SEARCH · PubMed Health

Results for “DOPAMINE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 757 records · Page 42Linked to original sources

PubMed1993

(-)-2-(N-propyl-N-2-thienylethylamino)-5-hydroxytetralin (N-0923), a selective D2 dopamine receptor agonist demonstrates the presence of D2 dopamine receptors in the mouse vas deferens but not in the rat vas deferens.

Experiments were carried out using the D2 dopamine receptor-selective agonist (-)-2-(N-propyl-N-2-thienylethylamino)-5-hydroxytetralin (N-0923) in the rat and the mouse isolated vas deferens to determine whether these tissues contained inhibitory D2 receptors in addition to their inhibitory alpha-2 adrenoceptors. In the mouse vas deferens N-0923 and the alpha-2 adrenoceptor agonist clonidine inhibited the electrically evoked twitch responses. The actions of clonidine, but not of N-0923, were antagonized by the alpha-2 antagonist idazoxan (pKb = 7.9), and responses to N-0923 were antagonized by the D2 antagonist sulpiride (pKb = 8.1). In the rat vas deferens, clonidine, but not N-0923, inhibited the twitch responses and these inhibitions were antagonized by idazoxan (pKb = 7.9) but not by sulpiride. Other D2 receptor agonists were tested in the mouse and in the rat vas deferens for their ability to activate D2 and alpha-2 receptors, respectively. At the D2 receptors in the mouse vas deferens (alpha-2 blocked) the potency order was (+)-propyl-9-hydroxy-naphtoxazine > pergolide > N-0923 = apomorphine > bromocriptine > quinpirole > dopamine. At the alpha-2 receptors in the rat vas deferens the potency order was pergolide > bromocriptine > (+)-propyl-9-hydroxynapthoxazine > apomorphine > quinpirole > or = dopamine. N-0923 was inactive but antagonized the responses to clonidine. N-0923 was therefore the most D2 receptor selective agonist tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1997

[PET study of dopamine metabolism and dopamine D2 receptor in juvenile parkinsonism].

Positron emission tomographic(PET) study using 18F-6-fluoro-L-dopa (18FDOPA) can provide efficient information on the pre-synaptic function of nigrostriatal dopaminergic neurons. In juvenile parkinsonism(JP), the accumulation of 18FDOPA is markedly decreased in the caudate nucleus and putamen on both hemispheres. This finding is different from those in dystonia syndromes such as dopa-responsive dystonia (DRD) and hereditary progressive dystonia with marked diurnal fluctuation(HPD), and it is rather similar to late onset of Parkinson's disease. Furthermore, we studied dopamine D2 receptor binding activity on the post-synaptic sites of the striatum using 11C-YM-09151-2(11C-YM), a highly selective dopamine D2 receptor antagonist. In JP, 11C-YM was highly accumulated in the striatum, and D2 receptor binding activity is not significantly different from that of age-matched young normal subjects, but much higher than that of aged subjects. This finding suggests that post-synaptic dopamine receptor function keeps still normal or hypersensitive in JP, and may be different from other degenerative disorders such as multiple system atrophy. Glucose metabolism using 18F-fluoro-2-deoxy-D-glucose(18FDG) was also within normal range in the cerebral cortex in JP, but was more increased in the striatum than in the cerebral cortex in some patients. These PET studies can provide efficient informations about the pathologic condition of JP.

Age of Onset↗

PubMed1995

The putative dopamine D3 agonist, 7-OH-DPAT, reduces dopamine release in the nucleus accumbens and electrical self-stimulation to the ventral tegmentum.

The present experiments were designed to test further the idea that 7-OH-DPAT (7-hydroxy-N,N-di-n-propyl-2-aminotetralin), a putative dopamine (DA) D3 agonist, has effects at DA autoreceptors to reduce intracranial DA levels and to reduce behaviours that are DA-dependent. Rats were trained to respond on a self-stimulation protocol for electrical stimulation to the ventral tegmental area (VTA). Each press of a lever delivered a 0.5 s train of square wave, 1.5 ms duration, 100 Hz, 90-120 mA stimulation. Systemic administration of 7-OH-DPAT at 0.01-0.3 mg/kg i.p., quickly dose-dependently reduced responding. Electrical stimulation using similar parameters to those that supported self-stimulation were then applied to the VTA of anaesthetized rats. Fast cyclic voltammetry (FCV) revealed that this stimulation released DA in the nucleus accumbens (NAC). 7-OH-DPAT i.p. (0.1-3.0 mg/kg) quickly and potently reduced the size of the DA-generated voltammetric signal. This effect of 0.3 mg/kg 7-OH-DPAT was not blocked by sulpiride (60 mg/kg, i.p.) a D2-specific antagonist that may preferentially block D2 autoreceptors. These data are discussed with reference to the possibility that 7-OH-DPAT reduces the release of dopamine in the NAC, at D3, but not at D2, autoreceptors and that this in turn may reduce the rewarding effect of VTA stimulation.

