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D H Versteeg

Publications and source records attributed to D H Versteeg.

At least 37 records · Page 2Linked to original sources
PubMed1993

Peptide-induced grooming behavior and caudate nucleus dopamine release.

We simultaneously measured the display of grooming behavior and, by monitoring the extracellular dopamine concentration via transversal microdialysis, the release of dopamine in the caudate nucleus in freely moving rats after i.c.v. administration of 1 micrograms adrenocorticotropic hormone-(1-24) (ACTH-(1-24)). During a period of 1 h after administration of the peptide, the incidence of excessive grooming behavior was increased. Concomitantly, the concentration of dopamine in the caudate nucleus dialysates was significantly increased (maximal effect 151% of basal release) whereas that of its metabolite DOPAC was unchanged. The potent alpha-melanocyte stimulating hormone (alpha-MSH) receptor agonist, [Nle4,D-Phe7]alpha-MSH, induced grooming behavior and stimulated caudate nucleus dopamine release (maximal effect 148% of basal release) whereas ACTH-(7-16)-NH2 did neither induce grooming behavior nor cause an increase in caudate nucleus dopamine release. Single-dose tolerance was observed for ACTH-induced grooming but not for ACTH-induced dopamine release. These data are in support of the proposed involvement of brain dopamine systems in grooming behavior of the rat but at the same time suggest that the effect of ACTH/MSH-like peptides on dopaminergic transmission in the caudate nucleus is proximal to the final neural pathway involved in ACTH-induced grooming behavior.

Animals↗
PubMed1993

The hemodynamic effects of gamma 2-melanocyte-stimulating hormone and related melanotropins depend on the arousal potential of the rat.

In conscious rats, i.v. administered adrenocorticotropic hormone (ACTH-(4-10)) and gamma 2-melanocyte-stimulating hormone (gamma 2-MSH) induced a dose-dependent increase in blood pressure (BP), heart rate (HR) and pulse pressure (PP). No circadian influence on these effects was observed. The structurally related peptide, alpha-melanocyte-stimulating hormone (alpha-MSH), only caused an increase in HR, which was not dose-dependent, whereas the stable ACTH-(4-9) analog, Org 2766, was without effect on these hemodynamic parameters. In rats under light urethane-induced anesthesia, which is known to maintain reflexes and sufficient sympathetic tone, gamma 2-MSH caused hemodynamic responses similar to those observed in conscious rats. In contrast, gamma 2-MSH had an opposite effect in rats under deep pentobarbital-induced anesthesia: a depressor effect combined with a slight bradycardia. A comparative study with rats of a more arousable Wistar rat substrain (Riv:TOX) and of a less excitable rat substrain (U:WU) showed that the dose-pressor response curves for ACTH-(4-10) and gamma 2-MSH were shifted to the left in the more excitable rats as compared to the in the less excitable rats. We conclude that a restricted amino acid sequence in the N-terminal part of the pro-opiomelanocortin (POMC)-molecule (gamma 2-MSH/ACTH-(4-10)-like) is responsible for the stimulating effects on the cardiovascular system and that those effects are strongly dependent on the state of arousal, i.e. sympathetic tone, of the rat. These stimulatory effects override a depressor phenomenon which can only be detected during central depression.

Adrenocorticotropic Hormone↗
PubMed1993

Dopamine D1 and D2 receptors in the caudate nucleus of spontaneously hypertensive rats and normotensive Wistar-Kyoto rats.

A series of studies was carried out to characterize the binding properties of dopamine D1 and D2 receptors in membrane homogenates of the caudate nucleus of spontaneously hypertensive rats (SHR). Binding in SHR was studied at the age of 4 weeks when the rats were still in the prehypertensive phase, and at the age of 8 weeks, during the phase in which blood pressure is increasing dramatically; age-matched normotensive Wistar-Kyoto rats (WKY) were used as controls. Binding to dopamine D1 receptors was studied using [3H]SCH 23390. Antagonist binding of dopamine D2 receptors was performed with [3H]spiperone. At both ages no differences were found between SHR and WKY in affinity (Kd) or concentration (Bmax) of dopamine D1 and D2 receptors. Binding to the high affinity state of the dopamine D2 receptor was measured using the agonist [3H]N-n-propylnorapomorphine (NPA). No differences in Bmax or Kd were found between SHR and WKY at both ages studied, indicating that the ratio between dopamine D2 receptors in the high and in the low affinity state is not altered in spontaneous hypertension. Although the results do not reveal differences in affinities or concentrations of dopamine D1 or D2 receptors in the caudate nucleus between SHR and WKY, a role in the development of hypertension for the here described lack of receptor up-regulation in connection with our previous observation of lower release of dopamine in the caudate nucleus of SHR, cannot be excluded.

