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PubMed1972

Comparison of geographical strains of Schistosoma mansoni in the rhesus monkey.

Rhesus monkeys were infected with strains of Schistosoma mansoni from Puerto Rico, St Lucia, Brazil, and Tanzania. Monkeys were killed 11-14 weeks after exposure to 600-650 cercariae. Some differences in the behaviour of different strains were noted, but the similarities between the strains were more remarkable. The only strain difference observed in both mice and monkeys was a prolonged prepatent period in animals infected with the Mwanza strain. The results of experimental infections are believed to be of little value in predicting possible differences in the pathogenicity of schistosome strains for man.

Animals↗
PubMed1982

Intravenous buspirone self-administration in rhesus monkeys.

Rhesus monkeys trained to press levers for intravenous cocaine injections were tested with saline and various doses of buspirone, chlordiazepoxide, and clorazepate. Buspirone was not self-administered at rates significantly above saline control levels. Chlordiazepoxide and clorazepate also failed to serve as reinforcers under these conditions. The lack of reinforcing properties, taken together with the results of other preclinical behavioral studies, suggests a low potential for recreational use of buspirone in man.

Animals↗
PubMed1984

The effect of oral contraceptives in malaria infections in rhesus monkey.

Rhesus monkeys, Macaca mulatta, were treated with the oral contraceptives Brevicon (norethisterone with ethinylestradiol) and Ovral (norgestrel with ethinylestradiol), and subsequently inoculated with the simian malaria parasites Plasmodium cynomologi bastianellii or P. coatneyi. Parasitological, serological, and serum biochemical studies indicated that although there were some significant differences, in general the patterns of response to infection in both treated and control animals were similar. During the primary infection, however, Brevicon resulted in increased levels of parasitaemia, whereas Ovral resulted in decreased parasitaemias, as compared with the untreated control animals. There were no differences in the responses following secondary parasite infection.

Animals↗
PubMed1981

Pharmacological evaluation of narcotic antagonist delivery systems in rhesus monkeys.

Rhesus monkeys were chronically restrained, intravenously catheterized, and allowed to self-administer morphine, methamphetamine, and saline. Various sustained-release systems containing naltrexone were then implanted in the animals and examined for selective morphine blockade. Similarly, continuous intravenous infusions of naltrexone, buprenorphine, and methadone were tested against morphine or heroin self-administration.

Animals↗
PubMed1982

Unlimited access intravenous drug self-administration in rhesus monkeys.

Rhesus monkeys implanted with intravenous catheters readily self-inject a wide variety of psychoactive drugs. Under conditions where access to drug is not limited, pharmacological variables are important determinants of the rate and pattern of drug-reinforced responding. Data for unlimited access phencyclidine self-administration are presented to illustrate the types of findings obtained from unlimited access studies. The results with phencyclidine indicate a pattern of drug intake that progressed from variable day-to-day response rates at a low dose to relatively stable daily response rate with greater drug intake at a higher dose. The pattern of responding, toxicity, and development of physical dependence seen in these subjects were similar in many respects to results found with several other drugs under conditions of unlimited access. These findings demonstrate that unlimited access studies are particularly useful for revealing toxic consequences of self-administered doses. Moreover, a review of the literature indicated that procedures allowing unlimited access by drug-naive monkeys were at least as likely to reveal reinforcing properties of drugs as limited access procedure using drug-experienced subjects.

Animals↗
PubMed1976

A comparison of immunologic asthma to two types of cholinergic respiratory responses in the rhesus monkey.

Rhesus monkeys were used to characterize the respiratory response (RR) to aerosolized physostigmine (Phy) and compare the response to the acute, reagin-mediated RR and the carbachol response. In the latter two responses, there are characteristic increases in frequency of respiration (f), pulmonary resistance (PR), and decreases in peak expiratory flow rate (PEFR), tidal volume (TV), and dynamic compliance (C). In contrast, a Phy RR characteristically shows no change in TV and f. The Phy RR is inhibited by atropine and lidocaine. The carbachol RR is inhibited by atropine but not lidocaine. The Phy RR mimics a vagally induced RR more closely than carbachol because it is inhibited by pharmacologic and physiologic vagal blockade produced by atropine and lidocaine, respectively, whereas the carbachol RR is blocked by atropine but not lidocaine. The carbachol block by atropine is primarily not a block of vagal action, but a general pharmacologic block of cholinergic action. The reagin-mediated RR is not inhibited by pharmacologic or physiologic vagal blockade. We conclude that a Phy-induced vagomimetic RR differs from a reagin-mediated, immediate-type RR. Although a minor portion, at most, of a reagin-mediated, immediate-type RR may be mediated via the vagus nerve, the major portion of a reagin-mediated RR occurs independent of the influences of the parasympathetic innervation of the lung.

