as that of probenecid (which increases 5-hydroxyindoleacetic acid), suggests that 5-hydroxyindoleacetic acid rather than serotonin is measured. Blockade of the presynaptic serotoninergic autoreceptors by methiothepin, metergoline or quipazine led to an increase in differential current of the peak attributed to 5-hydroxyindoleacetic acid in hippocampus, hypothalamus and striatum. Stimulation of these receptors by m-chlorophenylpiperazine, MK-212 or LSD decreased the signal attributed to 5-hydroxyindoleacetic acid. A decrease in the signal was also seen with cinanserin. Stimulation of presynaptic alpha 2-adrenoreceptors by clonidine decreased the signal. Metergoline, quipazine and cinanserin showed biphasic effects, and no effect was observed with methysergide. In general, a reasonable agreement with the results of Baumann & Waldmeier obtained in vitro with electrically stimulated [3H]serotonin prelabelled cortex slices was achieved with differential pulse voltammetry. Only partial agreement with the results of voltammetry was obtained if 5-hydroxyindoleacetic acid was determined biochemically under comparable conditions. Qualitatively, the effects observed with methiothepin, m-chlorophenylpiperazine, clonidine and LSD were in good agreement with those measured with voltammetry as well as with the in vitro effects obtained in electrically stimulated cortex slices. No, or only partial correlation with the results obtained with voltammetry was found with MK 212, cinanserin, metergoline and quipazine. It is concluded that voltammetry preferentially measures extraneuronal 5-hydroxyindoleacetic acid rather than overall changes of this metabolite.

Animals↗

PubMed1987

Factors affecting the stability and separation of biogenic amines and their metabolites. Simultaneous measurement by HPLC with electrochemical detection.

We describe a simple and sensitive method for the rapid and simultaneous quantification of dopamine, 3-methoxytyramine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, serotonin, 5-hydroxyindoleacetic acid, and 5-hydroxytryptophan in the picogram range in small samples of brain tissue. After minimal sample preparation the amines were analyzed utilizing isocratic separation and reversed-phase high-performance liquid chromatography with amperometric detection. The effects of pH and methanol concentration in the solvent on the retention times of the amines on two different C-18 columns were investigated. Stabilities of the amines in solution were determined under various conditions. Light and air were found to be detrimental to the stability of indoles. In the absence of light, their stability was dependent on temperature and the presence of air; however, in the absence of air, light and/or temperature had little effect. The catechols were stable under most of these conditions. The assay has been applied to study the postmortem stability of dopamine, serotonin, and their metabolites in the striatum of rat brain. In the striatum 4 hr after death, the content of dopamine and 3,4-dihydroxyphenylacetic acid decreased by less than 20%, and 3-methoxytyramine increased by 158%, with no changes in serotonin, 5-hydroxyindoleacetic acid, and homovanillic acid.

Animals↗

PubMed1990

Changes in selected brain neurotransmitters and their metabolites in the lamb after thyroidectomy during the last two trimesters of gestation or the early neonatal period.

To evaluate in a development context the effect of congenital hypothyroidism on concentrations of the neurotransmitters norepinephrine, dopamine, and serotonin (5HT) in selected brain areas of the ovine fetus, we studied the effect of thyroidectomy at three ages on the concentrations of these neurotransmitters and their major metabolites, homovanillic acid and 5-hydroxyindoleacetic acid. Fetuses underwent thyroidectomy at 90-95 or 105-115 d gestation (term = 147-150 d) or 1-5 d after birth. Approximately 25 d after thyroidectomy, at d 120-125 or 130-135 of gestation or 25-30 d after birth, respectively, the ewes were killed and fetal brains removed. Neurotransmitters and their metabolites were measured by HPLC with electrochemical detection. Thyroidectomy in the 2nd trimester increased 5HT in five brain areas: anterior hypothalamus, dorsal medial hypothalamus, pons, medulla, and cerebellum. Thyroidectomy in the 3rd trimester increased 5HT in the pons and medulla, increased norepinephrine in the dorsal medial hypothalamus and pons, and increased homovanillic acid in the posterior hypothalamus. Thyroidectomy in the newborn period decreased NE in the anterior hypothalamus, ventral medial hypothalamus, and midbrain, decreased 5-hydroxyindoleactic acid in the posterior hypothalamus, lateral hypothalamus, dorsal medial hypothalamus, and ventral medial hypothalamus, and decreased homovanillic acid in the dorsal medial hypothalamus and ventral medial hypothalamus. From these data we conclude the following: 1) Hypothyroidism causes changes in neurotransmitter concentrations only in selected brain areas of the ovine fetus, rather than causing generalized and similar changes in all brain areas; and 2) 5HT 5-hydroxyindoleacetic acid concentrations are affected more often than the other neurotransmitters evaluated, perhaps because the 5HT neurotransmitter system is developing at these times.

