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At least 775 records · Page 43Linked to original sources

PubMed1983

Presynaptic alpha 2- and dopamine-receptor-mediated inhibitory mechanisms and dopamine nerve terminals in the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine was measured. The potassium (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was reduced by adrenaline 10(-7) M, with a potent alpha 2-agonist action, and was reduced by a dopamine receptor agonist, apomorphine 10(-7) M, in the presence of yohimbine 10(-6) M. These inhibitory effects were antagonized by an alpha 2-antagonist, yohimbine 10(-6) M, and a dopamine receptor antagonist, (-)-sulpiride 10(-7) M, respectively. The electrically evoked release of DA was enhanced by (-)-sulpiride but not by the (+)-isomer. Taking into consideration that yohimbine at a relatively high concentration (10(-6) M) increases the electrically evoked DA release, it is suggested that DA release in the rat hypothalamus may be mediated not only via autoreceptors but also in part via presynaptic alpha 2-receptors on the DA nerve terminals.

Animals↗

PubMed1984

The cholecystokinin analogue, caerulein, does not modulate dopamine release or dopamine-induced locomotor activity in the nucleus accumbens of rat.

We have investigated the effect of the cholecystokinin (CCK) analogue, caerulein, in the nucleus accumbens on dopamine (DA) release and locomotor activity. Caerulein (10(-9)-10(-4) M) did not affect the resting or K+-evoked release of [14C]DA, although concentrations within this range have been shown to modulate transmitter release in cerebral cortex. When injected bilaterally into the nucleus accumbens, caerulein (30 ng-1 microgram) did not affect spontaneous locomotor activity as compared to vehicle-injected controls. Similarly, bilateral injections of caerulein (1 microgram) into the nucleus accumbens did not modulate locomotor hyperactivity induced by bilateral injections of DA (20 microgram) into the nucleus accumbens. It is concluded that CCK in the nucleus accumbens has no direct effect on dopamine release or dopamine-stimulated locomotor activity.

Animals↗

PubMed1979

Protein phosphorylation in rat caudate homogenate: stimulatory effects of dopamine and enhancement of dopamine response following 6-hydroxydopamine treatment.

Dopamine (3-hydroxytyramine) stimulates the incorporation of 32P into proteins endogenous to a homogenate of rat caudate nucleus when 10 microM [gamma-32P]-ATP is used as a substrate following preincubation with 400 microM ATP. The increase in 32P incorporation has pharmacological characteristics similar to caudate tissue. Chronic depletion of striatal dopamine in vivo by stereotaxic injection of 6-hydroxydopamine in the nigrostriatal pathway results in a significant enhancement of the dopamine stimulation of 32 p incorporation in vitro. Cyclic AMP-stimulated phosphorylation of caudate proteins remains unchanged following 6-hydroxydopamine treatment.

Adenosine Triphosphate↗

PubMed1983

The metabolism of dopamine in the blood of ruminant animals: an enzyme system to metabolize dopamine released from the mast cells in these species?

Following the i.v. administration of 3,4-dihydroxyphenylethylamine (dopamine) to sheep, 3,4-dihydroxyphenylethanol and 3,4-dihydroxyphenylacetic acid rapidly appeared in the blood. 3,4-Dihydroxyphenylethanol can be formed from dopamine by blood plasma of ruminants in vitro. It is suggested that this plasma enzyme system might serve to inactive dopamine released from mast cells in ruminant species.

3-Methoxy-4-hydroxyphenylethanol↗

PubMed2005

Lack of effect of reserpine-induced dopamine depletion on the binding of the dopamine-D3 selective radioligand, [11C]RGH-1756.

