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At least 1,495 records · Page 83Linked to original sources
PubMed1994

Antiparkinsonian activity of talipexole in MPTP-treated monkeys: in combination with L-dopa and as chronic treatment.

We examined whether or not the antiparkinsonian activity of talipexole (B-HT 920, 6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]-azepine) could be optimised by combination with L-3,4-dihydroxyphenylalanine (L-dopa). Additionally, the effects of chronic treatment with talipexole on motor behavior were investigated using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated and normal common marmosets. Administration of MPTP (0.5 mg/animal i.v. once or twice) to marmosets induced persistent parkinsonian motor deficits. The antiparkinsonian activity of talipexole (40 micrograms/kg s.c.) was significantly enhanced by its combination with L-dopa (30 mg/kg i.p.). This may further support the postulated postsynaptic dopamine D2 receptor agonist properties of talipexole. Chronic treatment with talipexole (a daily dose of 40 micrograms/kg s.c. for 21 days) did not lead to tolerance to the antiparkinsonian activity in MPTP-treated animals. No obvious dyskinesia was seen throughout the chronic treatment. In contrast, in normal marmosets, talipexole at a dose of 80 micrograms/kg which is a dose sufficient to induce hyperactivity did not increase motor activity during the treatment repeated for 21 days. These results suggest that talipexole is a selective dopamine D2 receptor agonist drug of potential use in the treatment of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Pharmacological profile of ME3221, a novel angiotensin II receptor antagonist.

The pharmacological profile of a new surmountable angiotensin AT1 receptor antagonist, ME3221, 3-methoxy-2,6-dimethyl-4-[[2'-(1H-tetrazol-5-yl)-1,1'-biphenyl-4- yl]methoxy]pyridine, was studied in several animal models, and was compared with that of losartan. EF2831, 3-hydroxy-2,6-dimethyl-4-[[2'-(1H-tetrazol-5-yl)-1,1'-biphenyl-4- yl]methoxy]pyridine, a metabolite of ME3221, is also a surmountable angiotensin AT1 receptor antagonist, whose potency was 1/30 that of ME3221 in vitro, but equal to or 1/3 of that of ME3221 in in vivo experiments. In rats and marmosets, ME3221 antagonized angiotensin II-induced pressor responses, but did not affect bradykinin-induced depressor responses. ME3221 lowered the blood pressure in renal hypertensive rats and spontaneously hypertensive rats (SHR), and its ED25 value was 3 times that of losartan. Repeated administration of ME3221 to SHR had a stable and long-lasting antihypertensive effect without influencing heart rate. Thus ME3221, like losartan, may be useful in the treatment of renal and essential hypertension.

Angiotensin II↗
PubMed1995

Short- and long-term changes in striatal and extrastriatal dopamine uptake sites in the MPTP-treated common marmoset.

The 'short-term' (15-30 days) and 'long-term' (18-42 months) effects of the systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on [3H]mazindol binding to dopamine uptake sites was investigated in the common marmoset. In the 'short-term' MPTP-treated group, [3H]mazindol binding was reduced in the caudate-putamen (by -82 to -98% with respect to controls), substantia nigra pars compacta (-71 to -84%), ventral tegmental area (-72%) and nucleus accumbens (-54%). [3H]Mazindol binding in the globus pallidus, frontal cortex and substantia nigra pars reticulata was much lower and was unaffected by MPTP treatment. In the 'long-term' MPTP-treated group [3H]mazindol binding was still greatly reduced in the substantia nigra pars compacta (by -76 to -89%), ventral tegmental area (-71%) and most of the caudate-putamen (-69 to -98%), although the reduction in [3H]mazindol binding in the nucleus accumbens (-27%) and rostroventral caudate nucleus (-69%) was less than in the 'short-term' MPTP-treated group. The motor deficits induced by MPTP treatment in the common marmoset are largely reversible with increasing survival times (Ueki et al., 1989, Neuropharmacology 28, 1089). In the present study, the apparent 'recovery' in [3H]mazindol binding in the rostroventral caudate nucleus and nucleus accumbens may indicate regeneration of dopamine neurone terminals in these regions and this may contribute to the behavioural recovery seen in this primate model of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Modulation of glutamate release by a kappa-opioid receptor agonist in rodent and primate striatum.