Animals↗

PubMed1993

Cerebrospinal fluid monoamine precursors and metabolites in human neonates following in utero cocaine exposure: a preliminary study.

BACKGROUND: Cocaine acts in the central nervous system by increasing dopamine release and inhibiting the reuptake of dopamine and other monoaminergic neurotransmitters. Prenatal cocaine exposure may cause neurochemical changes in developing monoaminergic neurons and might alter brain structure and function. No data have been published on central nervous system monoamine precursors and metabolites in human neonates exposed prenatally to cocaine. METHODS: Cerebrospinal fluid (CSF) was obtained from neonates undergoing lumbar puncture to rule out infection. The CSF was analyzed for the neurotransmitter precursors and metabolites tryptophan, tyrosine, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, and 5-hydroxyindoleacetic acid. Drug exposure was ascertained by medical record review and urine and meconium assays. RESULTS: Eleven neonates were cocaine-exposed, based on positive meconium or urine assays for benzoylecgonine; 20 were unexposed, based on both negative history and assay. The exposed and unexposed groups did not differ significantly in gender, perinatal stress, clinical illness, or exposure to other illicit drugs, but did differ in mean gestational age, growth parameters, and exposure to cigarettes. Cocaine-exposed neonates had significantly lower levels of CSF homovanillic acid (mean 148.1 vs 218.5 ng/mL, P = .01). The magnitude of this difference was similar after correcting for each of four potential confounding factors, although no longer statistically significant in all cases (P values ranged from .044 to .17). No significant differences were observed for tyrosine, tryptophan, 5-hydroxyindoleacetic acid, or 3-methoxy-4-hydroxyphenylglycol. CONCLUSIONS: These preliminary results suggest an association between prenatal cocaine exposure and decreased CSF homovanillic acid, the principal metabolite of dopamine. Prenatal cocaine exposure may result in changes in central dopaminergic systems in the human neonate.

Biogenic Monoamines↗

PubMed1987

Plasma monoaminergic metabolites and catecholamines in subarachnoid hemorrhage. Clinical implications.

We examined plasma catecholamines and monoaminergic metabolites (3-methoxy-4-hydroxyphenylethyleneglycol [MHPG], homovanillic acid [HVA], and 5-hydroxyindoleacetic acid) in patients with stroke successively up to three weeks after the initiation of symptoms. Plasma levels of free catecholamines were significantly elevated in patients with subarachnoid hemorrhage (SAH). However, no significant differences in plasma catecholamines were found when the patients with SAH were subdivided into noncomatose and comatose groups. In contrast, plasma HVA, MHPG, and 5-hydroxyindoleacetic acid levels in comatose patients with SAH significantly increased as compared not only with normal controls but also with noncomatose patients with SAH, and the peak levels of HVA and MHPG occurred within seven days poststroke. Such trends as observed in SAH were not observed in patients with cerebral hemorrhage. Our results suggest the usefulness of plasma monitoring of possibly centrally originating monoaminergic metabolites for predicting the degree of cerebral dysfunction in patients with SAH.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1975

3-Methoxy-4-hydroxy-phenylglycol sulfate (MOPEG-SO4) in ventricular and cisternal cerebrospinal fluid of dogs.

Cerebrospinal fluid was collected from the lateral ventricles and cisternal space from beagle dogs under light pentobarbital anesthesia. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglyco-sulfate (MOPEG-SO4) levels in the liquor taken from these two regions were evaluated, and the ventricular-cisternal ratio (V/C) was calculated for each monoamine metabolite. A marked similarity in the V/C ratio of 6:1 for 5-HIAA and 5:1 for MOPEG-SO4, as compared to a much higher V/C ratio of 18:1 for HVA, perhaps reflects the more diffuse distribution of norepinephrine and serotonin, precursor amines, as compared to dopamine in the CNS and also emphasizes the probable existence of an active transport mechanism for the removal of MOPEG-SO4, as has been well documented for 5-HIAA and HVA.

Animals↗

PubMed1977

Evidence for a probenecid-sensitive transport system of acid monoamine metabolites from the spinal subarachnoid space.