Animals↗
PubMed1993

Effects of ACTH-(1-24) on dopamine and noradrenaline release, B-50 phosphorylation and calmodulin binding to B-50 in vitro.

ACTH-(1-24), 1 microM, enhanced the Ca(2+)-dependent release of [3H]dopamine ([3H]DA) from intact septal synaptosomes by approximately 30%, but had no effect on the release of [3H]noradrenaline ([3H]NA) from intact cortical synaptosomes. Since a strong correlation has been reported between B-50 (phosphorylation) and [3H]NA release from intact or streptolysin-O- (SL-O-) permeated cortical synaptosomes, we investigated whether the effects of ACTH-(1-24) on the release of radiolabelled transmitters are mediated by B-50. We observed that the increment in the release of [3H]DA from SL-O-permeated septal synaptosomes as a result of exposure to a high Ca2+ concentration was much less pronounced than that of the release of [3H]NA from SL-O permeated septal and cortical synaptosomes. ACTH-(1-24) concentration-dependently inhibited [3H]NA release from SL-O-permeated cortical synaptosomes (IC50 value of approximately 10 microM) when ACTH-(1-24) was added 150 s prior to the Ca2+ trigger. Simultaneous addition of ACTH-(1-24), SL-O and Ca(2+)-buffers to cortical synaptosomes did not lead to a change in [3H]NA release at any of the ACTH-(1-24) concentrations tested. ACTH-(1-24) had no effect on B-50 phosphorylation in intact synaptosomes, whereas it concentration-dependently inhibited B-50 phosphorylation in permeated cortical synaptosomes (IC50 value of 100 microM). ACTH-(1-24) inhibited (IC50 value of 10 microM) B-50/calmodulin binding in vitro. We conclude that the effects of high concentrations of ACTH-(1-24) on various biochemical B-50 related parameters are not likely to represent the mechanisms underlying the action of ACTH-(1-24) on neurotransmitter release.

Adenosine Triphosphate↗
PubMed1993

Effect of ACTH-(4-10) and gamma 2-MSH on blood pressure after intracerebroventricular and intracisternal administration.

After intracerebroventricular (i.c.v.) administration of ACTH-(4-10) or gamma 2-MSH in doses of < or = 1,500 pmol, no changes were observed in mean arterial pressure (MAP) of conscious and urethane-anesthetized rats. When gamma 2-MSH was administered intracisternally (i.c.), a significant increase in MAP of approximately 15 mm Hg was observed after the two highest doses used (500 and 1,500 pmol) in conscious rats and also, though less pronounced, in urethane-anesthetized rats. Although the pressor effect of gamma 2-MSH after intravenous (i.v.) administration to conscious rats was maximal within 25 s and MAP had returned to preinjection values < or = 60 s, the pressor response after i.c. administration was slower in onset (maximal effect after 1-2 min) and of longer duration (return to preadministration values after 5 min). ACTH-(4-10) had a slight pressor effect after i.c. administration in doses of 1,500 and 2,500 pmol in conscious rats, but had no effect in urethane-anesthetized rats. These results indicate that sustained leakage of the peptides after i.c. administration, but not after i.c.v. administration, to the periphery is the causal factor of a modest pressor response. These results do not support the suggestion that the central nervous system (CNS) is the principal target of gamma-MSH-like peptides with respect to their pressor effect.

Adrenocorticotropic Hormone↗
PubMed1993

Adrenocorticotropin/alpha-melanocyte-stimulating hormone (ACTH/MSH)-like peptides modulate adenylate cyclase activity in rat brain slices: evidence for an ACTH/MSH receptor-coupled mechanism.