Acetylcholine↗
PubMed1993

Neural substrates of visual stimulus-stimulus association in rhesus monkeys.

Rhesus monkeys learned 10 visual stimulus-stimulus association, or paired associates. They then received bilateral removals of either the amygdaloid complex and underlying cortex, the hippocampal formation and underlying cortex, or both combined, or they were retained as unoperated controls. After surgery or rest, the monkeys were tested for their retention of the preoperatively learned set of paired associates, as well as for their ability to learn new associations of the same type. Both unoperated controls and hippocampectomized monkeys relearned the preoperatively trained set of paired associates almost immediately. By contrast, monkeys with amygdala removals were moderately retarded in relearning, and monkeys with combined amygdala and hippocampal ablations were severely retarded. When confronted with new sets of visual stimuli, monkeys with amygdala removals or hippocampal removals learned new sets of paired associates at the same rate as the controls, whereas monkeys with the combined ablation were again profoundly retarded. Only one monkey with the combined lesion was able to learn new stimulus-stimulus associations to criterion, and then only after extensive training, despite the ability of all three animals in this group to perform delayed matching-to-sample with the same stimuli and the same intraatrial delays as those used in the paired associate task. At the end of the main experiment, two of the unoperated controls received bilateral ablations of the rhinal cortex. These monkeys showed the same level of difficulty in learning new paired associates as the animals in the main experiment that had received the combined amygdala plus hippocampal ablations. The results implicate the medial temporal lobe, and particularly the rhinal cortex, in the formation of stimulus-stimulus associative memories.

Amygdala↗
PubMed1996

Anterior rhinal cortex and amygdala: dissociation of their contributions to memory and food preference in rhesus monkeys.

Rhesus monkeys were trained on 2 versions of delayed nonmatching-to-sample, one with multiple pairs of objects and the other with a single pair, to evaluate their ability to remember objects. They then received either bilateral aspiration lesions of the anterior rhinal cortex or bilateral excitotoxic lesions of the amygdala, or were retained as unoperated controls. On re-presentation of the multiple-pair task, monkeys with anterior rhinal cortex lesions failed to show the improvement observed in both other groups in remembering the objects over delay intervals ranging from 10 to 60 s. Also, monkeys with anterior rhinal cortex lesions were impaired relative to the controls in relearning the single-pair version of the task. Conversely, on a formal test of food preference, monkeys with amygdala lesions showed abnormal patterns of food choice, whereas monkeys with anterior rhinal cortex lesions did not. Visual memory impairments formerly attributed to amygdala damage are probably due to the rhinal cortex damage associated with aspiration lesions of the amygdala.

Amygdala↗
PubMed1996

Effects of cholinergic drugs on scopolamine-induced memory impairment in rhesus monkeys.

Rhesus monkeys were trained to perform matching-to-sample responses in which monkeys had to choose one of two stimuli that had the same color as the previously presented sample. Half of a daily session consisted of simultaneous trials where the sample was present during the trial, and the other half consisted of delayed trials, where the sample had been presented at the start of the trial but was withheld at the time of choosing. With vehicle control, the percentage of correct responses (CR%) in both trials exceeded 85%. Scopolamine (4-32 micrograms/kg, SC) selectively decreased the CR% for delayed trials in five out of eight animals, suggesting impairment of short-term memory. Physostigmine (2-16 micrograms/kg, SC), arecoline (16-128 micrograms/kg, SC) and nicotine (4-32 micrograms/kg, SC) attenuated the scopolamine-induced impairment of CR% in delayed trials with concurrent administration with scopolamine. Methamphetamine (16-64 micrograms/kg, SC) did not show such effects. These results suggested that scopolamine-induced memory impairment could be recovered by cholinergic agonists.

Animals↗
PubMed1981

Comparative pharmacokinetics of antipyrine (phenazone) in the baboon, cynomolgus monkey and rhesus monkey.

The pharmacokinetics of antipyrine (phenazone) in 3 species of non-human primate have been evaluated following its intravenous administration at a dose level of 92 mg/kg. Mean peak plasma concentrations of antipyrine of 132, 137 and 155 microgram/ml in the rhesus monkey, the cynomolgus monkey and the baboon respectively were not observed until 5 min after intravenous injection. Thereafter, concentrations declined with an apparent half-life of elimination of 1.5-2 h. The time-course of plasma antipyrine concentrations was adequately described by a one-compartment open model and no notable differences in pharmacokinetic parameters utilising a 2-compartment open model were observed. Antipyrine was mainly distributed in total body water. The mean volume of distribution was equivalent to 88, 73 and 66% of body weight in rhesus monkey, the cynomolgus monkey and the baboon, respectively. An analysis of variance of volumes of distribution, apparent half-lives of elimination and systemic clearances showed that there was a statistically significant species-related difference in systemic clearance (P less than 0.05) and volumes of distribution (P less than 0.01) which were lower in the cynomolgus monkey than in the other 2 species. The pharmacokinetics of antipyrine in the non-human primate are more similar to those of other laboratory animal species than to those of humans.

