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PubMed1984

Effect of some serotoninergic agents on the rectal temperature of the domestic fowl (Gallus domesticus).

The information currently available in the literature on the effects of serotonergic drugs on thermoregulation in the avian species is very scanty. Therefore, it was the objective in this project to study the influence of 5-hydroxytryptamine (5-HT), 5-hydroxytryptophan (5-HTP), benserazide, carbidopa (Mk 486), citalopram, cyproheptadine, methysergide, xylamidine, p-chlorophenylalanine (PCPA) and lysergic acid diethylamide (LSD-25) on the rectal temperature of young chicks. 5-hydroxytryptamine (0.8 mg/kg), produced significant dose-dependent hypothermia in young chicks. Similarly, 5-HTP (16 mg/kg) profoundly lowered the rectal temperature of young chicks. The hypothermic effect of 5-HTP was potentiated by benserazide (1.25-2.5 mg/kg). Pretreatment with carbidopa (50 mg/kg) potentiated 5-HTP induced hypothermia. Citalopram (5 mg/kg) significantly potentiated hypothermia induced by 5-HT. Pretreatment with PCPA (200 mg/kg, 24 hr previously) alone resulted in hyperthermia while the hypothermic effect of 5-HTP (16 mg/kg) was antagonised by pretreatment with PCPA. Cyproheptadine (1.25 mg/kg) antagonised the hypothermic effect of 5-HT (0.1 and 0.8 mg/kg). The antagonistic effect was weak when the chicks were pretreated with larger doses of cyproheptadine (i.e. 2.5-10 mg/kg). The hypothermia induced by 5-HT (0.8 mg/kg) was antagonised by smaller doses of methysergide (0.125-1.0 mg/kg) but potentiated by larger doses of methysergide (2.0 and 4.0 mg/kg). Xylamidine (1-2 mg/kg) alone induced hyperthermia and effectively antagonised hypothermia induced by 5-HT (0.8 mg/kg). D-Lysergic acid diethylamide (2.5-10 micrograms/kg) alone induced hypothermia. The interaction between LSD and 5-HT was dose-dependent and biphasic.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Hydroxytryptophan↗
PubMed1986

Nicotinic acid or N-methyl nicotinamide prolongs elevated brain dopa and dopamine in L-dopa treatment.

A peripheral dopa decarboxylase inhibitor, benserazide, was given ip, followed by intubation with L-dopa. Brain dopa and DA levels were elevated maximally between 0.5-2.5 hr and 1.0-2.5 hr, respectively. Dopa in serum, liver, and brain were at control values after 4 hr. Supplementation of dopa with NAM or NAC, as possible methyl group acceptors to lower catabolism of DA, showed that NAM had no effect on DA levels or on SAM. However, with both NAC and N-methyl NAM (a methylated compound intended as a control) at time periods where dopa and DA were normally decreasing, the brain levels were increased over control values with benserazide and dopa alone. NAC or N-methyl NAM appeared to extend the period of elevated brain DA levels with L-dopa treatment. The mechanism responsible for these results is uncertain.

Animals↗
PubMed1992

Differential effects of the novel antidepressant tianeptine on L-5-hydroxytryptophan (5-HTP)-elicited corticosterone release and body weight loss.

Biochemical and behavioural experiments have indicated that the novel antidepressant tianeptine stimulates 5-hydroxytryptamine (5-HT) reuptake. The present study has explored the influence of acute tianeptine pretreatment upon corticosterone release and body weight loss following L-5-hydroxytryptophan (5-HTP) administration in conscious rats. Administration of 5-HTP (20 mg/kg i.v.) increased plasma corticosterone levels to a similar extent in rats pretreated either with saline or tianeptine (10 mg/kg i.p., 60 min beforehand). Besides, prior administration of benserazide (50 mg/kg i.p., 30 min beforehand), an inhibitor of peripheral aromatic L-amino acid decarboxylase, prevented 5-HTP-induced corticosterone release in both saline- and tianeptine-pretreated rats. However, combined administration of benserazide and 5-HTP decreased overnight body weight in saline-, but not in tianeptine-pretreated rats. These results suggest that tianeptine preferentially activates 5-HT reuptake in central serotonergic neurones.

5-Hydroxytryptophan↗
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↗
PubMed1986

Reduction in paradoxical sleep after L-dopa administration in rats.