The regulation of adenylate cyclase activity by adrenocorticotropin/alpha-melanocyte-stimulating hormone (ACTH/MSH)-like peptides was investigated in rat brain slices using a superfusion method. Adenylate cyclase activity was concentration-dependently increased by ACTH-(1-24), alpha-MSH (EC50 values 16 and 6 nM, respectively), and [Nle4,D-Phe7]alpha-MSH (EC50 value 1.6 nM), in the presence of forskolin (1 microM, optimal concentration). 1-9-Dideoxyforskolin did not augment the response of adenylate cyclase to ACTH-(1-24). Various peptide fragments were tested for their ability to enhance [3H]cyclic AMP production. [Nle4,D-Phe7]alpha-MSH increased [3H]cyclic AMP formation with a maximal effect of 30% and was more potent than ACTH-(1-24), ACTH-(1-16)-NH2, alpha-MSH, ACTH-(1-13)-NH2, [MetO4]alpha-MSH, [MetO2(4),D-Lys8,Phe9]ACTH-(4-9), ACTH-(7-16)-NH2, ACTH-(1-10), and ACTH-(11-24), in order of potency. This structure-activity relationship resembles that found for the previously described peptide-induced display of excessive grooming. ACTH-(1-24) stimulated adenylate cyclase activity in both striatal (maximal effect, approximately 20%) and septal slices (maximal effect, approximately 40%), but not in hippocampal or cortical slices. Lesioning of the dopaminergic projections to the striatum did not result in a diminished effect of [Nle4,D-Phe7]alpha-MSH on [3H]cyclic AMP accumulation, which indicates that the ACTH/MSH receptor-stimulated adenylate cyclase is not located on striatal dopaminergic terminals. ACTH-(1-24) did not affect the dopamine D1 or D2 receptor-mediated modulation of adenylate cyclase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1992

Effect of SCH 23390 and quinpirole on novelty-induced grooming behaviour in spontaneously hypertensive rats and Wistar-Kyoto rats.

Grooming behaviour induced by exposure to a novel environment was studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The dopamine D1 receptor antagonist, SCH 23390, and the dopamine D2 receptor agonist, quinpirole, were used to study brain dopamine systems in these rat strains, via their effects on grooming behaviour. The total grooming behaviour displayed in a 50-min observation period was significantly lower in SHR than in WKY. Except for the paw licking component no differences between the two strains were observed in the separate behavioural elements of grooming behaviour. SCH 23390 and quinpirole were found to suppress novelty-induced grooming behaviour of both strains. In SHR, grooming behaviour was less suppressed by SCH 23390, whereas the suppression by quinpirole was more pronounced than in WKY. These results indicate that there are alterations in central dopamine systems in SHR, probably involving changes both in dopamine D1 and D2 receptor mechanisms in the brain.

Animals↗
PubMed1992

Characterization of the inhibitory effect of adrenocorticotropin/melanocyte-stimulating hormone-like peptides on the binding of dopamine receptor ligands to the dopamine D2 receptor in vitro.

Adrenocorticotropin (ACTH)-(1-24) decreased the binding of the dopamine D2 agonist [3H]N-n-propylnorapomorphine [3H](NPA) to the dopamine D2 receptor in rat striatal membranes in vitro. The association and dissociation of [3H]NPA to the dopamine D2 receptor was inhibited by ACTH-(1-24), suggesting an apparent competitive interaction between ACTH-(1-24) and the binding of [3H]NPA. ACTH-(1-24) was able to inhibit the binding of the dopamine D2 receptor antagonist [3H]spiperone to the dopamine D2 receptor, both in the high- and the low-affinity state. These observations suggest a G-protein-independent mechanism of action. The inhibitory effect of ACTH-(1-24) and ACTH-(7-16)-NH2 was diminished after the addition of polylysine chains, presumably via a blockade of the attachment sites for ACTH-(1-24) on the dopamine D2 receptor. The effect of ACTH-(1-24) on membrane fluidity and on the inhibition of the binding of [3H]NPA to the dopamine D2 receptor appeared to be unrelated because lowering the incubation temperature from 25 degrees C to 4 degrees C, which causes a strong decrease of membrane fluidity, did not diminish the effect of ACTH-(1-24) on the binding of [3H]NPA to the dopamine D2 receptor. Furthermore, in both young and old rats, whose membranes are reported to differ in lipid composition and membrane fluidity, ACTH-(1-24) inhibited the binding of [3H]NPA to the dopamine D2 receptor to nearly the same extent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1991

Effect of the dopamine D2 receptor agonist quinpirole on the in vivo release of dopamine in the caudate nucleus of hypertensive rats.