Animals↗

PubMed1996

Preferential vulnerability of nucleus accumbens dopamine binding sites to low-level lead exposure: time course of effects and interactions with chronic dopamine agonist treatments.

This study examined the hypotheses that low-level lead (Pb) exposure would increase dopamine (DA) binding sites, would do so preferentially in nucleus accumbens, and that such effects would be modified by concurrent DA agonist treatment. D1-like and D2-like binding sites and the dopamine transporter (DT) were measured autoradiographically in caudate-putamen and nucleus accumbens of rats exposed from weaning to 0, 50, or 150 ppm Pb acetate drinking solutions with or without concurrent chronic intermittent intraperitoneal injections of the D1-like agonist SKF 82958 or the DA agonist apomorphine after 2 weeks (no injections), 8 months, or 12 months of Pb exposure. Pb selectively decreased DA binding in nucleus accumbens. Decreases in D2-like and DT sites were sustained across the 12-month exposure, whereas D1-like sites evidenced recovery at 12 months. Chronic intermittent DA agonist treatments reversed these effects of Pb in nucleus accumbens, restoring receptor and DT binding levels to normal, despite decreasing binding sites of non-Pb-treated rats. These studies implicate increased DA availability as a mechanism of Pb-induced DA system changes. They also raise the possibility that Pb exposure could serve as a predisposing factor in neurodegenerative diseases associated with DA system dysfunction or could alter the course of DA-based therapeutic treatments.

Administration, Oral↗

PubMed1994

Characterization of the functional activity of dopamine ligands at human recombinant dopamine D4 receptors.

The human D4 dopamine receptor has been expressed in Sf9 insect cells where it appears to couple to endogenous G proteins. Increased guanine nucleotide exchange to G proteins is a reflection of receptor activation and can be followed using a [35S]GTP gamma S binding assay. By measuring D4 receptor stimulation of [35S]-GTP gamma S binding we have been able to characterize several dopaminergic compounds for their functional activity at this receptor. In Sf9 cells expressing the D4 receptor, dopamine, quinpirole, and dp-2-aminodihydroxy-1,2,3,4-tetrahydronaphthalene were all full agonists, whereas (-)-apomorphine appeared to be a partial agonist. No increase in [35S]GTP gamma S binding was observed for noninfected cells or cells infected with an unrelated sequence. The quinpirole-stimulated [35S]GTP gamma S binding could be inhibited by the antagonists clozapine, eticlopride, and haloperidol, and a Schild analysis of these data showed that all three compounds were acting as competitive antagonists of D4 receptors. The rank order of affinities derived from the Schild analysis correlated with that obtained from [3H]spiperone competition binding assays. In conclusion, we have shown that, using this assay system, it is possible to investigate functionally the pharmacology of a recombinant G protein-coupled receptor in the absence of any information regarding the eventual second messenger pathways involved.

Animals↗

PubMed1993

Modification of the behavioral effects of the selective dopamine D2 agonist (+)-4-propyl-9-hydroxynaphthoxazine by dopamine antagonists in monkeys.

