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At least 1,279 records · Page 71Linked to original sources
PubMed1990

Physical model simulations of brain injury in the primate.

Diffuse brain injuries resulting from non-impact rotational acceleration are investigated with the aid of physical models of the skull-brain structure. These models provide a unique insight into the relationship between the kinematics of head motion and the associated deformation of the surrogate brain material. Human and baboon skulls filled with optically transparent surrogate brain tissue are subjected to lateral rotations like those shown to produce diffuse injury to the deep white matter in the brain of the baboon. High-speed cinematography captures the deformations of the grids embedded within the surrogate brain tissue during the applied load. The overall deformation pattern is compared to the pathological portrait of diffuse brain injury as determined from animal studies and autopsy reports. Shear strain and pathology spatial distributions mirror each other. Load levels and resulting surrogate brain tissue deformations are related from one species to the other. Increased primate brain mass magnified the strain amplified without significantly altering the spatial distribution. An empirically-derived value for a critical shear strain associated with the onset of severe diffuse axonal injury in primates is determined, assuming constitutive similarity between baboon and human brain tissue. The primate skull physical model data and the critical shear strain associated with the threshold for severe diffuse axonal injury were used to scale data obtained from previous studies to man, and thus derive a diffuse axonal injury tolerance for rotational acceleration for humans.

Animals↗
PubMed1986

Production of primate monoclonal antibodies.

Monoclonal antibodies of primate origin were produced by direct fusion of peripheral blood lymphocytes with two different fusion cell lines: SP2/0, a mouse plasmacytoma line and SBC-H2O, a human-mouse heteromyeloma. The fusion of primate lymphocytes with SP2/0 cells was not successful and only transient production of antibodies was found. The fusion of primate lymphocytes with SBC-H2O cells was more successful and resulted in the establishment of stable monoclonal antibody-producing lines especially when chimpanzee cells were used.

Animals↗
PubMed1985

Differences in the metabolism of MPTP in the rodent and primate parallel differences in sensitivity to its neurotoxic effects.

Primates and rodents show marked differences in sensitivity to the neurotoxic effects of MPTP. We and others have previously shown that the toxic effects of MPTP on nigrostriatal cells are dependent on the oxidative metabolism of MPTP to the quaternary species MPP+. We have therefore compared the distribution and metabolism of MPTP in the monkey and several rodent species. Three major differences have been identified: 1) the primate, but not the rodents, showed a persistently high concentration of MPTP metabolites in the caudate nucleus compared to other brain regions; 2) the rodent brains cleared MPTP and its metabolites much more rapidly than did the monkey, and; 3) the predominant metabolite retained by the monkey brain was MPP+, while MPP+ cannot be detected in rodent brains for more than a few hours after injection. The persistence of MPP+ in the primate brain may explain the heightened toxicity of MPTP in this species.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Direct inhibitory effect of atriopeptin III on renin release in primate kidney.

Patterns of in vitro renal renin release and the ability of atriopeptin to directly inhibit renin release have been examined in the rat, rabbit, and dog, but have been unstudied in the primate kidney. Accordingly, we examined renin release from superficial renal cortical slices of the squirrel monkey (Samiri sciuresus). The average age of the 5 animals was 10.2 +/- 2.5 yr at the time of study. Renin release was stimulated significantly by the beta-adrenergic agonist isoproterenol in concentrations of 10(-5) M (1.67-fold) and 10(-4) M (1.84-fold). Isoproterenol-induced renin release was inhibited by atriopeptin III (ANP, 2 X 10(-8) M) and the adenylate cyclase inhibitor dideoxadenosine (DDA, 10(-5) M). Similarly, the incubation of the superficial cortical slices with arachidonic acid (10(-3) M) resulted in a 4-fold increase in tissue renin release which was blocked by the calcium ionophore A23187 (17 X 10(-6) M) and ANP; interestingly, DDA did not block arachidonic acid-induced renin release. These results suggest that ANP exerts a direct inhibitory effect on B-adrenergic and arachidonic acid-induced renin release in the primate kidney. Further, the inhibitory action of A23187 on renin release suggests, as in other species, an integral role for intracellular calcium in the renin release process. These patterns of renin release in primate kidney are similar to those observed in the rodent kidney in vitro.

Animals↗
PubMed1986

The suitability of East African primates as animal models of visceral leishmaniasis.

The susceptibility of four East African primate species to experimental infection with Leishmania donovani was investigated. Vervet monkeys (Cercopithecus aethiops), Sykes monkeys (C. mitis) and baboons (Papio cynocephalus) all supported low grade infections for periods ranging between four and eight months and subsequently showed evidence of self-cure. Greater bushbabies (Galago crassicaudatus) remained completely refractory throughout the course of the experiment. The significance of hepatic histiocytic nodules in the infected primates, similar to those observed in asymptomatic human visceral leishmaniasis, and the susceptibility of Old World primates to experimental infection are discussed.