The EEG and EMG activity of two groups of rats (N = 8 each) was recorded during one experimental and 5 control days. On the experimental day, one group received 125.0 mg/kg L-dopa preceded by 50.0 mg/kg benserazide hydrochloride. The other group received 1.0 mg/kg haloperidol, immediately before the recording session. After L-dopa plus benserazide administration the total time and the number of episodes of paradoxical sleep and slow wave sleep decreased significantly compared to control sessions.

Animals↗
PubMed1975

Urinary excretion of monoamines and their metabolites in patients with Parkinson's disease. Response to long-term treatment with levodopa alone or in combination with a dopa decarboxylase inhibitor and clinical correlations.

Urinary excretion of DA, DOPAC, 3-MT, HVA, NMA, MA, VMA and 5-HIAA were studied in 33 parkinsonian patients treated with 1.5-7.5 g of levodopa daily for up to six months and in 30 patients receiving levodopa (800-1,000 mg) combined with a dopa decarboxylase inhibitor, benserazide (200-250 mg). Basal urinary excretions were within normal limits except for that of 3-MT which was significantly lower in parkinsonian patients as compared to controls. Levodopa induced an increase of about 400 fold in urinary DA; DOPAC was increased about 300 fold, 3-MT only about 70 fold, but HVA about 300 fold. Urinary NMA and MA did not change but VMA was increased significantly. On the other hand, urinary 5-HIAA was significantly decreased. The amounts of excreted DA and its subsequent metabolities were increased with the continuation of treatment, suggesting inductive phenomena in enzyme systems. During combined treatment with levodopa and benserazide urinary DA was increased, but only to about one tenth the extent seen with levodopa alone. The excretion of DOPAC was about one 20th, of 3-MT about one fourth and of HVA one 25th that seen during levodopa treatment. No signs of enzyme induction were seen. NMA was lowered significantly but MA remained unchanged. VMA was increased and significantly more than during therapy with levodopa alone. 5-HIAA was again significantly decreased and the decrease was significantly greater than that seen with levodopa alone. Some statistically significant correlations were seen between the excretions of NMA, MA and VMA and cardiovascular side effects, indicating an affection on the NA-ergic system by levodopa treatment. Significant correlation between 5-HIAA excretion and clinical improvement of tremor during levodopa treatment may suggest that participation of 5-HT in the mechanism of tremor.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

Chiral and non chiral determination of Dopa by capillary electrophoresis.

The suitability of capillary electrophoresis for determining the enantiomeric purity of levodopa in a pharmaceutical formulation also containing benserazide was assessed. To this end, the pharmaceutical components were separated in a non-chiral medium that allowed the total amount of Dopa and that of benserazide to be quantified. The addition of a chiral crown ether to the background electrolyte allows to separate the enantiomers of this compounds. Optimizing the variables influencing the enantioresolution of Dopa affords a resolution high enough resolution to determine the amount of dextrodopa (the distomer) contained in levodopa (the eutomer) in a pharmaceutical. A relative limit of detection (RLD) is proposed as a measure of the lowest detectable enantiomeric impurity. The RLD for the determination of dextrodopa contained in levodopa was 0.1% and found to depend on the enantiomer migration order. The enantiomeric purity of levodopa in the pharmaceutical preparation and dextrodopa from Sigma was 99.5 and 99.95%, respectively.

Benserazide↗
PubMed1998

Evidence for the involvement of P-glycoprotein on the extrusion of taken up L-DOPA in cyclosporine A treated LLC-PK1 cells.