The influence of the kappa-opioid receptor agonist, enadoline, on endogenous glutamate release was investigated in rat and marmoset striatal synaptosomes. Enadoline decreased 4-aminopyridine (2 mM)-stimulated glutamate release (rat: IC50 approximately 8.7 microM, marmoset: IC50 approximately 2.9 microM). The effect of enadoline was reversed by nor-binaltorphimine (5 microM). These data indicate that, in the striatum of the rat and marmoset, kappa-opioid receptor agonists can modulate glutamate release. These findings may have implications for the treatment of Parkinson's disease.

4-Aminopyridine↗
PubMed1995

Peptoid CCK receptor antagonists: pharmacological evaluation of CCKA, CCKB and mixed CCKA/B receptor antagonists.

Several novel cholecystokinin (CCK) receptor ligands with differing degrees of receptor selectivity were characterised in both in vitro and in vivo models. In radioligand binding assays, the dipeptoid PD 135666 ((benzenebutanoic acid, beta-[[3-(1H-indol-3-yl)-2-methyl-1-oxo-2- [[(tricyclo[3.3.1.1(3,7)]dec-2-yloxy)carbonyl]amino]propyl] amino],-[R-(+*,S*)]) selectively inhibited [125I]Bolton Hunter CCK-8 binding to CCKB receptors in mouse cerebral cortex (CCKB IC50 = 0.1 nM) but was weaker as an inhibitor of CCKA receptor binding in the rat pancreas (IC50 = 26 nM). In contrast, its enantiomer PD 140548 ((benzenebutanoic acid, beta-[[3-(1H-indol-3-yl)-2-methyl-1-oxo-2-[[(tricyclo[3.3.1.1(3,7] dec-2-yloxy)carbonyl]amino]propyl] amino],-[S-(R*,S*)) displayed the reverse selectivity (CCKA IC50 = 2.8 nM, CCKB IC50 = 260 nM). PD 142898 ([benzenebutanic acid, beta-[[3-(1H-indol-3-yl)-2-methyl-2-[[[(2- methylcyclohexyl)oxy]carbonyl]amino]-1-oxopropyl]amino]-,[1S-[1 alpha[S*(R*)],2 beta ]]) possessed nanomolar affinity for both receptor subtypes (CCKB IC50 = 4.2 nM, CCKA IC50 = 3.8 nM) whereas its corresponding enantiomer PD 142896 ([benzenebutanic acid, beta-[[3-(1H-indol-3-yl)-2-methyl-2-[[[(2- methylcyclohexyl)oxy]carbonyl]amino]-1-oxopropyl]amino]-, [1R-[1 alpha[S*(R*)],2 beta]]) displayed 147-fold selectivity for the CCKA receptor (CCKA IC50 = 7.9 nM, CCKB IC50 = 1160 nM). The pyrazolidinone PD 141479 (trans-5-(2-chlorophenyl)-3-oxo-4-phenyl-N-[4- (trifluoromethyl)phenyl]-1-pyrazolidinecarboxamide) was found to interact selectively with the CCKB receptor (CCKB IC50 = 36 nM, CCKA IC50 = 1100 nM). PD 140548, PD 142896, PD 135666 and PD 142898 antagonised the CCKA receptor-mediated contraction of guinea pig gall bladder with respective pA2 values of 7.2, 7.4, 6.6 and 8.5. In the rat elevated X-maze, PD 135666 and PD 141479, together with the mixed CCKA/B receptor antagonist PD 142898 produced anxiolytic effects with respective minimum effective doses (MEDs) of 0.01, 0.001 and 0.01 mg/kg s.c. Furthermore, the selective CCKB receptor antagonist CI-988 (0.01-1 mg/kg) and PD 142898 (0.001-0.1 mg/kg), dose dependently induced behavioural changes suggestive of anxiolysis in the marmoset human threat test with respective MED values of < 0.01 and < 0.001 mg/kg s.c. In contrast, compounds with the CCKA selective profile were either inactive in the two behavioural models or showed activity only at doses of 1 mg/kg and above. These data suggest that the anxiolytic effects of CCK receptor antagonists parallel their affinity for the CCKB rather than the CCKA receptor.