The present studies were conducted to evaluate the modification of the behavioral effects of the selective D2 agonist (+)-4-propyl-9-hydroxynaphthoxazine [(+)-PHNO] by dopamine receptor blockade. In squirrel monkeys responding under a fixed-ratio schedule of stimulus-shock termination, the effects of (+)-PHNO were determined alone and in combination with the selective D2 antagonist eticlopride, the selective D1 antagonist (-)-trans-6,7,7a,8,9,13b- hexahydro-3-chloro-2-hydroxy-N-methyl-5H-benzo(d)naphtho-(2,1)azepine (SCH 39166), the nonselective D1/D2 antagonist cis-flupentixol or the atypical neuroleptic clozapine. When administered alone, (+)-PHNO produced dose-dependent decreases in rates of responding. Pretreatment with eticlopride and cis-flupentixol resulted in dose-dependent right-ward shifts of the (+)-PHNO dose-effect curve, indicative of surmountable antagonism. Pretreatment with SCH 39166 and clozapine failed to antagonize the effects of (+)-PHNO and resulted in a downward shift of the (+)-PHNO dose-effect curve. Other experiments were conducted to determine the duration of either catalepsy-associated behavior or repetitive scratching produced by (+)-PHNO alone and in combination with selected dopamine receptor blockers. Low doses of (+)-PHNO (0.001-0.003 mg/kg) increased the duration of catalepsy-associated behavior, whereas higher doses (0.003-0.01 mg/kg) restored the duration of catalepsy-associated behavior to control values and produced increases in the duration of repetitive scratching.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Development of catecholaminergic neurons in the pond snail, Lymnaea stagnalis: I. Embryonic development of dopamine-containing neurons and dopamine-dependent behaviors.

The embryonic development of the catecholaminergic system of the pond snail, Lymnaea stagnalis, was investigated by using chromatographic and histochemical methods. High performance liquid chromatography suggested that dopamine was the only catecholamine present in significant concentrations throughout the embryonic development of Lymnaea. Dopamine first became detectable at about embryonic stage (E) 15 (15% of embryonic development) and then increased in amount during early development to reach about 120-140 fmol per animal by around E40. Dopamine content remained stable during mid-embryogenesis (E40-65), increased slowing for the next couple of days, and then increased rapidly to culminate at about 400 fmol per animal by hatching. The detection of aldehyde- and glyoxylate-induced fluorescence and of tyrosine hydroxylaselike immunoreactivity indicated that the first catecholaminergic cells appeared in the late trochophore or early veliger stage of embryonic development (E32-35). The paired perikarya of these transient apical catecholaminergic (TAC) neurons were located beneath the apical plate, remained outside of the central ganglia during embryogenesis, and no longer contained detectable catecholamines close to hatching. TAC neurons bore cilia on the ends of short processes that penetrated the overlying epithelium; their long processes branched repeatedly under the ciliated apical plate. Several smaller catecholaminergic cells first appeared in the anterior margin of the foot at a stage when the embryos began to metamorphose from the veliger form (E55). Similar bipolar cells later appeared in the tentacle and lips. The axons of all of these small peripheral cells projected centrally and terminated within the neuropil of different central ganglia. Central catecholaminergic neurons, including RPeD1, differentiated only after metamorphosis was complete (E75). Development of locomotor, respiratory, and feeding behaviors correlated with maturation of catecholaminergic neurons, as indicated by histology and chromatography.

Animals↗

PubMedDate not supplied

Distribution of dopamine receptors and dopamine receptor homologs in the brain of the honey bee, Apis mellifera L.

In the brain of the honey bee, Apis mellifera, the radioligands [3H]-SCH23390 and [3H]-spiperone recognise D1- and D2-like receptors, respectively. In addition to being pharmacologically distinct and exhibiting significantly different expression profiles during the lifetime of the bee, [3H]-SCH23390- and [3H]-spiperone-binding sites differ markedly in their distribution within the brain. Estimates of [3H]-SCH23390-binding site density are highest in the somatal rind, whereas [3H]-spiperone-binding sites are most concentrated in the beta lobe neuropil of the mushroom bodies. Molecular cloning techniques have been used to identify two honey bee genes encoding dopamine receptor homologs. The first is the honey bee counterpart of a Drosophila D1-like dopamine receptor and is expressed in the mushroom bodies of both workers and drones. The second is related to D2-like dopamine receptors from vertebrates and is expressed in the brain of the bee, but the precise distribution of expression is not yet known.

Animals↗

PubMed1990

Pharmacokinetic analysis of absorption and metabolism of dopamine and a dopamine prodrug in dogs.