Animals↗
PubMed1984

Delineation of lymphocyte subsets in lymph nodes of nonhuman primates.

Monoclonal antibodies which recognize specific surface antigens on human lymphocytes were used with an avidin-biotin immunoperoxidase technique to stain lymph nodes from nonhuman primates. Cells in lymph nodes from three macaque species and two new-world primate species could be stained to define T11, T4, T8, and B1 lymphocyte subsets. This approach will facilitate the study of many important spontaneous and experimentally induced diseases of nonhuman primates.

Animals↗
PubMed1995

Arachidonic acid inhibits hCG-stimulated progesterone production by corpora lutea of primates: potential mechanism of action.

Arachidonic acid (AA) is a precursor of metabolites known to affect the corpus luteum (CL) in many species, including primates. We have shown that some of these products (prostaglandins F2 alpha and E2) inhibit pro-gesterone (P4) production and activate the phosphatidylinositol (PI) pathway in CL of rhesus monkeys. A direct role of AA in luteal function has also been suggested. The current experiments were designed to investigate the effect of AA on P4 synthesis and to examine the ability of AA to activate the PI pathway in CL of rhesus monkeys. Basal and hCG-stimulated P4 production by luteal cells collected during the midluteal phase was measured after treatment with AA (1, 5, and 10 microM) or linoleic acid (1, 5, and 10 microM). Dispersed cells (50,000/tube) were incubated at 37 degrees C for 2 h. AA elicited a dose-dependent decrease in hCG-stimulated, but not in basal, P4 production. hCG-stimulated P4 production was reduced (P < 0.01) at AA doses of 5 microM (12.1 +/- 1.5 ng/mL) and 10 microM (8.6 +/- 1.8 mg/mL) to hCG alone (18 +/- 1.6 ng/mL). There was no significant effect of 1 microM AA (15.2 +/- 1.6). Response to linoleic acid was dissimilar and was not dose-dependent. Viability of cells was not affected by any treatment. Indomethacin, a prostaglandin synthesis inhibitor, and nordihydroguaiaretic acid, an inhibitor of lipoxygenase, did not interfere with the inhibitory effect of AA. Activation of the PI pathway was assessed by monitoring the hydrolysis of phosphatidylinositol-4,5-bisphosphate (PIP2) to inositol phosphates and by monitoring increases in intracellular free calcium concentrations ([Ca2+]i) in individual cells. Moreover, the ability of AA to activate protein kinase C (PKC) in luteal cells was measured using a [3H]phorbol dibutyrate (PDBu) binding assay. AA did not alter PIP2 hydrolysis or [Ca2+]i, however, AA (10 microM) increased specific binding of [3H]PDBu to luteal cells (P < 0.05). We conclude that AA inhibits hCG-stimulated P4 production by primate luteal cells. AA exerts this action without being converted to prostaglandins or leukotrienes. This inhibition may be mediated through the activation of PKC. These results suggest a possible role for AA in the regulation of luteal function in primates, and that PKC-activation by AA may promote its effects.

Animals↗
PubMed1986

Intrinsic 5HT-immunoreactive neurons in the spinal cord of the fetal non-human primate.

Serotonin (5HT) immunoreactive neurons were identified in the late-term fetal spinal cord of normal non-human primates. These neurons were distributed throughout the spinal cord, being concentrated in lamina X and the subjacent ventral median fissure, while their immunoreactive fibers and terminals innervated the zone surrounding the central canal and the ventral spinal artery. Even at this late fetal stage, the dorsal and ventral spinal gray matter was virtually devoid of any positive 5HT immunoreactivity, in contrast to that seen in the adult primate. These findings suggest that the intrinsic 5HT neurons of the primate during development may modulate CSF composition or provide cues for spinal cord differentiation rather than regulate sensorimotor functions as they do in the adult.

Animals↗
PubMed1996

Calcium-binding proteins in primate basal ganglia.