Using an in vivo microdialysis method, we found that the extracellular concentrations of dopamine and its main metabolite dihydroxyphenylacetic acid (DOPAC) were lower in the caudate nucleus of 8-week-old spontaneously hypertensive rats (SHR) than in the same area of age-matched normotensive Wistar-Kyoto rats (WKY). No differences in the extracellular concentrations of dopamine and DOPAC were found between renal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats when compared to their respective controls. After subcutaneous administration of the dopamine D2 receptor agonist quinpirole (10, 33 and 100 micrograms/kg), the amount of dopamine and DOPAC in the dialysates was diminished dose dependently. The quinpirole-mediated inhibition of dopamine release was more pronounced in SHR than in WKY, whereas inhibition of the extracellular DOPAC concentration was not different. Compared to WKY, the dose-response curve for the inhibition of dopamine release by quinpirole was shifted to the left in SHR and the maximal inhibition in response to the highest dose was significantly greater. Renal and DOCA-salt hypertensive rats showed no differences in the quinpirole-induced inhibition of the extracellular concentrations of striatal dopamine and DOPAC compared to their controls. The present findings on changes in dopaminergic neurotransmission and D2 autoreceptor-mediated modulation of dopamine release in genetically hypertensive rats but not in rats with experimentally induced hypertension provide further evidence for the hypothesis that alterations in the nigrostriatal dopamine system may be involved in the initiation of the development of spontaneous hypertension.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

ACTH/MSH-like peptides inhibit the binding of dopaminergic ligands to the dopamine D2 receptor in vitro.

ACTH-(1-24) decreased the binding of the dopamine D2 receptor agonist, [3H]N-propylnorapomorphine ([3H]NPA), to rat striatal membranes in a concentration-dependent manner, with a Ki of 5 x 10(-7) M. Saturation curves for [3H]NPA binding in the presence of increasing concentrations of ACTH-(1-24) were performed. Scatchard analysis in the presence of ACTH-(1-24) revealed an increased dissociation constant (Kd), while the binding capacity (Bmax) was not affected by the peptide, suggesting an apparent competitive interaction between ACTH-(1-24) and [3H]NPA. ACTH-(1-24) also reduced the binding of the dopamine D2 receptor antagonist [3H]spiperone to striatal membranes, with a Ki of 10(-6) M. Much higher concentrations of ACTH-(1-24), up to 10(-4) M, were needed for the displacement of appropriate radiolabelled ligands from dopamine D1 receptors, serotonin 5-HT1A, serotonin 5-HT1B, muscarinic M1 acetylcholine and histamine H1 receptors. ACTH-(1-24) also inhibited the binding of [3H]spiperone to dopamine D2 receptors in membranes of the pituitary gland, the septum and the substantia nigra. ACTH-(1-39) and most ACTH fragments and analogs were less potent than ACTH-(1-24) in displacing [3H]NPA from the dopamine D2 receptor in striatal membranes. In general there was a relationship between displacing potency and chain length. ACTH-(7-16)-NH2 and benzyloxycarbonyl-ACTH-(8-16)-NH2, however, were more potent than ACTH-(1-24) in reducing the binding of [3H]NPA to dopamine D2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

The electrically stimulated release of [3H]noradrenaline from nucleus tractus solitarii slices in vitro is modulated via mu-opioid receptors.

