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At least 1,081 records · Page 60Linked to original sources
PubMed1995

Effects of subchronic treatments with SM-9018, a novel 5-HT2 and D2 antagonist, on dopamine and 5-HT receptors in rats.

1. Receptor binding and behavioral studies were performed to compare the effects of subchronic treatments with SM-9018, a novel 5-HT2 and D2 antagonist, and with haloperidol (HAL) on dopamine and 5-HT receptors in rats. 2. SM-9018 treatment (10 mg/kg/day p.o.) for 2 weeks did not significantly change the density (Bmax) of striatal D2 receptors or the incidence of stereotyped behavior induced by apomorphine (APO). By contrast, HAL treatment (3 mg/kg/day p.o., for 2 weeks) significantly increased the D2 receptor density by about 55% and markedly enhanced the behavioral response to APO. 3. The density of 5-HT2 receptors in the cerebral cortex was significantly reduced (about 20%) by SM-9018 treatment without being affected by HAL. However, the hyperthermic response of rats to p-chloroamphetamine (p-CAMP, a putative 5-HT releaser) was unaltered by either treatment. 4. Neither SM-9018 nor HAL treatment changed the density of 5-HT1A receptors in the hippocampus. 5. These findings suggest that SM-9018 is weaker than HAL in inducing up-regulation and supersensitivity of the striatal D2 receptors after the subchronic treatment.

Animals↗
PubMed1995

Persistent, specific and dose-dependent effects of toluene exposure on dopamine D2 agonist binding in the rat caudate-putamen.

Exposure to toluene (40-320 ppm; 4 weeks, 6 h/day, 5 days/week), followed by a postexposure period of 29-40 days, decreased the wet weight of the caudate-putamen and of the subcortical limbic area (maximal effect of 10% attained at 80 ppm toluene) of the male rat. Furthermore, toluene exposure decreased the IC50 values (significant effects attained at 80 ppm), the KH, the KL, and the RH% values of dopamine on [3H]raclopride-binding in the caudate-putamen. Toluene exposure did not significantly affect either the body weights, the wet weights of the whole brain, the serum prolactin levels, the KD or the Bmax values of [3H]raclopride-binding in the caudate-putamen and the subcortical limbic area, or the IC50 values of dopamine at [3H]raclopride-binding sites in the subcortical limbic area. Exposure to xylene or styrene (80 and 40 ppm, respectively; 4 weeks, 6 h/day, 5 days/week), followed by a postexposure period of 26-32 days, had no effect on the parameters described above (prolactin levels were not analyzed). The present study indicates that long-term exposure to low concentrations of toluene (> or = 80 ppm), but not xylene (80 ppm) or styrene (40 ppm), leads to persistent increases in the affinity of dopamine D2 agonist binding in the rat caudate-putamen.

Aging↗
PubMed1984

Binding of a spin-labelled photoallergen to human serum albumin.

The binding site for 3,3',4',5-tetrachlorosalicylanilide (T4CS), a potent photoallergen, on human serum albumin (HSA) was studied by electron spin resonance spectroscopy using a spin-labelled analogue 3,5-dichlorosalicylamido-4-(2,2,6,6-tetramethylpiperidine 1-oxyl) (DCS-TEMPO) of T4CS in the absence of ultraviolet irradiation. DCS-TEMPO bound non-covalently (K = 5.8 X 10(6) M-1) to one major binding site on HSA. This binding site could be blocked by the photochemical binding of T4CS to the protein. Limited tryptic digestion of HSA or chemical modification of its single tryptophan residue with 2-hydroxy-5-nitrobenzyl bromide was found to reduce the binding constant of the T4CS/DCS-TEMPO-binding site. These observations are in good agreement with earlier conclusions on the nature of the T4CS-binding site and suggest a location for this site close to the single tryptophan residue of the HSA molecule.

Allergens↗
PubMed1986

Autoradiographic visualization of dopamine D-2 receptors in the monkey brain using the selective benzamide drug [3H]raclopride.

Using the novel substituted benzamide drug [3H]raclopride in combination with in vitro receptor autoradiography, the distribution of dopamine D-2 receptors was studied in the monkey brain. Highest densities of D-2 receptors are present in dopamine-rich areas and the distribution shows the following rank order: caudatus and putamen greater than nucleus accumbens greater than olfactory tubercle greater than substantia nigra (pars compacta) greater than insular cortex greater than piriform and entorhinal cortex greater than substantia nigra (pars reticulata). In all of these areas [3H]raclopride binding was blocked by dopamine (1 microM) and by D-2 receptor antagonists such as (+)-butaclamol, eticlopride and raclopride, while the D-1 receptor antagonist SCH 23390 (1 microM) reduced [3H]raclopride binding by 15-20% in some restricted parts of the caudatus and putamen exclusively.