1. The present work has examined the effects of short- (30 min) and long-term (14 h) exposure to cyclosporine A (CsA) on the uptake of L-DOPA, its decarboxylation to dopamine and the cellular extrusion of taken up L-DOPA and of newly-formed amine in monolayers of LLC-PK1 cells. 2. In the presence of benserazide (50 microM), L-DOPA was rapidly accumulated in LLC-PK1 cells (cultured in collagen-treated plastic) attaining equilibrium at 30 min of incubation. Non-linear analysis of the saturation curves revealed a Km of 113+/-16 microM and a Vmax of 5581+/-297 pmol mg(-1) protein 6 min(-1). 3. In the absence of benserazide, LLC-PK1 cells incubated with increasing concentrations of L-DOPA (10 to 500 microM) for 6 min accumulate newly-formed dopamine by a saturable process with apparent Km and Vmax values of 31+/-6 microM and 1793+/-91 pmol mg(-1) protein 6 min(-1), respectively. The fractional outflow of newly-formed dopamine was found to be 20%. Up to 200 microM of intracellular newly-formed dopamine, the outward transfer of the amine was found to be a non-saturable process. 4. Short-term exposure to CsA (0.3, 1.0 and 3.0 microg ml(-1)) was found not to change the intracellular concentrations of newly-formed dopamine, but increased the levels of dopamine in the incubation medium (143% to 224% increase) and the total amount of dopamine formed (31% to 59% increase). Long-term exposure to CsA (0.03 to 3.0 microg ml(-1)) reduced the total amount of dopamine (15% to 39% reduction) and the intracellular levels of the amine (11% to 56% reduction), without changing dopamine levels in the incubation medium. Both short- and long-term exposure to CsA resulted in a concentration-dependent increase in the fractional outflow of newly-formed dopamine. 5. Short-term exposure to CsA (3.0 microg ml(-1)) reduced the apical extrusion of intracellular L-DOPA by 15% (P<0.05), whereas long-term exposure to CsA reverted this effect and decreased its intracellular availability (15% reduction; P<0.05). 6. Detection of P-glycoprotein activity was carried out by measuring verapamil- or UIC2-sensitive rhodamine 123 accumulation. Both UIC2 (3 microg ml(-1)) and verapamil (25 microM) significantly increased the accumulation of rhodamine 123 in LLC-PK1 cells. A 30 min exposure to CsA was found not to affect the accumulation of rhodamine 123 in the presence of verapamil (25 microM), whereas a 14 h exposure to CsA was found to reduce the accumulation of rhodamine 123. 7. In conclusion, the increase and the reduction in the formation of dopamine after short- and long-term exposure to CsA, respectively, correlate with the effects of the immunosuppressant on the apical cell extrusion of taken up L-DOPA, suggesting the involvement of P-glycoprotein. The effects of CsA on the fractional outflow of newly-formed dopamine appear to be mediated by a different mechanism.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Locally formed dopamine modulates renal Na-Pi co-transport through DA1 and DA2 receptors.

The involvement of dopamine (DA) receptor subtypes in regulation of renal phosphate transport by DA, either exogenous or locally synthesized from L-dihydroxyphenylalanine (L-dopa) was evaluated in opossum kidney (OK) cells with proximal tubular phenotype. DA synthesis from L-dopa by OK cells was abolished by carbidopa and benserazide, two dissimilar inhibitors of aromatic L-amino acid decarboxylase. L-Dopa stimulated cyclic AMP generation and inhibited Na-dependent Pi uptake, and these effects were abolished by carbidopa and benserazide. The effects of L-dopa or DA on cyclic AMP generation and on Na-Pi co-transport were mimicked by SKF 38393, a DA1 receptor agonist, and were potentiated by S-sulpiride, a DA2 receptor antagonist. Bromocriptine, a DA2 receptor agonist, blunted in a pertussis toxin-dependent manner parathyroid hormone (PTH)-induced cyclic AMP generation and inhibition of Pi uptake. In contrast with PTH, neither L-dopa nor DA affected significantly the cytosolic calcium concentration. These results support the involvement of DA1 and DA2 receptors, positively and negatively coupled into adenylate cyclase respectively, in modulation of renal phosphate transport.

Adenylate Cyclase Toxin↗
PubMed1997

L-hydroxytryptophan amplifies pulsatile secretion of LH in the follicular phase of normal women.