The effect of reserpine induced dopamine depletion on the binding of the putative dopamine-D3 receptor ligand, [(11)C]RGH-1756 was examined in the monkey brain with positron emission tomography (PET). In a previous series of experiments, we have made an attempt to selectively label D3 receptors in the monkey brain using [(11)C]RGH-1756. Despite high selectivity and affinity of RGH-1756 in vitro, [(11)C]RGH-1756 displayed only low specific binding to D3 receptors in vivo. The aim of the present study was to examine whether low specific binding of [(11)C]RGH-1756 is caused by insufficient in vivo affinity of the ligand, or by high physiological occupancy of D3 receptors by endogenous dopamine (DA). PET experiments were performed in three monkeys under baseline conditions and after administration of reserpine (0.5 mg/kg). The results of the baseline measurements corresponded well to our earlier observations with [(11)C]RGH-1756. Reserpine caused no evident change in the regional distribution of [(11)C]RGH-1756 in the monkey brain, and no conspicuous regional accumulation of activity could be observed. After reserpine treatment there was no evident increase of specific binding and binding potential (BP) of [(11)C]RGH-1756. The lack of increased [(11)C]RGH-1756 binding after reserpine treatment indicates that competition with endogenous DA is not the predominant reason for the failure of the radioligand to label D3 receptors. Therefore, the low binding of [(11)C]RGH-1756 could largely be explained by the need for very high affinity of radioligand for D3 receptors in vivo, to obtain a suitable signal for the minute densities of D3 receptors expressed in the primate brain.

Adrenergic Uptake Inhibitors↗

PubMed2003

Nurr1 regulates dopamine synthesis and storage in MN9D dopamine cells.

Nurr1, a transcription factor belonging to the nuclear receptor family, is essential for the generation of midbrain dopamine (DA) cells during embryonic development. Nurr1 continues to be expressed in adult DA neurons but the role for Nurr1 in inducing and regulating basic dopaminergic functions such as dopamine synthesis and storage has remained unknown. We have previously used MN9D dopamine cells to analyze the role of Nurr1 and retinoids in DA cell maturation. These studies demonstrated that both Nurr1 and retinoids induce cell cycle arrest and a mature morphology. Here we used MN9D cells to investigate how Nurr1 regulates dopaminergic functions. Our results demonstrate that Nurr1, but not retinoids, increases DA content and the expression of aromatic L-amino acid decarboxylase (AADC) and vesicular monoamine transporter-2 (VMAT2) in MN9D cells. In a Nurr1-inducible cell line upregulation of VMAT2 is dependent on continuous Nurr1 expression. Moreover, AADC and VMAT2 are deregulated in midbrain DA cells of Nurr1 knockout embryos as revealed by in situ hybridization. Together, the results provide evidence indicating an instructive role for Nurr1 in controlling DA synthesis and storage.

Animals↗

PubMed1984

Comparison of high-performance liquid chromatography with electrochemical detection and gas chromatography-mass fragmentography for the assay of salsolinol, dopamine and dopamine metabolites in food and beverage samples.

High-performance liquid chromatography with electrochemical detection (HPLC-ED) and combined gas chromatography--mass spectrometry in the single-ion monitoring mode (GC--MS-SIM) have been used for the determination of salsolinol, dopamine, 3,4-dihydroxyphenylacetic acid, 3,4-dihydroxyphenylethanol and norepinephrine in a selection of food and beverage samples. The unique specificity of the SIM mode allows a simple one-step extraction to be used even for complex sample matrices. We have been able to demonstrate the quantitative and qualitative advantages offered by GC--MS over HPLC--ED by direct comparison of the chromatographic data obtained. We demonstrate that the specificity of SIM and the benefits offered by the incorporation of deuterated internal standards make GC--MS-SIM the method of choice for valid identification and precise quantitation of salsolinol, dopamine and dopamine metabolites in a complex sample matrix.

Beer↗

PubMed2000

Determination of dopamine and dopamine-derived (R)-/(S)-salsolinol and norsalsolinol in various human brain areas using solid-phase extraction and gas chromatography/mass spectrometry.