The electrically stimulated release of [3H]noradrenaline ([3H]NA) from slices of the nucleus tractus solitarii (NTS) from the rat in vitro was inhibited by the alpha 2-adrenoceptor agonist, clonidine, in a concentration-dependent manner and enhanced by the alpha 2-adrenoceptor antagonist, yohimbine. Phenylephrine, isoprenaline, carbachol, quinpirole and SKF 38393, all at 10(-6) M, did not affect the stimulus-evoked release of [3H]NA. The opioid peptides, alpha- and gamma-endorphin, did not have a significant effect on the stimulus-evoked release of [3H]NA; however, beta-endorphin reduced it in a concentration-dependent manner. [Leu5]Enkephalin also reduced [3H]NA release, but higher concentrations were necessary. The selective delta opioid receptor agonists, [D-Pen2,D-Pen5]enkephalin (DPDPE) and [D-Ser2(O-tert-butyl),Leu5]enkephalyl-Thr6 (DSTBULET), as well as the selective kappa opioid receptor agonist, U-69593, were not effective. The selective mu opioid receptor agonist, [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO), concentration dependently reduced the stimulus-evoked release of [3H]NA to the same extent as beta-endorphin did. Naloxone, while having no effect on stimulus-evoked [3H]NA release, antagonized the effect of DAGO. These results corroborate that the release of NA from noradrenergic terminals in the NTS region of the medulla oblongata of the rat is modulated via alpha 2-adrenoceptors and suggest that the release of NA in the NTS in rats is also modulated via mu opioid receptors.

Adrenergic alpha-Agonists↗
PubMed1991

Stimulus-evoked release of tritiated monoamines from rat periaqueductal gray slices in vitro and its receptor-mediated modulation.

The periaqueductal gray is a brain region of considerable interest. It is innervated by monoamine-containing neurons as well as by a variety of peptidergic fiber systems, and it participates in the regulation of various functions. Virtually nothing is known about monoamine release in the periaqueductal gray and its receptor-mediated modulation. We therefore studied the release of radioactivity from periaqueductal gray slices preloaded with tritriated monoamines, using an in vitro superfusion method. The release of radioactivity from superfused periaqueductal gray slices after preloading of the tissue with [3H]noradrenaline increased upon electrical stimulation in a frequency-dependent manner. The stimulus-evoked release of radioactivity was Ca(2+)-dependent. Clonidine reduced and yohimbine enhanced the release. The inhibition curve for the effect of clonidine was shifted to the right in the presence of 10(-6) M yohimbine. While phenylephrine, isoprenaline, SK & F 38393, quinpirole, carbachol, [Arg8]vasopressin, alpha-MSH and ACTH-(1-24), at a concentration of 10(-6) M, did not influence the electrically evoked release of radioactivity, [Leu5]enkephalin reduced it. The selective mu-opioid receptor agonists [D-Ala2,NMePhe4,Gly-ol5]enkephalin and [D-Arg2,Lys4]-demorphin-(1----4)-amide reduced the release of radioactivity, whereas the selective delta opioid receptor agonist [D-Pen2,D-Pen5] enkephalin and the selective kappa opioid receptor agonist U-69593 had no effect. In the presence of naloxone, which by itself had no effect on the release of radioactivity, the effect of [D-Arg2,Lys4]dermorphin-(1-4)-amide was abolished. These results show that the release of noradrenaline from periaqueductal gray slices is via a Ca(2+)-dependent exocytotic process, and that it is modulated through alpha 2-adrenoceptors as well as via mu-opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Role of brain dopamine systems in the development of hypertension in the spontaneously hypertensive rat.

We studied the role of central dopamine in the development of hypertension. Earlier work had shown that depletion of brain dopamine can inhibit the age-related rise in blood pressure in spontaneously hypertensive rats (SHR). In an open-field test, locomotor activity of Wistar-Kyoto controls was inhibited by haloperidol, apomorphine and sulpiride, but these drugs had less effect in SHR. The stimulation-evoked release of [3H]-dopamine from slices of the striatum of SHR was smaller than that from slices of WKY. The inhibition of the stimulation-evoked release of [3H]-dopamine by quinpirole was greater in SHR than in WKY. The results from the lesion experiments and from the behavioural activity studies would suggest an enhanced release of central dopamine in SHR, which might contribute to the development of hypertension in these animals. However, the in vitro release experiments (and subsequent in vivo microdialysis experiments) do not support such an enhanced release but rather showed decreased release of striatal dopamine in SHR.

Animals↗
PubMed1990

Evidence for a relationship between B-50 (GAP-43) and [3H]noradrenaline release in rat brain synaptosomes.