Animals↗
PubMed1988

D1- and D2-receptor antagonists induce catalepsy via different efferent striatal pathways [corrected].

The D1- and D2-receptor antagonists SCH 23390 and raclopride produced a dose-dependent catalepsy as studied by a vertical grid test in the male rat. The benzodiazepine antagonist Ro 15-1788 antagonized catalepsy induced by the D2-receptor antagonist raclopride while it failed to block the action of SCH 23390. The antimuscarinic drug scopolamine reduced and the gamma-aminobutyric acid (GABA) agonist muscimol enhanced catalepsy induced by both SCH 23390 and raclopride. The results suggest that D2-antagonist-induced catalepsy is mainly mediated via activation of the strio-pallidal GABA pathways whereas D1-receptor antagonist induced catalepsy is mainly mediated via increased activity in the nigrothalamic GABA pathways.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Synergy between a selective D1 antagonist and a selective D2 antagonist in the induction of catalepsy.

The cataleptogenic effects of the selective D1 dopamine receptor antagonist, SCH 23390, and the selective D2 dopamine receptor antagonist, raclopride, when administered alone or in combination were studied in rats using the vertical grid and horizontal bar methods. In either model both agents, given alone, produced dose-dependent catalepsy. When administered together, there was a marked synergy between the two drugs. Thus, a low dose of SCH 23390 resulted in a 10-fold shift to the left of the raclopride dose-effect curve. When the same low dose of SCH 23390 was administered together with a subcataleptogenic dose of raclopride, marked catalepsy was produced. The finding of synergy between selective D1 and D2 dopamine antagonists in the induction of catalepsy suggests that mixed antagonists may possess greater antipsychotic activity than neuroleptics acting mainly on one receptor subtype.

Animals↗
PubMed1989

Evidence for the role of dopamine D1 receptors in morphine induced stereotypic behavior.

In the course of studying the effects of morphine on the escape from electrical stimulation to the rat medial forebrain bundle, we observed that a combination of low doses of morphine and stimulation, neither of which caused stereotypy in the rat, resulted in marked stereotypic behavior that was similar to that seen with high doses of morphine alone. This behavior could be blocked by either naloxone or by the D1 antagonist SCH 23390, but not by the D2 antagonist raclopride. Furthermore, the stereotypy caused by chronically administered high doses of morphine was blocked by naloxone and the D1 antagonist. These results strongly implicate the role of dopamine D1 activation in morphine-induced stereotypies.

Animals↗
PubMed1990

A10 somatodendritic dopamine autoreceptor sensitivity following withdrawal from repeated cocaine treatment.

The mesoaccumbens dopamine (DA) pathway is known to be involved in both the rewarding properties of cocaine and in behavioral sensitization to its locomotor-stimulating effects. We investigated changes in DA neurons in this pathway following withdrawal from repeated cocaine treatment. Rats were injected with 10 mg/kg cocaine or 1 ml/kg saline twice daily for 14 days. One day, 4 days and 8 days after treatment, inhibition of cell firing by the DA agonist apomorphine was measured in DA neurons using in vivo single cell recording techniques. As previously reported, the somatodendritic autoreceptor appeared subsensitive one day after treatment. This autoreceptor subsensitivity persisted four days, but not eight days, after treatment. Although not a persistent alteration, autoreceptor subsensitivity may be necessary to trigger other permanent changes involved in behavioral sensitization.

Animals↗
PubMed1990

Lack of effect of chronic dopamine receptor blockade on D2 dopamine receptor mRNA level.

The chronic treatment of rats with antipsychotic drugs which increase striatal D2 dopamine receptors did not measurably increase the level of D2 receptor mRNA indicating that the observed increase in receptors was not primarily due to transcriptional regulation. These and other data suggest that the molecular mechanisms involved in receptor regulation in response to denervation or neurotransmitter depletion may be different from those which occur in response to chronic receptor blockade by antagonist drugs.

Adrenergic alpha-Antagonists↗
PubMed1990

Effects of inactivation of D1 dopamine receptors on stereotypic and thermic responses to quinpirole (LY 171555).