Pharmacokinetic compartment models were constructed to describe the absorption and metabolism of dopamine (DA) and DA prodrug, N-(N-acetyl-L-methionyl)0,0-bis-eth-oxycarbonyl) dopamine(1). Plasma concentrations of DA, DA-SO4, and DOPAC after oral administration of DA to dogs, were analysed using the pharmacokinetic model assuming the contribution of first-pass metabolism for the formation of DA-SO4 and DOPAC. Though plasma concentration of DA was quite different from that of DA-SO4 or DOPAC, these data were simultaneously analysed with a good fitting curve. The apparent absorption rate constant of DA(K1) was proved to be much smaller than the apparent formation rate constants of DA-SO4(K2) or DOPAC(K3). It was found that the compartment model is useful for the evaluation of absorption and metabolic inactivation of DA. Plasma concentration of DA, N-(N-acetyl-L-methionyl)dopamine(2), DA-SO4, and DOPAC after oral administration of 1 were simultaneously analysed using the compartment model including the first-pass metabolism and two-fraction dissolution process. Good fitting curves were obtained. The apparent formation rate constant of 2(K4) is larger than that of DA-SO4(K5) or DOPAC(K6); thus it was shown that two protective groups of 1 reduced the metabolism of DA and 2 specially played an important role to the reduction of first-pass metabolism. From these results, it was found to be possible to give a pharmacokinetic interpretation for the mechanism of reduction of first-pass metabolism of DA.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1989

Chloral hydrate anesthesia alters the responsiveness of identified midbrain dopamine neurons to dopamine agonist administration.

Single-unit electrophysiological recording techniques were used to sample the basal activity of antidromically identified nigrostriatal and mesoaccumbens dopamine (NSDA and MADA, respectively) neurons and to examine the responsiveness of these cells to dopamine agonist-induced inhibition of cell firing rate in either chloral hydrate-anesthetized or paralyzed rats. Paralyzed rats exhibited a greater percentage of burst-firing cells (69%) than did anesthetized animals (37%). Furthermore, paralyzed rats were less sensitive to the mixed D1/D2 DA receptor agonist apomorphine and the selective D2 DA receptor agonist quinpirole. However, significantly higher doses of d-amphetamine were required in paralyzed animals only with respect to inhibiting MADA neurons. The abilities of apomorphine and quinpirole to inhibit NSDA cell firing were rate-dependent in both anesthetized and paralyzed rats, whereas d-amphetamine-induced inhibition was rate dependent only in anesthetized animals. In contrast, apomorphine- and quinpirole-induced inhibition of MADA neurons were rate-dependent only in anesthetized rats, whereas d-amphetamine-induced inhibition was rate-dependent only in paralyzed animals. These results suggest that general anesthesia exerts subtle effects on the basal activity and pharmacological responsiveness of midbrain dopamine neurons.

Action Potentials↗

PubMed1994

Isolation of DARP (dopamine-releasing protein) from fetal rat brain and effects of DARP immunoneutralization on fetal mesencephalic dopamine levels.

Recent work from this laboratory suggests a role for a novel dopamine-releasing protein (DARP) during rat fetal development. We have previously shown that intrafetal administration of an anti-DARP monoclonal antibody (DARP mAb) at Embryonic Day 17 (E17) induces fetal resorption in a dose-dependent manner (Kuhananthan et al., Mol. Cell. Neurosci., 2, 410-417). In this study we present evidence that (1) DARP is present in the rat brain at E17 and (2) in vivo immunoneutralization of DARP at E17 alters dopamine (DA) levels selectively in the prenatal mesencephalon. Enzyme-linked immunosorbent assay of supernatants of crude fetal (E17) brain homogenates using DARP mAb as a probe detects the presence of a DARP-like immunoreactive protein in the E17 rat brain. Purification of these homogenates with concanavalin A and immunoaffinity chromatography yielded a single 60-kDa protein that displayed dopamine-releasing activity in an in vitro superfusion assay. In addition, intrafetal administration of DARP mAb at E17 significantly elevated DA levels in the mesencephalon 24 and 48 h postinjection, while decreasing these levels 72 h postinjection. No changes in DA levels were detected in the diencephalon or in the telencephalon. These findings indicate that DARP is present in the rat brain at E17 and may play a role in the development of dopaminergic neurons of the mesencephalon.

Animals↗

PubMed2000

The molecular mechanism of dopamine-induced apoptosis: identification and characterization of genes that mediate dopamine toxicity.