The location of probenecid-sensitive elimination mechanisms of monoamine metabolites from the cerebrospinal fluid of the cat was determined with ventriculo-cisternal or ventriculo-lumbar perfusion techniques. These techniques were described in detail. Levels of endogenous homovanillic acid and 5-hydroxyindoleacetic acid were assayed in the perfusate. Probenecid administration induced the most marked increase of the levels of the monoamine metabolites in the ventriculo-lumbar perfusates. It was concluded that probenecid blocked the transport of both metabolites from the spinal subarachnoid space.

Animals↗

PubMedDate not supplied

Monoamine metabolism in the striatum of the rat brain during drug infusion into the nucleus accumbens.

Studies on conscious Sprague-Dawley rats using intracerebral dialysis in live animals combined with high-performance liquid chromatography with electrochemical detection showed that administration of apomorphine into the nucleus accumbens decreased the levels of dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid in the extracellular space of the dorsal striatum throughout the observation period and produced a transient reduction in the level of homovanillic acid in the dialysate from this structure. The studies demonstrated that reversible exclusion of the nucleus accumbens with procaine produced a transient increase in the levels of dopamine metabolites, without an increase in serotonin metabolites, in the extracellular space of the dorsal striatum. These results demonstrate that the nucleus accumbens affects dopamine metabolism in the striatum, this being mediated by the dopamine-reactive system in the nucleus accumbens.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

Effects of valproate on amino acid and monoamine concentrations in striatum of audiogenic seizure-prone Balb/c mice.

The effects of valproate on CNS concentrations of gamma-aminobutyric acid (GABA), glulamate (GLU), glutamine (GLN); dopamine (DA), serotonin (5-HT), and metabolites were examined in tissue extracts of caudate nucleus of genetic substrains of Balb/c mice susceptible (EP) or resistant (ER) to audiogenic seizures. Generalized tonic-clonic seizures observed in EP mice were inhibited by valproate, administered 1 h prior to testing, in a dose-response fashion. Concentrations of GABA, GLU, and GLN, which were lower in EP mice than in ER mice, were significantly increased by valproate at doses of 180 and 360 mg/kg. Concentrations of homovanillic acid (HVA) and hydroxyindoleacetic acid (5-HIAA), metabolites of DA and 5-HT, were substantially increased by valproate at these doses. The in situ activity of tyrosine hydroxylase (TH) was not significantly influenced by valproate, whereas a valproate-induced increase in tryptophan hydroxylase (TPH) activity was observed in both striatum and in midbrain tegmentum. The data are consistent with the interpretation that anti-convulsive doses of valproate influences the intraneuronal metabolism of monoamines, GABA, and glutamate concurrently. Valproate's influence on the metabolism of both major inhibitory (GABA) and excitatory (GLY amino acids in striatum could contribute to its anti-convulsive effects in genetically seizure prone mice, as well as to the accumulation of DA and 5-HT metabolites.

Acoustic Stimulation↗

PubMed1983

Direct correlation between level of morphine and its biochemical effect on monoamine systems in mouse brain. Evidence for involvement of dopaminergic neurons in the pharmacological action of acute morphine.

The pharmacokinetics (uptake and elimination) and pharmacodynamics (biochemical effects on monoamine systems) of morphine in the CNS were investigated concurrently. ICR mice, weighing about 25 g, were injected intravenously with several doses (2.5-80 mg/kg) of morphine. The animals were killed by microwave irradiation (5 kW, 0.6 sec) at 10 and 30 min, and 1, 2, 4, 8 and 24 hr after the injection. The intracerebral levels of morphine and metabolically related substances consisting of monoamines [noradrenaline, dopamine (DA), 5-hydroxytryptamine (5-HT), 3, 4-dihydroxyphenylacetic acid (DOPAC), 3-methoxy-4-hydroxyphenylacetic acid [homovanillic acid (HVA)], 5-hydroxyindoleacetic acid (5-HIAA), tyrosine and tryptophan] were determined in identical samples by a combination of organic extraction and high-performance liquid chromatography with electrochemical detection. The intracerebral level of morphine was found to depend on the dose injected, and the biological half-life of the drug was estimated to be about 1 hr. The morphine injection (2.5-80 mg/kg) caused significant increases in monoamine metabolites although only slight changes occurred in the concns of parent transmitters. The intracerebral level of morphine was significantly correlated with the ratios DOPAC/DA and HVA/DA (r = 0.7033, P less than 0.0001; and r = 0.6455, P less than 0.0001, respectively). On the other hand, the correlation between the morphine level and 5-HIAA/5-HT was lower than those for DOPAC/DA and HVA/DA. These results suggest that monoamine systems, especially DA, are closely involved in the biochemical effects of morphine. Furthermore, the proposed procedure is demonstrated to be useful as a new approach in biochemical pharmacology, where the direct correlation between the distribution of a drug (pharmacokinetics) and the biochemical effects of the drug (pharmacodynamics) can be measured.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1984