Phosphorylation of the neuron-specific substrate of protein kinase C (PKC), B-50 (GAP-43), was studied parallel with noradrenaline release in rat brain synaptosomes. Both could be evoked by treating the synaptosomes with high K+ or veratridine. Phorbol 12,13-dibutyrate enhanced depolarization-induced B-50 phosphorylation and noradrenaline release. To investigate the involvement of PKC-mediated B-50 phosphorylation in noradrenaline release, we applied a variety of kinase inhibitors. Prior to measuring the effects of these inhibitors in intact synaptosomes, we determined their effectivity and specificity in a membrane phosphorylation assay. H-7 most specifically inhibited PKC-dependent phosphorylation, whereas calmidazolium inhibited calmodulin-dependent phosphorylation. Polymyxin B affected both protein kinase systems. Only polymyxin B effectively inhibited noradrenaline release in the intact synaptosomes. We conclude that PKC as well as calmodulin-dependent processes are important for the release event. Data are discussed in view of the presumed function of B-50 as a calmodulin-binding protein.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Electrically stimulated [3H]dopamine and [14C]acetylcholine release from nucleus caudatus slices: differences between spontaneously hypertensive rats and Wistar-Kyoto rats.

Using an in vitro superfusion method it was found that nucleus caudatus slices of 8- and 12-week-old spontaneously hypertensive rats (SHR) release significantly less [3H]dopamine and [14C]acetylcholine upon electrical stimulation than do slices of normotensive Wistar-Kyoto rats (WKY) at all frequencies tested. At 4 weeks similar trends were seen, but the difference in [14C]acetylcholine release was not significant. That the difference in release of dopamine was already present prior to the onset of the development of hypertension, i.e. at the age of 4 weeks, indicates that it is probably not a consequence of, but rather associated with the development of hypertension. Addition of the dopamine uptake inhibitor nomifensine to the superfusion medium caused an increase in the net release of [3H]dopamine by inhibiting re-uptake, but did not influence the difference in release between SHR and WKY. The release of labelled dopamine and acetylcholine was inhibited in the presence of the dopamine D2 receptor agonist quinpirole. The concentration-response curve for the inhibition of the release of [3H]dopamine, but not that of [14C]acetylcholine, by quinpirole was shifted to the left and the maximum inhibition was higher for SHR than for WKY. These results suggest that the difference in stimulus-evoked release of labelled dopamine in the nucleus caudatus is not the consequence of changes in the uptake mechanism of dopamine, but is associated with differences between SHR and WKY in dopamine D2 autoreceptor regulation.

Acetylcholine↗
PubMed1990

4-Aminopyridine stimulates B-50 (GAP43) phosphorylation and [3H]noradrenaline release in rat hippocampal slices.

In situ phosphorylation of the presynaptic protein kinase C substrate B-50 was investigated in rat hippocampal slices incubated with the convulsant drug 4-aminopyridine (4-AP). Phosphorylation of B-50 was significantly enhanced 1 min after the addition of 4-AP (100 microM). This increase by 4-AP was concentration dependent (estimated EC50 30-50 microM). Concomitant with the changes in B-50 phosphorylation, 4-AP also dose-dependently stimulated [3H]noradrenaline [( 3H]NA) release from the slices. 4-AP stimulated [3H]NA release within 5 min to seven times the control level. The B-50 phosphorylation induced by 4-AP remained elevated after removal of the convulsant, this is contrast to B-50 phosphorylation induced by depolarization with K+. A similar persistent increase was observed for [3H]NA release after a 5-min incubation period with 4-AP. These results give more insight into the molecular mechanisms underlying 4-AP-induced epileptogenesis and provide further evidence for the correlation between B-50 phosphorylation and neurotransmitter release in the hippocampal slice.

4-Aminopyridine↗
PubMed1989

Dopamine D-1 and D-2 receptor agonists and antagonists and neuropeptide-induced excessive grooming.

The administration of the dopamine D-1 receptor antagonist, SCH 23390, but not of the dopamine D-2 receptor antagonist, sulpiride, suppressed the excessive grooming induced by a new environment or by various neuropeptides. In addition, administration of the dopamine D-1 agonist, SK & F 38393, induced excessive grooming but that of the dopamine D-2 agonist, quinpirole, did not. It is suggested that dopamine D-1 rather than D-2 receptor stimulation is an important mechanism underlying novelty-induced as well as neuropeptide-induced excessive grooming.

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