Parkinson's disease (PD) is a progressive neurological disorder caused by rather selective degeneration of the dopaminergic (DA) neurons in the substantia nigra. Though subject to intensive research, the etiology of this nigral neuronal loss is still enigmatic and treatment is basically symptomatic. The current major hypothesis suggests that nigral neuronal death in PD is due to excessive oxidative stress generated by auto- and enzymatic oxidation of the endogenous neurotransmitter dopamine (DA), the formation of neuromelanin and presence of high concentrations of iron. We have found that DA toxicity is mediated through its oxidative metabolites. Whereas thiol-containing antioxidants provided marked protection against DA toxicity, ascorbic acid accelerated DA-induced death. Using the differential display approach, we sought to isolate and characterize genes whose expression is altered in response to DA toxicity. We found an upregulation of the collapsin response mediator protein (CRM) and TCP-1delta in sympathetic neurons, which undergo dopamine-induced apoptosis. The isolation of these genes led us to examine the expression and activity of CRM and TCP-1delta related genes. Indeed, we found a significant induction of mRNAs of the secreted collapsin-1 and the mitochondrial stress protein HSP60. Antibodies directed against collapsin-1 provided marked and prolonged protection of several neuronal cell types from dopamine-induced apoptosis. In a parallel study, using antisense technology, we found that inhibition of TCP-1delta expression significantly reduced DA-induced neuronal death. These findings suggest a functional role for collapsin-1 and TCP-1delta as positive mediators of DA-induced neuronal apoptosis.

Animals↗

PubMed1986

The effect of the dopamine agonist pergolide on tyrosine hydroxylase activity in rat striatal and limbic miniprisms in vitro: a model for the dopamine autoreceptor?

A method for the assay of tyrosine hydroxylase activity in rat striatal and limbic (nucleus accumbens + olfactory tubercle) brain miniprisms is described. The dopamine agonists apomorphine (1 mumol/l) and pergolide (0.01-100 mumol/l) inhibited the tyrosine hydroxylase activity in both regions. The inhibition produced by 1 mumol/l pergolide was antagonised partially in striatal miniprisms and completely in limbic miniprisms by 1 mumol/l haloperidol. The dopamine D2-selective antagonist raclopride, at concentrations up to 300 nmol/l, did not antagonise the inhibition produced by pergolide in striatal miniprisms, but appeared partially to antagonise the inhibition in limbic miniprisms. It is concluded that whilst pergolide potently inhibits tyrosine hydroxylase activity in striatal and limbic miniprisms, the inhibition is of doubtful value as a predictive model of dopamine autoreceptor function in striatal miniprisms, but may be useful when limbic miniprisms are used.

Animals↗

PubMed1977

Correlation between serum dopamine-beta-hydroxylase activity and dopamine-beta-hydroxylase and tyrosine hydroxylase activities in central and peripheral adrenergic neurons and adrenal glands.

Serum dopamine-beta-hydroxylase activity in spontaneously hypertensive rats and Wistar-Kyoto rats had a positive correlation with dopamine-beta-hydroxylase and tyrosine hydroxylase activities in mesenteric vessels, vas deferens, and adrenal glands at 14-16 weeks of age, a negative correlation with dopamine-beta-hydroxylase activity in locus coeruleus at 3 weeks and 14-16 weeks of age, and a positive correlation with tyrosine hydroxylase activity only at 3 weeks of age, but not at 14-16 weeks of age.

Adrenal Glands↗

PubMed1983

Dopamine uptake inhibiting versus dopamine releasing properties of fencamfamine: an in vitro study.

To elucidate its mechanism of action, the effects of fencamfamine, a norcamphanethylamine derivative, were studied in vitro on the release of newly accumulated dopamine in superfusion experiments using slices of rat corpus striatum and substantia nigra in comparison to nomifensine and d-amphetamine. Furthermore, the activity of fencamfamine on biogenic amine uptake in synaptosome preparations and on monoamine oxidase activity was evaluated. As compared to d-amphetamine, fencamfamine exhibited roughly 10 times less dopamine releasing activity in striatal slices at concentrations at which dopamine uptake into synaptosomes was almost completely blocked although, at high concentrations, what was probably non-specific release due to interactions with neuronal membranes could also be demonstrated. In addition, fencamfamine, unlike d-amphetamine did not inhibit monoamine oxidase. It is concluded that, at least in the models employed, the in vitro profile of fencamfamine is more similar to that of nomifensine, a reportedly pure uptake inhibitor, than to d-amphetamine.

Animals↗

PubMed1983

Differentiation of dopamine agonists using drug-induced rotation in rats with unilateral or bilateral 6-hydroxydopamine destruction of ascending dopamine pathways.