Using a solid-phase extraction procedure and a gas chromatographic-mass spectrometric (GC/MS) method the levels of dopamine and the levels of dopamine-derived salsolinol (SAL) and norsalsolinol (NorSAL) were determined in human brain areas involved in the etiology of alcoholism, parkinsonism and other diseases. The possibility that biosynthesis of salsolinol occurs through a stereospecific enzymatic reaction was considered. Using a two-step derivatization with N-methyl-N-trimethylsilyltrifluoracetamide (MSTFA) and the chiral reagent (R)-(-)-2-phenylbutyryl chloride, baseline separated peaks of (R)- and (S)-SAL were obtained. Both enantiomers were found in human brain samples with no correlations between levels of salsolinol and dopamine. These findings do not support the hypothesis that only an enantio-selective synthesis of (R)-SAL by a putative salsolinol synthase is responsible for the in vivo formation. In our opinion, non-enzymatic formation of salsolinol via the Pictet-Spengler reaction reveals both salsolinol enantiomers and an additional enzymatic synthesis of only (R)-SAL explains the enantiomer ratio (R)-/(S)-SAL of approximately 2.

Adult↗

PubMed2003

Relationship between methamphetamine-induced dopamine release, hyperthermia, self-injurious behaviour and long term dopamine depletion in BALB/c and C57BL/6 mice.

Differential sensitivity to neurotoxic effects of methamphetamine on striatal dopaminergic neurones between C57BL/6 and BALB/c mice has been established. In the present studies, the interaction of methamphetamine-induced dopamine release, self-injurious behaviour, the neural immune response, and the long-term (3 day) dopamine depletion were examined in these strains after administration of 8 mg/kg methamphetamine. BALB/c mice showed increased hyperthermia compared to the C57BL/6 strain, as well as induction of interleukin-1beta. Additionally, homovanillic acid (HVA) levels, as well as HVA/DA turnover ratios were elevated in the striatum and frontal cortex of BALB/c mice, both compared to untreated mice and to the C57BL/6 strain after a single injection of methamphetamine. Pretreatment with acetaminophen eliminated the methamphetamine-induced hyperthermia in BALB/c mice and reduced body temperature in C57BL/6 mice. However, acetaminophen pretreatment did not affect any parameters of dopaminergic toxicity in the striatum or frontal cortex of the BALB/c strain following repeated methamphetamine injections. Furthermore, acetaminophen pretreatment did not alter the incidence of self-injurious behaviour in BALB/c mice. Therefore, hyperthermia and methamphetamine-induced toxicity appear to be independent phenomena while self-injurious behaviour may provide a better predictor of toxicity, which, in turn, may be related to dopamine release.

Actins↗

PubMed1999

Oral administration of the dopamine prodrug docarpamine shortens need for drip infusion of dopamine in patients with low cardiac output syndrome after cardiac surgery.

BACKGROUND: Docarpamine (DOC) is a dopamine prodrug which can be orally administered. It has been found that oral docarpamine transforms into dopamine in vivo, and increases cardiac output and renal blood flow as effectively as intravenous dopamine. METHODS: We reviewed the records of 26 patients who had developed low cardiac output syndrome (LOS) after cardiac surgery and received docarpamine during the early postoperative course. Five patients discontinued docarpamine within 2 days due to arrhythmia. There were 3 hospital deaths. The remaining 18 patients were divided into two groups according to the timing of docarpamine administration. In group A docarpamine was administered during and after weaning from intravenous catecholamines, in group B only on demand after weaning from intravenous catecholamines. RESULTS: There were 12 patients in group A and 6 in group B, and the severity of LOS was relatively milder in group B than in group A. Stable hemodynamics and sufficient daily urinary output were maintained by oral administration of DOC in both groups just as well as by drip infusion of catecholamines. CONCLUSION: Sinse continuous drip infusion of catecholamine commonly slows recovery in LOS patients, it is considered that switching from drip infusion of catecholamines to oral DOC administration is safe and useful for earlier recovery in LOS patients after cardiac surgery.

Administration, Oral↗

PubMed2000

Diazepam in the ventral striatum dissociates dopamine-dependent and dopamine-independent place conditioning.