OBJECTIVES: The hypothalamus possesses serotoninergic fibres which arise from neuronal cell bodies located in the raphe nuclei and have synapse on GnRH-secreting neurones. Hitherto, no firm evidence has been produced to support a role for serotoninergic control of LH in humans. Our first objective was to investigate whether pulsatile administration of L-5-hydroxytryptophan--the immediate precursor of serotonin--affects pulsatile LH secretion in the medium-late follicular phase of normal women. Since the results of the first experiment suggest that L-5-hydroxytryptophan amplifies LH release, our second objective was to investigate whether, in the absence of GnRH, L-5-hydroxytryptophan can release LH. This was done by studying LH response in patients with hypogonadotrophic hypogonadism of hypothalamic origin. PATIENTS: Twenty-two normal women (18-25 years old) and 8 patients with hypogonadotrophic hypogonadism (2 men with Kallmann's syndrome and 6 women with anorexia nervosa). DESIGN: Serum LH levels in the 22 subjects (reference population) were monitored at 10-minute intervals over an 8-hour period (1000-1800h) during medium-late follicular phase. In 7 of these subjects, serum LH levels were monitored in their next medium-late follicular phase while L-5-hydroxytryptophan was administered at hourly intervals from 1000 to 1800 h; the peripheral conversion of L-5-hydroxytryptophan to serotonin was inhibited by 150 mg of benserazide at 0930 and 1430h. To investigate whether, in the absence of GnRH, L-5-hydroxytryptophan can release LH, two patients with Kallmann's syndrome were monitored over a 7-hour period and 6 patients with anorexia nervosa over a 9-hour period. After a 2-5 hour control period the subjects received 150 mg of benserazide, and pulsatile L-5-hydroxytryptophan (every 30 minutes in the Kallmann's patients and every 45 minutes in the subjects with anorexia nervosa). MEASUREMENTS: LH pulses were identified and analysed according to number, amplitude, interpulse interval and pulse duration. RESULTS: In the normal women, L-5-hydroxytryptophan increased pulse amplitude (mean +/- SD; 3.02 +/- 1.42 IU/l vs. 1.75 +/- 0.98 IU/l before L-5-hydroxytryptophan and 1.90 +/- 1.04 IU/l in the reference population; P < 0.01 in both cases), but had no significant effects on pulse duration, interpulse interval or number of pulses. L-5-hydroxytryptophan had no effect on LH in patients with Kallmann's syndrome. In the anorexia nervosa group, the mean serum LH level increased significantly after L-5-hydroxytryptophan (3.90 +/- 2.46 IU/l vs. 3.06 +/- 1.23 IU/l, P < 0.001) but, as in Kallmann's patients, the three women in this group without residual LH pulsatility did not respond to L-5-hydroxytryptophan. CONCLUSION: Pulsatile administration of L-5-hydroxytryptophan increases LH pulse amplitude in the follicular phase of normal women. In the absence of GnRH, L-5-hydroxytryptophan does not stimulate pituitary LH secretion.

5-Hydroxytryptophan↗
PubMed1984

[Combined treatment of the early stages of Parkinson's syndrome with bromocriptine and levodopa. The results of a multicenter study].

125 patients in the early stages of Parkinson's syndrome were randomized and subjected to prearranged treatment adaptation period. Subsequently they were treated with either a mean dosage of 444 mg levodopa and benserazide (47 patients) or a combination of a mean of 298 mg levodopa and benserazide plus 17 mg bromocriptine (32 patients). Follow-up was done up to three years. Combined treatment permitted reduction of the levodopa dosage by 39%. As assessed by improvement of symptoms of Parkinson's syndrome in patients with a minimum treatment period of 1 or 3 years combined treatment was shown to be superior to monotherapy.

Aged↗
PubMed1994

Reduction of nerve growth factor receptor immunoreactivity in ischaemic gerbil hippocampal CA1 neurons after treatment with L-threo-3,4-dihydroxyphenylserine (DOPS).

Nerve growth factor (NGF) synthesis in cultured mouse L-M fibroblast and astroglial cells can be increased after the treatment with L-threo-3,4-dihydroxyphenylserine (DOPS). Since the increase of NGF is not blocked by the treatment with decarboxylase inhibitor, DOPS may have direct effect to increase the NGF content. NGF and its receptor (NGFR) are suggested to play an important role in the neuronal survival and regeneration under pathologic conditions. In this study, we studied a possible protective effect of DOPS against the hippocampal CA1 cell death after transient forebrain ischaemia in gerbils in relation to the change of NGFR immunoreactivity. We found that treatment with DOPS (300 mg kg-1) in combination with a decarboxylase inhibitor (benserazide, 10 mg kg-1) protected ischaemic hippocampal CA1 cell against delayed neuronal death (neuronal density = 125 +/- 24 mm-1) as compared to the treatment with vehicle (49 +/- 11 mm-1) (p < 0.01). The immunoreactivity for NGFR was scarcely present in the sham-control CA1 area but was induced from 1 h and markedly expressed at 7 days after recirculation in the vehicle group. However, it was slightly and transiently induced from 8 h to 2 days in the DOPS plus benserazide treated group. These data suggest that the protective role of DOPS on the ischaemic hippocampal CA1 cells may act through the NGF and its receptor system.