The purpose of the present study was to investigate reports that the expression of dopamine agonist-induced behaviours is dependent upon the ratio of D1 to D2 receptor activation. Selective inactivation of the D1 dopamine receptor was achieved using the irreversible antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) while D2 receptors were maintained at control levels by the use of a D2 antagonist, raclopride. Stereotypic and hypothermic responses to quinpirole (LY 171555) were assessed and related to striatal D1 and D2 receptor concentrations. Results showed that the incidence of stereotyped sniffing behaviour induced by LY 171555 was reduced in parallel with D1 receptor loss and sniffing behaviour was abolished at low D1 receptor (less than 40% of control) concentrations. Hypothermic responses to LY 171555 were unaffected by D1 receptor loss. These findings suggest that activation of D1 receptors is a critical component of stereotypic, but not hypothermic, responses to LY 171555, the magnitude of the sniffing response being positively associated with D1 receptor concentration.

Animals↗
PubMed1991

The serotonin (5-HT)1A agonist, LY 165,163, induces contralateral rotation in unilateral substantia nigra-lesioned rats via dopamine receptors.

The serotonin (5-HT)1A agonist, LY 165,163 (1-[2-(4-aminophenyl)ethyl]-4-(3-trifluoromethylphenyl)-piperazine) , also known as PAPP, has been suggested to exert effects via an interaction with dopamine receptors. Thus, in this study, we examined its ability to induce rotation in rats sustaining unilateral 6-hydroxy-dopamine lesions of the substantia nigra, an in vivo model of dopaminergic activity. In analogy to the direct dopamine (mixed D1/D2) agonist, apomorphine, (0.01-0.63 mg/kg), LY 165,163 (0.16-10.0 mg/kg) dose-dependently elicited robust and sustained contralateral rotation. Its maximal effect was comparable to that of apomorphine and its duration of action more extended. Rotation elicited by LY 165,163 (10.0 mg/kg) was resistant to the 5-HT1A antagonist, (-)-alprenolol. It was also unaffected by the selective D1 antagonist, SCH 23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5,tetrahydro-1H-3-be nza zepine) (2.5 mg/kg) or the selective D2 antagonist, raclopride (10.0 mg/kg) when each was administered alone. However, upon joint administration they clearly diminished the effect of LY 165,163. The dopamine antagonist, haloperidol (D2 greater than D1) also reduced the action of LY 165,163. This profile of partial antagonism by mixed D1 and D2 receptor blockade has been reported previously for apomorphine and contrasts to that seen with selective D1 or D2 agonists, the actions of which are completely blocked by D1 or D2 antagonists, respectively. In conclusion, the present data demonstrate that LY 165,163 exerts pronounced rotation in nigral-lesioned rats: this reflects a mixed D1/D2 action rather than an activation of 5-HT1A sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprenolol↗
PubMed1991

Striatal dopamine metabolism increases during long-term haloperidol administration in rats but shows tolerance in response to acute challenge with raclopride.

The release and metabolism of dopamine (DA) in the striatum of rats during long-term haloperidol administration (32 weeks) was assessed using in vivo microdialysis. Basal levels of homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC) were significantly elevated over control values, while basal DA release was not significantly increased. The specific DA D2 receptor antagonist, raclopride (0.5 mg/kg, i.p.), increased DA release and metabolism in control animals, but this effect was profoundly blocked in the haloperidol treated group. These results suggest that chronic haloperidol treatment may induce compensatory increases in basal DA activity even though response to an acute D2 antagonist shows significant tolerance.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Different laminar distributions of dopamine D1 and D2 receptors in the rat hippocampal region.

The distribution of dopamine (DA) D1 and D2 receptors in the hippocampal region was studied using in vitro receptor autoradiography with 125I-SCH 23982 and 125I-NCQ 298, respectively. The specific binding of both ligands indicated the existence of D1 as well as D2 receptors in the rat hippocampal region. A closer analysis revealed, however, a different laminar distribution of the two receptor subtypes: layers with a high density of one DA receptor subtype had low density of the other. Thus, in the entorhinal cortex, which contained the highest densities of both subtypes, the following pattern was seen. Layers 2, 4, 5 and 6 had high densities of D1 receptors and low densities of D2 receptors while layers 1 and 3 had high densities of D2 receptors and low densities of D1 receptors. The parasubiculum contained D1 receptors but not D2 receptors and the presubiculum had D2 receptors in layer 2 but few D1 receptors. Similar patterns were recorded in Ammon's horn: the part of stratum lacunosum-moleculare which was rich in D1 was poor in D2 receptors. The interdigitating laminar distribution of D1 and D2 receptors suggests that the effects of DA are mediated via D1 and D2 receptors located at different levels along the intrinsic hippocampal circuit.