We have previously shown that diazepam blocks both the formation and the expression of amphetamine-induced conditioned place preference (CPP), but has no effect on the CPP induced by morphine. Because diazepam reduces dopamine activity in the nucleus accumbens, three experiments were conducted in order to investigate whether diazepam selectively blocks the expression of place conditioning dependent on mesolimbic dopamine. The first experiment found that systemic diazepam blocked the expression of conditioned place aversion induced by the kappa-receptor agonist U50-488. The second and third experiments demonstrated that intra-cranial injections of diazepam in the nucleus accumbens blocked the expression of amphetamine CPP but not of morphine CPP. It is concluded that diazepam interferes with mesolimbic dopamine-dependent motivational effects of drugs.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1993

FGF-2 modulates dopamine and dopamine-related striatal transmitter systems in the intact and MPTP-lesioned mouse.

Following a previous study in which we showed ameliorative effects of basic fibroblast growth factor (FGF-2) locally applied to the nigrostriatal system in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mice, we investigated FGF-2 actions at different time intervals after the lesion and effects on non-dopaminergic striatal transmitter systems. A triple intraperitoneal injection of 30 mg/kg MPTP at 24 h intervals caused a reduction of striatal dopamine to 23% of control levels that lasted for at least 4 weeks. Four micrograms FGF-2 soaked into gel foam and placed onto the right striatum partially and bilaterally restored dopamine levels and tyrosine hydroxylase activity after 2 weeks, when the treatment started simultaneously or 1 day after the toxin lesion. FGF-2 was ineffective, if administration commenced with a delay of 7 days. Striatal neurotransmitters that are known to be linked to the dopaminergic system were also altered by the MPTP treatment. GABA was significantly increased, while somatostatin levels were reduced. Upon FGF-2 administration both GABA and somatostatin levels were partially normalized. Our data are consistent with the notion that FGF-2 protects and rescues acutely and subacutely MPTP-lesioned nigrostriatal neurons and that its effects must be mainly indirect. Likewise, positive effects of FGF-2 on non-dopaminergic neurons may be due to the partial restoration of striatal dopamine.

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

PubMed1977

Dopamine enhances the action of prolactin on rat blood vessels. Implications for dopamine effects on plasma prolactin.

It has been claimed that dopamine enhances peripheral uptake of prolactin. Dopamine at 2.1 x 10(-9)M, a concentration which had no effect by itself, enhanced both the potentiation of rat mesenteric vascular reactivity caused by 50ng/ml ovine prolactin and the inhibition of reactivity caused by 500ng/ml prolactin. These observations are consistent with the proposal that dopamine can interact peripherally with prolactin.

Animals↗

PubMed1983

The effect of dopamine on L-fucose incorporation into hippocampal and striatal slices of dopamine-supersensitive rats.

The incorporation of L-[1-3H]fucose into total proteins was measured in hippocampal and striatal slices of dopamine-supersensitive and control rats. Compared with controls, striatal slices of supersensitive animals exhibited an augmented stimulation of L-fucose incorporation by 5 X 10(-5) M dopamine. This result supports former data about a dopamine-receptor mediated regulation of protein glycosylation in the nervous tissue.

Animals↗

PubMed1982

[Effect of nootropic drugs on the dopamine release and dopamine uptake in structures of the rat striatum].

Nootropics increase the overflow of dopamine from rat striatum slices in a concentration dependent manner, but without relation to their clinical effectiveness. The influence of a nootropic drugs and of amphetamine on the stimulus induced dopamine release points to a relationship between nootropic and nooanaleptic activity, on the one hand, and transmitter release, on the other. Dopamine re-uptake is not altered by nootropics like piracetam.

Animals↗

PubMed1981

[Haemodynamic effects of dopamine, sodium nitroprusside and the association dopamine-sodium nitroprusside. Comparison of their effects after extra-corporeal circulation under deep hypothermia for congenital heart defects in infants and small children (author's transl)].