Animals↗
PubMed1990

Paired arrangement of nonhomologous centromeres during vertebrate spermiogenesis.

Indirect immunofluorescence staining with human anti-kinetochore antibodies was used to study the position of centromeres during vertebrate spermiogenesis. Many species of Amphibia have a low chromosome number and very large spermatids and spermatozoa. The number of kinetochore dots correlates exactly with the haploid chromosome number. This implies that kinetochore duplication occurs in the interval between meiosis I and meiosis II. The nonhomologous centromeres are arranged in tandem during the entire course of spermiogenesis and in mature spermatozoa. A higher order centromere arrangement was found in spermiogenic cells of Anura and Urodela. In mammals, immunofluorescence analysis is complicated by the extreme condensation of chromatin during spermiogenesis and the high chromosome numbers. Nevertheless, centromere-centromere associations were observed in mammalian round spermatids and sporadically in testicular spermatozoa. This indicates that pair-wise association of centromeres is a universal principle of centromere arrangement at the postmeiotic stage.

Animals↗
PubMed1995

Neurotoxicity induced by prenatal exposure to MPTP on the monoaminergic and peptidergic systems of the marmoset brain.

The neurotoxicity induced by incidental prenatal exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied in three marmosets. The baby marmosets exposed in utero to MPTP looked normal in the first few weeks of life but around 8 to 10 weeks of life they started to behave abnormally and were sacrificed when they were 20 weeks old. A marked reduction in DA levels was found in the baby marmosets prenatally exposed to MPTP as compared to the corresponding age-matched controls and this was highly significant in the caudate nucleus, putamen, and nucleus accumbens. Serotonin content was normal in the caudate and putamen and was only significantly reduced in the nucleus accumbens, hypothalamus, and cingulate cortex. Met-enkephalin levels were reduced in the caudate nucleus, putamen, and globus pallidus. Substance P content tended to be lower in all regions examined; however, the decrease was only statistically significant in the substantia nigra. These results indicate that prenatal exposure to MPTP induces a marked and long-lasting alteration in monoaminergic and peptidergic systems of the primate brain. This observation may provide a new insight into the role of toxins in the etiology of Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Isolation of cytochrome P-450 components from marmoset liver microsomes by high-performance liquid chromatography.

A fast protein liquid chromatographic (FPLC) system with pre-packed and laboratory-packed columns was used for the analytical and preparative isolation of marmoset monkey cytochrome P-450 (P450) and NADPH-P450-reductase. Chromatographic separations also allowed the recovery of cytochrome b5, NADH-b5-reductase and epoxide hydratase. Cholate-solubilized liver microsomes from phenobarbital-induced marmosets were crudely purified on 8-aminooctyl-Sepharose or 6-aminohexyl-Sepharose and then fractionated into several isoenzyme groups using hydroxyapatite. Further purification on Mono S or CM-Sepharose and finally on phenyl-Superose, phenyl-Sepharose or octyl-Sepharose yielded a P450 fraction which was apparently homogeneous as judged by sodium dodecyl sulphate-polyacrylamide gel electrophoresis in the automated Phast system using silver staining. Removal of excess of non-ionic detergent was effected by hydroxyapatite columns, and this was compared with other methods. For the isolation of P450 isoenzymes from untreated marmosets, Mono Q columns were employed and yielded at least two highly purified forms. NADPH-P450-reductase was recovered from the 8-aminooctyl-Sepharose column or crudely fractionated on DEAE-Sepharose Fast Flow. Subsequent purification via 2',5'-ADP-Sepharose and Superose 12 chromatography resulted in a homogeneous preparation.