Differential pulse voltammetry: simultaneous in vivo measurement of ascorbic acid, catechols and 5-hydroxyindoles in the rat striatum.

This paper describes carbon fibre electrodes that can simultaneously monitor changes in ascorbic acid, dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid (HVA) in vivo in the rat striatum using differential pulse voltammetry. The separation between DOPAC and 5HIAA oxidation is improved and the size of the 5HIAA peak decreased by the removal of uric acid using the enzyme uricase indicating that uric acid oxidation may contribute to the oxidation peak at + 300 mV. Haloperidol (0.5 mg/kg) decreased ascorbic acid and 5HIAA but increased DOPAC and HVA while D-amphetamine (3 mg/kg) increased ascorbic acid, decreased DOPAC and HVA but had no effect on 5HIAA. These electrodes should be a useful means of investigating interactions between dopamine and serotoninergic systems in vivo.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1984

Increased transport of 3,4-dihydroxyphenylacetic acid from brain during performance of operant behavior in the rat.

Although the performance of positively reinforced operant behavior is accompanied by increased turnover of brain dopamine in the rat, the accumulation of 3,4-dihydroxyphenylacetic acid (DOPAC), the major metabolic product of dopamine in brain, is not increased during operant performance. The hypothesis that the lack of increased DOPAC accumulation stems from an increase in the rate at which DOPAC is eliminated from the brain was tested by measuring the relative rate of DOPAC transport from brain in rats performing operant behavior and in control rats. The transport of DOPAC was estimated following inhibition of monoamine oxidase with pargyline. The pargyline-induced depletions of DOPAC in the caudate putamen and amygdala were significantly greater in rats that performed operant behavior than in control rats. In the caudate putamen, the concentrations of homovanillic acid and 5-hydroxyindoleacetic acid were also depleted by pargyline to a greater extent in operant performing rats than in controls. These results suggest that in addition to the increased turnover of dopamine in central neurons during operant behavior, the rate of elimination of acidic amine metabolites from brain is also accelerated.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1975

Virus infections in infant mice causing persistent impairment of turnover of brain catecholamines.

Newborn mice were inoculated with attenuated Coxsackie type B4 virus. Three-to-4-day old mice were infected with yellow fever virus vaccine. A number of mice survived the acute infections. Some of these demonstrated residual neurological symptoms, some showed recovery from symptoms while others survived the infection without revealing symptoms of disease. Determinations of dopamine, noradrenaline, 5-hydroxytryptamine, homovanillic acid and 5-hydroxyindoleacetic acid in the inoculated brains indicated an imparied turnover of neurotransmitters. Subnormal concentrations of catecholamines and homovanillic acid were encountered in the acutely-infected mice as well as among the survivors. Failure to synthesize catecholamines was observed not only in mice demonstrating symptoms of disease or in animals which recovered from their infection but also among a proportion of the mice which never demonstrated neurological symptoms. In contrast, 6-week-old Swiss albino mice infected with West Nile virus showed no effect on the turnover of brain monoamines either in acutely infected mice or in animals which survived the acute infection. Herpes simplex virus infection of 3-week-old mice induced during the acute infection an increased release of neurotransmitters. When these mice were "cured" of the infection by increasing the environmental temperature the elevated turnover of monoamine metabolism was normalized. Two months later there were no differences in concentrations of catecholamines or homovanillic acid between infected animals or uninfected controls. Thus, persistent impairment of brain monoamine metabolism was induced in mice infected when very young. The possible importance of the observations, in particular the findings of an impaired turnover after subclinical infection, is discussed.

Age Factors↗

PubMed1987

Behavioral and biochemical changes following acute administration of MPTP and MPP+.