Animals↗
PubMed1992

Changes in striatal dopamine release and metabolism during and after subchronic haloperidol administration in rats.

The release and metabolism of dopamine (DA) in the striatum of rats during and after subchronic haloperidol (HAL) administration (3 weeks) was assessed using in vivo microdialysis. Basal extracellular levels of DA, DA metabolites (homovanillic acid and 3,4-dihydroxyphenylacetic acid) and the serotonin metabolite (5-hydroxyindoleacetic acid) were not significantly different from control values at 3 weeks of HAL administration and 3 days after drug withdrawal. The specific DA D2 receptor antagonist, raclopride (0.5 mg/kg, i.p.), significantly increased DA release and metabolism in control animals, but decreased DA release in the HAL-treated groups at 3 weeks of drug treatment. This effect was not significant following drug withdrawal. These results contrast with our previous finding that chronic HAL treatment (32 weeks) increases basal DA metabolism and further support the possibility that changes in DA function differ following short term vs. long term neuroleptic exposure.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Gpp(NH)p stimulates [3H]raclopride binding to homogenates from human putamen and accumbens.

The effects of the stable GTP analogue Gpp(NH)p (5'-guanylyl imido diphosphate) were examined on in vitro [3H]raclopride binding to dopamine D2 receptors in preparations from post mortem human brains. The estimated number of receptors in the brain was 29% and 38% higher in putamen and accumbens, respectively, when determined in the presence of Gpp(NH)p as compared to its absence. The interaction of agonists was biphasic confirming the two affinity state model of the receptor--G-protein complex. The addition of Gpp(NH)p to the assay abolished the two site competition of apomorphine with [3H]raclopride binding in both regions studied. The non-specific binding at high concentrations of apomorphine was not significantly affected by the addition of Gpp(NH)p, indicating that only the specific binding of [3H]raclopride to the dopamine D2 receptor is increased.

Apomorphine↗
PubMed1992

Specific binding of 3N-(2'-[18F]fluoroethyl)benperidol to primate cerebral dopaminergic D2 receptors demonstrated in vivo by PET.

3N-(2'-[18F]Fluoroethyl)benperidol ([18F]FEB) an 18F-labeled analogue of the D2 antagonist benperidol, was evaluated as a tracer for positron emission tomography (PET). PET imaging of a living baboon showed that the fluorinated ligand rapidly localized in vivo within D2 receptor-rich brain tissue, with selective retention lasting over 2 h after tracer injection. Pretreatment of the animal with unlabeled D2-specific antagonist eticlopride (4 mg/kg, i.v.) 1 h before [18F]FEB completely abolished the selective disposition of the radioligand, whereas the regional cerebral blood flow, blood volume and peripheral metabolism/protein binding of [18F]FEB were not changed. Tracer localization when the baboon was pretreated with unlabeled ketanserin (0.55 mg/kg, i.v.) or SCH 23390 (1.1 mg/kg, i.v.) was identical to that for the control case, indicating that the [18F]FEB did not bind to S2 of D1 receptors in vivo. [18F]FEB has advantages compared to previously used PET tracers, and may be an excellent radioligand for non-invasive study of D2 receptor binding.

Animals↗
PubMed1994

The role of 5-HT1A serotonin and D2 dopamine receptors in buspirone effects on cortical electrical activity in rats.

The effects of buspirone (5 and 10 mg/kg i.p.), 8-OH-DPAT (0.25 mg/kg) and raclopride (2.5 mg/kg) on the EEG power spectra of the sensorimotor cortex were studied in freely moving rats. Buspirone (5 mg/kg) and 8-OH-DPAT produced selective slowing of the theta-activity. Buspirone (10 mg/kg) produced slowing of the theta-activity and increased the power of the alpha-band (9-11 Hz). Raclopride alone did not influence EEG power spectra. Simultaneous injection of 8-OH-DPAT and raclopride produced marked slowing of the theta-activity and increased the power of the alpha-band. The role of 5 HT1A and D2 dopamine receptors in buspirone effects on cortical electrical activity in rats was discussed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