Animals↗
PubMed1992

Purification of cytochromes P-450 derived from liver microsomes of untreated and 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated marmoset monkeys.

The purification of multiple forms of cytochrome P-450 (P450) from 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated marmosets using fast protein liquid chromatography (FPLC) is described. The main aim was to achieve a better separation of certain closely related P450 sub-forms from each other than that previously obtained using conventional chromatography. An 8-aminooctyl-Sepharose fraction of cholate-solubilized microsomes was obtained first and, after fast desalting on Sephadex G-25, loaded on to a preparative Mono Q column. Five of the six gradient peaks contained P450 and were each rechromatographed on an analytical Mono Q column. The pass-through peak was fractionated further using a Mono S column. Other HPLC-quality anion- and cation-exchange gels were compared. For removal of excess of non-ionic detergent, five types of hydroxyapatite gels were compared. Seven purified forms of P450 and cytochrome b5 and P420 were isolated and characterized according to PHAST sodium dodecylsulphate-polyacrylamide gel electrophoretic apparent molecular masses, catalytic, spectral and magnetic properties and also TCDD-binding capacity (molar ratio of [14C]TCDD to P450). There are at least two sub-forms which appear to be TCDD inducible, one showing a substantial ethoxyresorufin-O-deethylase activity and the other having a high TCDD-binding molar ratio. Two other forms appear to be constitutive, as deduced from comparisons with forms purified from untreated animals.

Animals↗
PubMed1984

Undifferentiated carcinoma of the nasal tissues in the common marmoset.

The occurrence of undifferentiated carcinoma of the nasal tissues in 3 adult marmosets is described. The tumours appeared to arise from the respiratory epithelium of the turbinate bones and nasal septum. They were poorly differentiated, invaded the paranasal sinuses and hard palate and metastasized to the lungs or liver.

Animals↗
PubMed1984

Chronic inflammatory polyneuropathy. Reduction of nerve conduction velocities in monkeys by systemic passive transfer of immunoglobulin G.

In chronic (relapsing) inflammatory polyneuropathy (CRIP), successful treatment with plasma exchange has led to the concept of pathogenic humoral factors. In 6 patients with CRIP, 5 of whom improved after plasma exchange, the potential pathogenic role of circulating immunoglobulin (Ig) fractions was tested by applying the systemic passive transfer model to marmoset monkeys. After continuous treatment with intramuscular injections for 2-8 weeks, monkeys injected with the crude immunoglobulin fractions or with purified IgG from 5 of the 6 patients showed a significant and partially reversible reduction of the motor nerve conduction velocity (mean 34%, P less than 0.001) when compared with pre-treatment values. In control animals the reduction was 4%. Morphological examination revealed only minor ultrastructural changes of the myelin sheath. Immunocytochemistry revealed that human IgG was able to cross the blood-nerve barrier. It is concluded that the circulating IgG-fraction of patients with CRIP contains a factor that may contribute to the disordered nerve function after crossing the blood-nerve barrier. It may be the removal of this particular factor which is responsible for the rapid recovery of nerve conduction in patients after plasma exchange.

Animals↗
PubMed1992

Soman levels in kidney and urine following administration to rat, guinea pig, and marmoset.

Concentrations of C(+/-)P(+/-)-soman (1,2,2-trimethylpropyl methylphosphonofluoridate) in urine of anaesthetized, atropinized and artificially ventilated rats, guinea pigs and marmosets were determined 1-4 h after iv administration of 1-6 LD50 of the agent and in the kidneys 1 h after iv administration of 2-6 LD50 14C-C(+/-)P(+/-)-soman. The concentrations of the toxic C(+/-)P(-)-isomers in both urine and kidneys of the rat were at least two orders of magnitude higher than the corresponding levels in the two other species. Relatively high urine concentrations were also found for C(+/-)P(+/-)-soman-intoxicated (6 LD50) rats pretreated with the nontoxic soman analogue PDP (1,2,2-trimethyl dimethylphosphinate), which considerably decreases the persistence of C(+/-)P(-)-soman in rats, or the carboxylesterase inhibitor CBDP [2-(o-cresyl)-4H-1:3:2-benzodioxaphosphorin-2-oxide]. The lethal effect brought about by intravesical administration of C(+/-)P(+/-)-soman in rats showed that the agent can easily be reabsorbed from the bladder. It is concluded, that this reabsorption does probably not explain the previously observed persistence and "late toxicity" of C(+/-)P(+/-)-soman in rats, although the amount of renally excreted C(+/-)P(-)-soman (ca. 1% of the administered dose) should be sufficient for a toxicologically significant effect.