Eighteen compounds with dopamine agonist properties were examined in two rat rotational models. In the classical Ungerstedt model, a unilateral 6-hydroxydopamine (60HDA) lesion destroyed nigrostriatal and mesolimbic dopamine pathways on one side. Indirectly acting compounds, amphetamine, amantadine, methylphenidate and S1694, produced ipsiversive rotation, which was inhibited by pretreatment with alpha-methyl-p-tyrosine (AMPT). All other compounds produced contraversive rotation, but the rotation caused by CM 29-712, bromocriptine and ET 495 was reduced by AMPT. In animals with a bilateral 60HDA lesion removing both dopaminergic inputs to nucleus accumbens and the dopaminergic input into one striatum, indirectly acting drugs caused ipsiversive posturing prevented by AMPT, but little rotation. All other compounds produced contraversive rotation, but the effects of CM 29-712, bromocriptine and ET 495 were reduced by AMPT pretreatment. Inhibition of monooxygenase drug metabolising activity utilising SKF-525A inhibited contraversive turning induced by bromocriptine and ET 495 in the unilateral lesion model, but had no effect on rotation caused by apomorphine or CM 29-712. We conclude that, in addition to indirect pre-synaptically acting agonists and direct post-synaptic receptor agonists, there are a small group of compounds which produce rotation associated with direct receptor activation, which is inhibited by disruption of pre-synaptic dopamine function. The mechanism of action of this latter group is not understood, but cannot be attributed solely to active metabolite formation.

Animals↗

PubMed1976

The relationship between striatal and mesolimbic dopamine dysfunction and the nature of circling responses following 6-hydroxydopamine and electrolytic lesions of the ascending dopamine systems of rat brain.

The importance of extrapyramidal and mesolimbic function for circling behaviour was investigated by placing 6-hydroxydopamine (6-OHDA) and electrolesions in the cell bodies, axons and terminals of each system. Circling behaviour was weak when 6-OHDA was placed at the centre of the substantia nigra (SN), but the characteristic contralateral/ipsilateral turning to apomorphine/amphetamine were recorded. Circling was more marked when 6-OHDA was placed anterior to the SN but was generally absent following injections posterior to the SN. However, 6-OHDA placed in the medial forebrain bundle in the lateral hypothalamus resulted in intense contralateral/ipsilateral turning to apomorphine/amphetamine. Generally, the intensity of circling responses was related to the degree of striatal dopamine (DA) depletion but the more effective lesions also caused reductions in mesolimbic DA content. However, circling was not observed following any 6-OHDA injection into the mesolimbic DA system and it is concluded that mesolimbic DA function is not essential for the initiation of circling. In contrast to the 6-OHDA lesions, rats circled ipsilateral to both apomorphine and amphetamine when the SN was damaged by electrocoagulation to cause marked depletion of striatal dopamine. Lesser depletions of striatal dopamine after electrocoagulation in different regions of the medial forebrain bundle were associated with a lower intensity of ipsilateral circling to both drugs. In general, the differences between 6-OHDA and electrolesions could not be explained by additional damage to ascending noradrenaline or 5-hydroxytryptamine pathways. Lower doses of apomorphine were effective in the 6-OHDA circling rats, and the ipsilateral striatum of such rats was more sensitive to directly applied DA. Higher doses of apomorphine were required to produce circling after chronic electrolesions which rendered the ipsilateral striatum insensitive to DA. The contralateral circling to apomorphine after 6-OHDA lesions was abolished by chronic but not by acute electrolesion of the SN. It is suggested that electrolesions of the SN cause different effects to 6-OHDA because they destroy neuronal pathways in addition to the dopaminergic nigrostriatal tract. These appear to be required for the expression of circling behaviour caused by stimulation of the denervated striatum. Whereas 6-OHDA lesions result in super-sensitivity of the denervated strital DA receptors, electrolesions may cause a hypo-sensitivity of the same receptor sites.

Afferent Pathways↗

PubMedDate not supplied

CSF dopamine increased in depression: CSF dopamine, noradrenaline and their metabolites in depressed patients and in controls.

Some studies report reduced levels of the dopamine metabolite HVA in CSF in depression. In the present study including 24 depressed patients and 10 controls, we found significantly increased concentrations of total CSF dopamine in depressed patients. This finding suggests a dysfunction in central dopamine turnover in depression. No differences in CSF levels of noradrenaline or the amine metabolites homovanillic acid and 3-methoxy-4-hydroxy-phenylglycol were seen when comparing depressed patients with controls.

Adult↗