Animals↗
PubMed2003

Pathogenicity and neurovirulence of a mutagen-attenuated Rift Valley fever vaccine in rhesus monkeys.

Rhesus macaques, intravenously inoculated with virulent Rift Valley fever virus, develop viremia and biochemical evidence of liver damage and serve as a model for human disease. Some of these monkeys suffer more serious disease with hemorrhagic phenomena and approximately 20% die with frank hemorrhage. Presently, the only Rift Valley fever vaccine approved for use in humans is a formalin-killed product that requires annual booster vaccinations. Efforts to produce an improved vaccine to replace the present vaccine have led to a mutagen-attenuated strain of Rift Valley fever virus that was found to be markedly attenuated for rhesus macaques and showed promise as a vaccine candidate for human use. Neurovirulence testing in rhesus monkeys showed that, while the vaccine was not completely innocuous, residual lesions were no more severe than the currently used 17D yellow fever vaccine.

Animals↗
PubMed1995

Comparisons of phase I and phase II in vitro hepatic enzyme activities of human, dog, rhesus monkey, and cynomolgus monkey.

The metabolism of probe substrates of phase I and phase II enzymes in vitro were compared in hepatic subcellular fractions from humans, cynomolgus monkeys, rhesus monkeys, and beagle dogs. These studies were undertaken to compare the suitability of these species as models of metabolism in drug development. Eight cytochrome P450-dependent activities were measured in microsomal incubations: ethoxyresorufin O-deethylase, coumarin 7-hydroxylase, tolbutamide 4-hydroxylase, S-mephenytoin 4'-hydroxylase, bufuralol 1'-hydroxylase, N-nitrosodimethylamine N-demethylase, midazolam 1'-hydroxylase, and erythromycin N-demethylase. Seven phase II activities were determined in the appropriate subcellular fractions:acetaminophen UDP-glucurono-syltransferase, acetaminophen sulfotransferase, 17 alpha-ethinylestradiol UDP-glucuronosyltransferase, 17 alpha-ethinylestradiol sulfotransferase, 6-mercaptopurine methylase, dichloronitrobenzene (DCNB) glutathione S-transferase, and isoniazid N-acetylase. Hepatic subcellular fractions from cynomolgus and rhesus monkeys showed significantly higher activities than those from humans for ethoxyresorufin O-deethylase, bufuralol 1'-hydroxylase, midazolam 1'-hydroxylase, erythromycin N-demethylase, acetaminophen UDP-glucuronosyltransferase, acetaminophen sulfotransferase, and tolbutamide 4-hydroxylase. Cynomolgus monkey had higher activity than humans and rhesus monkeys for S-mephenytoin 4'-hydroxylase erythromycin N-demethylase. Rhesus monkey and human cytosol displayed an apparent genetic polymorphism in the N-acetylation of isoniazid, whereas cynomolgus monkey cytosol did not. All other monkey activities were not significantly different than human. Dog subcellular fractions showed higher activity than humans for midazolam 1'-hydroxylase, erythromycin N-demethylase, acetaminophen UDP-glucuronosyltransferase, acetaminophen sulfotransferase, 17 alpha-ethinylestradiol sulfotransferase, and DCNB glutathione S-transferase. Furthermore, dog samples had significantly lower activity for coumarin 7-hydroxylase and 6-mercaptopurine methylase, and no detectable activity for tolbutamide 4-hydroxylase or isoniazid N-acetylase. All other activities were not significantly different from human. These results reveal minor differences between the cynomolgus and rhesus monkey in drug metabolism capacities in vitro, but both species are generally more metabolically active than humans in both phase I and phase II metabolism, whereas dogs had more diverse deviations from humans.

Animals↗
PubMed2000

Comparison of celecoxib metabolism and excretion in mouse, rabbit, dog, cynomolgus monkey and rhesus monkey.

1. The metabolism and excretion of celecoxib, a specific cyclooxygenase 2 (COX-2) inhibitor, was investigated in mouse, rabbit, the EM (extensive) and PM (poor metabolizer) dog, and rhesus and cynomolgus monkey. 2. Some sex and species differences were evident in the disposition of celecoxib. After intravenous (i.v.) administration of [14C]celecoxib, the major route of excretion of radioactivity in all species studied was via the faeces: EM dog (80.0%), PM dog (83.4%), cynomolgus monkey (63.5%), rhesus monkey (83.1%). After oral administration, faeces were the primary route of excretion in rabbit (72.2%) and the male mouse (71.1%), with the remainder of the dose excreted in the urine. After oral administration of [14C]celecoxib to the female mouse, radioactivity was eliminated equally in urine (45.7%) and faeces (46.7%). 3. Biotransformation of celecoxib occurs primarily by oxidation of the aromatic methyl group to form a hydroxymethyl metabolite, which is further oxidized to the carboxylic acid analogue. 4. An additional phase I metabolite (phenyl ring hydroxylation) and a glucuronide conjugate of the carboxylic acid metabolite was produced by rabbit. 5. The major excretion product in urine and faeces of mouse, rabbit, dog and monkey was the carboxylic acid metabolite of celecoxib.