Animals↗
PubMed1991

Effect of L-dopa administration on islet monoamine oxidase activity and glucose-induced insulin release in the mouse.

Previous studies have shown that the amine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) is rapidly converted to its corresponding amine, dopamine, in islet beta-cells. In the present investigation, we studied the effect of acute L-DOPA administration on islet monoamine oxidase (MAO) activity and on glucose-induced insulin secretory response in mice. It was observed that at 2 min after intravenous L-DOPA administration, there was a marked increase (+35%) in islet MAO activity, with serotonin as substrate. At 7 min, MAO activity towards dopamine was enhanced by 32% and that towards serotonin and phenylethylamine (PEA) was decreased by 23 and 25%, respectively. The inhibitor of L-aromatic amino acid decarboxylase, benserazide, abolished L-DOPA-induced changes of MAO activity, suggesting that the formed dopamine, and not L-DOPA itself, was responsible for the observed effects. At 60 min, no effect by L-DOPA administration on islet MAO activity was noticed. L-DOPA (125 or 250 mumol/kg), given together with glucose, induced a decrease in glucose-induced insulin response. L-DOPA (125 mumol/kg), given 7 min before glucose, totally suppressed glucose-induced insulin response. This inhibition was eliminated through pretreatment with benserazide. Enhancement of glucose-stimulated insulin response, after deposition of horseradish peroxidase (HRP) in beta-cell vacuolar system, was suppressed by L-DOPA. We conclude that acute L-DOPA-induced dopamine accumulation in pancreatic islets is accompanied by rapid changes in MAO activity, concomitant with an inhibitory effect on glucose-stimulated insulin response. Increased hydrogen peroxide production, following increased MAO activity, may possibly augment the inhibitory effect of dopamine accumulation on insulin release.

Animals↗
PubMed1992

Extracellular concentrations of dopamine and metabolites in the rat caudate after oral administration of a novel catechol-O-methyltransferase inhibitor Ro 40-7592.

The effect of the systemic administration of a novel, orally active, catechol-O-methyltransferase (COMT) inhibitor, Ro 40-7592, on the in vivo extracellular concentrations of dopamine (DA) and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), was studied by transcerebral microdialysis in the dorsal caudate of freely moving rats. Ro 40-7592 (at doses of 3.0, 7.5, and 30 mg/kg p.o.) elicited a marked and long-lasting reduction of HVA, and at doses of 7.5 and 30 mg/kg, an increase of DOPAC output, but it failed to increase DA output. The administration of L-beta-3,4-dihydroxyphenylalanine (L-DOPA, 20 and 50 mg/kg p.o.) with a DOPA decarboxylase inhibitor (benserazide) increased both HVA and DOPAC output, but failed to modify significantly extracellular DA concentrations in dialysates; in contrast, combined administration of L-DOPA+benserazide with Ro 40-7592 (30 mg/kg p.o.) resulted in a significant increase in DA output. Ro 40-7592 prevented the L-DOPA-induced increase in HVA output and markedly potentiated the increase in DOPAC output. To investigate to what extent the increase in extracellular DA concentrations was related to an exocitotic release, tetrodotoxin (TTX) sensitivity was tested. Addition of TTX to Ringer, although abolishing DA output in the absence of L-DOPA, partially reduced it in the presence of L-DOPA+Ro 40-7592 and even more so after L-DOPA without the COMT inhibitor. The results of the present study suggest that metabolism through COMT regulates extracellular concentrations of DA formed from exogenously administered L-DOPA but not of endogenous DA.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Intrarenal dopamine participation in frusemide diuretic and natriuretic responses to frusemide.