Heart rate, cardiac index measured by thermodilution, systolic diastolic and mean arterial pressure, mean left and right atrial pressures, were measured immediately before and after 30 minutes of dopamine infusion at a rate of 7 micrograms/kg/minute, then after 30 minutes of nitroprusside infusion at a rate of 0.5 micrograms/kg/minute, and after 30 minutes of association dopamine-nitroprusside at the same doses. The statistical analysis shows that the best enhancement in the cardiac output is observed (P less than 0.01) after the association dopamine-nitroprusside, with a diminution of systemic vascular resistance (P less than 0.05) however less important than that observed with sodium nitroprusside alone (P less than 0.025).

Child, Preschool↗

PubMed1997

Differential reinnervation of retinal bipolar cell dendrites and axon terminals by dopamine interplexiform cells following dopamine depletion with 6-OHDA.

Depletion of retinal dopamine in goldfish increases light sensitivity at photopic backgrounds. As horizontal cells appear not to be involved with this effect (Yazulla and Studholme [1995] Vis. Neurosci. 12:827-837), we investigated the innervation patterns of the ON rod/cone bipolar cells (ON-BC) by dopaminergic interplexiform cells (DA-IPCs) normally and during the period of neogeneration of new DA-IPCs at the marginal zone following DA-IPC destruction. DA-IPCs were destroyed via intraocular injection of 6-hydroxydopamine over 2 successive days. Controls and 1 year post-injection retinas were double labeled for protein kinase C and tyrosine hydroxylase (TH) immunocytochemistry to identify the ON-BCs and the DA-IPCs, respectively. Double-labeled 25 microns tissue sections were examined on a confocal laser scanning microscope by using dual channel immunofluorescence acquisition. Image stacks were analyzed for DA-IPC/ON-BC contacts in the distal inner nuclear layer (INL) and inner plexiform layer (IPL). Image stacks were rotated 180 degrees with respect to each other and reanalyzed to determine potential randomness of the contacts. For control retinas there were 1.8 contacts/axon terminal in the IPL (n = 165) and 9.4 contacts/ON-BC in the distal INL (n = 28). At 1 year after injection, reinnervation of TH-immunoreactive boutons in the retina recovered to 16% of control in the IPL but only 10% in the distal INL. Establishment of DA-IPC/ON-BC contacts recovered to 36% of control for ON-BC axon terminals (n = 103), whereas there was no recovery of contacts in the distal INL (n = 30). Reinnervation of ON-BC by DA-IPCs preferentially targets the axon terminals. The absence of reinnervation of bipolar cell dendrites by DA-IPCs may account for the persistence of the increased light sensitivity following retinal dopamine depletion. Thus, dopamine input to ON-BCs in the outer retina maybe involved in setting background sensitivity under photopic conditions.

Animals↗

PubMed1989

Distribution of dopamine D1 and D2 receptors in rabbit cortical areas, hippocampus, and neostriatum in relation to dopamine contents.

The densities of dopamine D1 and D2 receptors were measured by using [3H]SCH23390 and [3H]raclopride, respectively, in the rabbit cingulate, visual, sensorimotor, and entorhinal-piriform cortical areas; the dorsal and ventral hippocampus; and the putamen as well as the medial and lateral caudate. Endogenous dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), 4-hydroxy-3-methoxyphenylacetic acid (HVA), and 3-methoxytyramine (3-MT) were assayed by HPLC with electrochemical detection. The distributions of [3H]SCH23390 and [3H]raclopride binding were heterogenous with the greatest densities in the neostriatum. The concentrations of DA and its metabolites were also highest in this structure. Regions with low DA content, i.e., cortex and hippocampus, had lower densities of [3H]SCH23390 and [3H]raclopride binding. Furthermore, these sites were differentially localized within the various regions and there were substantially more D1 than D2 receptors. The functional significance and heterogeneities in the distribution of D1 and D2 receptors are discussed in relation to the dopaminergic innervation and the turnover estimated by the ratios between endogenous DA and its metabolites.

Animals↗