Animals↗
PubMed1996

Cerebrovascular amyloidosis in squirrel monkeys and rhesus monkeys: apolipoprotein E genotype.

Some neuropathological changes characteristic of aging and Alzheimer's disease (AD) in humans are present also in senescent non-human primates. The human apoE4 allele is associated with an increased risk of developing late-onset familial and sporadic AD. We found that rhesus monkeys and three subspecies of squirrel monkeys are homozygous for apoE phenotype with arginine at positions 112 and 158 as in human apoE4. However, in both species threonine replaces arginine at position 61 of human apoE. It was previously shown that arginine 61 was critical in determining apoE4 lipoprotein distribution in humans.

Alzheimer Disease↗
PubMed1991

SIV vaccine protection of rhesus monkeys.

Rhesus macaques (M. mulatta), immunized with an inactivated whole SIVmac vaccine and muramyl dipeptide or Freund's incomplete adjuvant, were protected against IV challenge infection with 10 animal infectious doses of the homologous virus. The protection in these animals appeared to be complete, with no breakthrough of latent virus infection over a 10-month period. Vaccine protection in this model was correlated generally with a high level of SIVmac envelope antibody by ELISA and immunoblot, high titers of syncytial inhibiting antibody, and, more specifically, with the presence of antibodies binding to a putative V3 loop synthetic peptide of the SIVmac outer envelope. This model can now be used for further identification of the protective epitopes and protective host immune responses as well as for development of novel and better AIDS vaccines.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1997

Lymphocyte subsets and expression of differentiation markers in blood and lymphoid organs of rhesus monkeys.

Rhesus macaques are invaluable experimental animals in biomedical research. Using three color flow cytometry, we screened anti-human antibodies for crossreactivity with macaque cells in order to determine the distribution of functionally important lymphocyte subsets in blood, lymph nodes (LN), and spleen. NK-cells are almost completely absent in LN. The percentage of B-cells expressing CD80, CD86, and the level of expression of CD20 is higher in blood than in LN. In contrast, a higher proportion of B-cells in LN stains positive for CD21 and CD35. Whereas the number of CD29hi expressing T-cells is lower, CD69 is expressed on more T-cells in LN than in blood. About one-third of CD8+ T-cells in blood are CD28-, a subset with a unique pattern of antigen expression which cannot be found in LN. In contrast to humans, a relatively high proportion of T-cells in blood also express the co-stimulatory molecules CD80 and CD86. With increasing age, the proportion of B-cells in blood declines, whereas the percentage of T-cells rises. In addition, the proportion of CD29hi expressing T-cells increases among both the CD4+ and CD8+ subsets.

Animals↗
PubMed1993

Conserved T-cell receptor repertoire in simian immunodeficiency virus-infected rhesus monkeys.

Studies to assess the possibility that the HIV may encode a superantigen that plays a role in the depletion of functional CD4+ lymphocytes in the infected individual have yielded discrepant results. The problem in performing conclusive examinations of this issue may be attributed, at least in part, to the difficulty of prospectively studying individuals from before their infection until the time of profound CD4+ lymphocyte loss. To determine whether the AIDS virus deletes particular subpopulations of V beta-expressing lymphocytes, we have employed an animal model of AIDS, the simian immunodeficiency virus (SIV)-infected macaque monkey. Rhesus monkeys were experimentally infected with SIVmac and studied prospectively. A PCR-based quantitative method for assessing TCR repertoire was employed to analyze the expression of 24 V beta and 30 V alpha gene families in the monkeys. Although circulating PBL were increased in number by 3 wk after SIVmac infection, the expanded lymphocyte populations exhibited no significant perturbation in their TCR V beta repertoires. PBL obtained from monkeys before and 0.5 to 3 years after infection displayed no significant change in V beta and V alpha gene family expression. Finally, no deletion of V beta-expressing cell subpopulations could be demonstrated in purified CD4+ lymphocytes from infected monkeys. This was true even for monkeys whose blood contained less than 200 CD4+ lymphocytes/microliters. These results indicate that the TCR repertoire is conserved in SIVmac-infected rhesus monkeys and suggests that mechanisms other than superantigen-induced deletion must be responsible for CD4+ lymphocyte loss in these animals.

Animals↗