Administration, Intravesical↗
PubMed1992

The competitive NMDA antagonist CGP40.116 enhances L-dopa response in MPTP-treated marmosets.

Experiments in MPTP-treated non-human primates testing potential antiparkinsonian action have shown both, beneficial and adverse effects of gutamate receptor antagonists. To investigate this matter further, the novel competitive NMDA antagonist CGP40.116 was administered systemically to three adult MPTP-treated marmosets. When coadministered subcutaneously with a subthreshold dose of L-DOPA, 2 mg/kg, CGP40.116 25-250 micrograms/kg, increased locomotor activity. However, when administered alone, CGP40.116 had no effect on locomotor activity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

A selective MAOB inhibitor Ro19-6327 potentiates the effects of levodopa on parkinsonism induced by MPTP in the common marmoset.

The effects of the selective and reversible MAOB inhibitor Ro19-6327 on parkinsonism in common marmosets, induced by MPTP were studied. Combined administration of Ro19-6327 with benserazide/levodopa potentiated the effects of levodopa to reverse akinesia. In a microdialysis study, the administration of Ro19-6327 was found to minimize the increase in metabolites of dopamine (DA) following injection of levodopa. These results suggest that Ro19-6327 suppresses the metabolism of DA, resulting in increased effects of levodopa on parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Thus, Ro19-6327 should be useful in the treatment of patients with Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Naloxone reversal of stress-induced suppression of LH release in the common marmoset.

There is considerable evidence suggesting that endogenous opioid peptides (EOP) might play a role in the defensive response to stressful stimuli. The stress associated with receipt of aggression from a female conspecific and physical restraint for collection of serial blood samples (at 10-min intervals) resulted in a significant (p less than 0.05) suppression of LH secretion in the oestradiol primed ovariectomized marmoset. Administration of the opioid receptor antagonist, Naloxone (1 mg/kg) immediately before and after receipt of aggression completely prevented the stress-induced decrease in LH release. This suggests that EOP may mediate, at least in part, this stress induced decline in LH release in the marmoset.

Aggression↗
PubMed1993

Sound levels in rooms housing laboratory animals: an uncontrolled daily variable.

High sound levels are known to have adverse effects on the behaviour and physiology of laboratory animals, yet their acoustic environment is rarely monitored. In particular, high-frequency sounds that are above the limit of human hearing, but are well within the limits of many laboratory species (i.e., ultrasounds), are usually ignored. In this study, the acoustic environment of laboratory animals was investigated in a variety of different animal facilities. Sound pressure levels (dB SPL) were monitored for periods up to 24 h over two frequency ranges: a relatively low range (0.01-12.5 kHz), and a high range (12.5-70 kHz). While background sound levels in undisturbed situations were generally low (i.e., below 50 dB SPL), marked increases in sound levels often occurred during the working day, producing characteristic daily variations in the sound profile. Peak SPLs commonly reached values of 80-95 dB in the low-frequency range and 50-75 dB in the higher range. In most cases, sound levels were low over weekends. The results suggested that human activities were a very important source of sound in most animal facilities. In a few situations (e.g., rabbits, marmosets, dogs), the animals themselves provided a significant contribution to the acoustic environment. It is clear that the acoustic environment of laboratory animals is a daily variable that is usually uncontrolled and that may have important implications for behavioural and physiological experiments and for animal welfare.

Animal Welfare↗