The acute effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ion (MPP+) on mouse locomotor activity and striatal dopamine (DA) and 5-hydroxytryptamine (5-HT) levels were investigated. A single dose of either MPTP (10-30 mg/kg, i.p.) or MPP+ (5-20 ug/mouse, i.c.v.) decreased locomotor activity 10-40 min after injection: this locomotor effect was significantly suppressed by either pretreatment with nomifensine or 1-deprenyl alone, or by the combination of desmethylimipramine and 6-hydroxydopamine. Pretreatment with clorgyline did not suppress this behavior and a single dose of haloperidol enhanced the effect. The striatal levels of DA, 3-methoxytyramine and 5-HT increased in parallel with the decrease in locomotor activity caused by MPTP or MPP+. In contrast, levels of 3,4-dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindoleacetic acid were decreased by injection of either MPTP or MPP+. Possible mechanism(s) of the behavioral and biochemical changes caused by the acute actions of MPTP and MPP+ with respect to their neurotoxic effects on the nigrostriatal DA system are discussed.

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

PubMed1991

Acute effects of 3,4-methylenedioxymethamphetamine (MDMA) on monoamines in rat caudate.

Extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and serotonin (5-HT) were assayed in the caudate of freely moving rats using microdialysis and high performance liquid chromatography with electrochemical detection (HPLC-EC) to detect changes in their release. Dialysates were assayed at 20-minute intervals for four hours after an intraperitoneal (IP) injection of MDMA (10 mg/kg). In a separate study to determine MDMA effects on total caudate levels of the above neurochemicals, animals were injected IP with MDMA (10 mg/kg) and then sacrificed at 20, 60, 120 and 180 minutes after treatment. Brains were quickly removed, and caudate nuclei were dissected for neurochemical analysis using HPLC-EC. MDMA elicited an amphetamine-like increase in DA release, followed by an increase in DA content. DOPAC and HVA were both reduced in homogenate. 5-HT release was also increased, followed by a drop in caudate homogenate levels by three hours. DA extracellular content was 686% of control at 80 minutes; caudate homogenate levels were 122% at 120 minutes. 5-HT extracellular release was 123% at 20 minutes, then decreased thereafter. It is concluded that the acute effect of MDMA on caudate is at least as great on the DA as it is on the 5-HT system.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1988

Increased 3,4-dihydroxyphenylacetic acid (DOPAC) levels in spontaneously hypertensive rats (SHR) during the development of hypertension.

Central dopaminergic neuronal activity was investigated in the spontaneously hypertensive rat (SHR) using an in vivo cerebrospinal fluid (CSF) sampling technique. Increased central dopaminergic activity in the SHR was indicated by a significant (P less than 0.05) elevation in CSF levels of DOPAC relative to both Wistar-Kyoto and Sprague-Dawley control strains. The increased levels of CSF DOPAC were present at 5, 10 and 16 weeks of age. Homovanillic acid and 5-hydroxyindoleacetic acid levels were significantly (P less than 0.05) greater in SHR than WKY at 16 weeks. The possible role of central dopaminergic neurons in the pathogenesis of hypertension in the SHR was discussed.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

Alcohol stimulates the release of dopamine and serotonin in the nucleus accumbens.

The effects of acute IP administration (0.5, 1.0 or 2.0 g/kg) and local perfusion (25, 50 or 100 mM) of ethanol on the extracellular concentrations of dopamine (DA), serotonin (5-HT) and their metabolites in the nucleus accumbens (ACC) of the rat were studied with in vivo microdialysis coupled with a small-bore HPLC electrochemical detection procedure. The IP administration of 1.0 and 2.0 g/kg ethanol significantly (p less than 0.05) increased the extracellular levels of DA and 5-HT in the ACC whereas the 0.5 g/kg dose caused no change. In general, the extracellular levels of the 3 monoamine metabolites were not altered by IP ethanol except for a slight increase in the levels of homovanillic acid following the 2.0 g/kg dose. Local perfusion of 50 and 100 mM ethanol (but not 25 mM) through the microdialysis probe markedly increased (170-200% of control) the extracellular levels of DA in the ACC. Only the 100 mM concentration of ethanol altered the extracellular levels of 5-HT (2-fold increase), 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid. Addition of 100 microM ICS 205-930 (a 5-HT3 antagonist) to the perfusate markedly reduced the 100 mM ethanol-stimulated release of DA and 5-HT. Overall, the data suggest that ethanol can stimulate the release of both DA and 5-HT in the ACC and that the action of ethanol within the ACC may be mediated in part by 5-HT3 receptors.

3,4-Dihydroxyphenylacetic Acid↗