1. Dopamine (DA) involvement in the renal response to frusemide was analysed using the isolated perfused rat kidney preparation. Endogenous DA levels were increased through the infusion of its precursor levodopa (LD) (0.5 or 1 microM) whereas benserazide (50 or 100 microM), an inhibitor of the enzyme L-dopa-decarboxylase, was used to decrease DA synthesis. 2. Frusemide administration (0.3-20 nmols) induced a dose-dependent increase in fractional excretion of water (FE H2O), sodium (FE Na+) and glucose (FEG). FE Na+ elicited by the diuretic was enhanced 30-40% by 0.5 microM of LD (n = 5, P < 0.05), and 60-80% by LD 1 microM (n = 5, P < 0.05). FE H2O produced by the diuretic was enlarged 80-100% by 0.5 microM (n = 5, P = 0.05), and 130-170% by 1 microM of LD (n = 5, P < 0.01). The increase produced by both concentrations of LD on FEG was 200% for the lowest dose of the diuretic (n = 5, P < 0.01), and 90% for the highest (n = 5, P < 0.05). 3. Benserazide (BZ) (100 microM) decreased the F.E. Na+ induced by frusemide (n = 5, P < 0.05) by 32-42%, and completely abolished frusemide effects on FE H2O and FEG (n = 5). 4. In conclusion, our results suggest that endogenous dopamine participates in the frusemide-induced diuresis and sodium excretion within the kidney, and that the participation of extrarenal factors is not essential for this effect. Dopamine may be involved in frusemide-induced inhibition of proximal sodium reabsorption.

Animals↗
PubMed1976

Parkinson's disease treated with Sinemet or Madopar. A controlled multicenter trial.

92 patients with Parkinson's disease not previously treated with levodopa were considered as eligible for this triple-blind trial. Patients were allocated at random to treatment with either levodopa + benserazide ratio 4:1 (Madopar) or levodopa + carbidopa ratio 10:1 (Sinemet) using dosage schedules recommended by the manufacturers which they had to adhere to for 6 months. Unless prohibitive side-effects occurred daily maximum dosage of 800 mg levodopa + 200 mg benserazide respectively 1,500 mg levodopa + 150 mg carbidopa were obtained after 6 weeks and 3 weeks, respectively. The effect of the two schedules on the Parkinsonian symptoms were equal and appeared equally fast. The frequency of gastrointestinal side-effects and involuntary movements were significantly higher and more severe for Sinemet than for Madopar. These side effects are usually symptoms of levodopa overdosing, but whether or not a different dosage schedule with Sinemet would have given fewer side-effects without concurrent lower efficacy remains open to speculation. The treatment schedules did not differ with regard to other side-effects and influence on blood pressure. Neither treatment seemed to influence liver function, renal function and hematological parameters in a statistically way.

Aged↗
PubMed1984

The effects of phenylpropanolamine and other sympathomimetics on food consumption and motor activity in mice.

The effects of phenylpropanolamine on motor activity and on food intake were compared with those of S-amphetamine, ephedrine, 2-aminoindane and fenfluramine in groups of mice. Motor activity was additionally measured in mice pretreated with levodopa and benserazide, and food intake in mice pretreated with alpha-methyl-p-tyrosine. Amphetamine (2.5 mg kg-1) increased motor activity, phenylpropanolamine (10-40 mg kg-1) and 2-aminoindane (2.5-10 mg kg-1) decreased activity whilst ephedrine (2.5-40 mg kg-1) had a biphasic effect. Fenfluramine (10-40 mg kg-1) had negligible effect on activity. In mice pretreated with levodopa and benserazide both phenylpropanolamine and 2-aminoindane caused a massive increase in motor activity whilst fenfluramine's action was not affected in the same way. Whilst the anorectic action of fenfluramine was considerably potentiated in mice pretreated with alpha-methyl-p-tyrosine, that of amphetamine, ephedrine, 2-aminoindane and phenylpropanolamine was either unaffected or initially antagonized. It is concluded that the mechanisms of motor and anorectic actions of phenylpropanolamine are similar to those of amphetamine.

Animals↗
PubMed1975

Effect of peripheral decarboxylase inhibition on HVA and 5HIAA in cerebrospinal fluid of depressed patients.

The effects of benserazide on the level of homovanillic acid and 5-hydroxyindoleacetic acid in CSF have been investigated in 1 manic and 11 depressed patients. Benserazide induced no change on both metabolites. This negative result supports the view that monoamine metabolites in CSF, in the absence of loading with an exogenous precursor, originate mostly from brain parenchyma, without significant contribution of the metabolism in capillary walls.

Adult↗