This paper describes the distribution of the calcium-binding proteins calbindin-D28k. Parvalbumin and calretinin in primate basal ganglia. The data derive from immunocytochemical studies undertaken in squirrel monkeys (Saimiri sciureus) and in normal human individuals. In the striatum, calbindin labels medium-sized spiny projection neurons whereas parvalbumin and calretinin mark two separate classes of aspiny interneurons. The striatal matrix compartment is markedly enriched with calbindin while striatal patches (striosomes) display a calretinin-rich neuropil. In the pallidum, virtually all neurons contain parvalbumin but none express calbindin. Calretinin occurs only in a small subpopulation of both large and small pallidal neurons. In the subthalamic nucleus, there exists a multitude of parvalbumun-positive cells and fibers but the number of calretinin and calbindin-positive neuronal elements is small. In the substantia nigra/ventral tegmental area complex, calbindin and calretinin occur principally in dopaminergic neurons of the dorsal tier of the pars compacta and in those of the ventral tegmental area. Parvalbumin is strictly confined to the GABAergic neurons of the pars reticulata and lateralis. Calbindin-rich fibers abound in the pars reticulata and lateralis, while calretinin-positive axons are confined to the pars compacta. These results indicate that calbindin and parvalbumin are distributed according to a strikingly complementary pattern in primate basal ganglia. Calretinin is less ubiquitous but occurs in all basal ganglia components where it labels distinct subsets of neurons. Such highly specific patterns of distribution indicate that calbindin, parvalbumin and calretinin may work in synergy within primate basal ganglia.

Animals↗
PubMed1985

Cross-reactivity of a normal human cell surface antigen with primate retrovirus glycoproteins.

Normal human cells express a human-specific antigen, HuLy-m5 (defined by the E4.3 monoclonal antibody), cross-reactive with determinants of the primate retroviruses, MPMV(Mason Pfizer monkey virus) and GALV (gibbon ape leukemia virus). Purified virus preparations of MPMV and GALV absorbed E4.3 antibody activity while antisera to these retroviruses blocked the binding of E4.3 antibody to human target cells. Sequential immunoprecipitation and two-dimensional gel analysis both indicated that the anti-primate retrovirus sera recognize the same molecular entity (a two-chain glycoprotein of Mr60 and 69Kd) as does the E4.3 antibody. These results suggest that normal human cells express primate retroviral proteins (most probably viral envelope glycoprotein, gp69) at the cell surface.

Animals↗
PubMed1989

Distinct morphologic classes of serotonergic axons in primates exhibit differential vulnerability to the psychotropic drug 3,4-methylenedioxymethamphetamine.

Immunohistochemical methods were used to analyse the distribution and morphology of serotonergic axons in normal macaque monkeys and in monkeys given (+/-)3,4-methylenedioxymethamphetamine. In untreated monkeys, we observed two morphologic classes of serotonergic axon terminals, which differ in regional and laminar distribution. These two axon types, fine and beaded, correspond to the serotonergic axon types which have been described in the rat. In 3,4-methylenedioxymethamphetamine-treated monkeys, there is a profound loss of serotonergic axon terminals, yet some are consistently spared. The surviving axon terminals are nearly all of the beaded type; in contrast, fine serotonergic axons are markedly reduced in density. There are regional differences in the magnitude of denervation, which reflect differences in the distribution of these two types of serotonergic axons in controls. The present study demonstrates that 3,4-methylenedioxymethamphetamine has differential neurotoxic effects on fine and beaded serotonergic axons. These results indicate that in the primate there are two distinct classes of serotonergic axon terminals, which differ in morphology, distribution, and vulnerability to psychotropic drugs. We hypothesize that in the primate, as demonstrated in the rat, these two classes of serotonergic axon terminals may arise from different raphe nuclei. In both rodent and primate, the dorsal and median raphe nuclei give rise to parallel ascending serotonergic projections, which are likely to have different pharmacologic properties and functions.

3,4-Methylenedioxyamphetamine↗
PubMed1980

An ancestral amplification of DNA in primates.

Newly evolved, tandemly arrayed, highly repeated DNAs from three primates were compared using Markov-chain and random-simulation approaches. Markov-chain calculations suggested that the repeated DNA sequences derived from the amplification of a progenitor sequence some 55 million years ago. Divergence of the products of this ancestral amplification could have created a library of related DNA sequences from which newly evolved repeated DNA was drawn - by recent amplifications of library members. The ancestral DNA amplification may have provided the genetic flexibility for creating the primate order; more recent amplifications in old-world primates probably led to the present subfamilies. The random-simulation approach verified the idea that repeated DNA evolves nonrandomly. A variable region was identified within the sequence.

Animals↗
PubMed1982

The nucleotide sequence of cDNA coding for preproinsulin from the primate Macaca fascicularis.

DNA complementary to preproinsulin messenger RNA from the primate Macaca fascicularis has been cloned into the PstI endonuclease site of the plasmid pBR322. One clone contains the entire preproinsulin coding region as well as 59 nucleotides of the 5'-untranslated region. The results predict an amino acid sequence for the Macaca fascicularis preproinsulin and establish for the first time that the primary structures of human and primate insulins are identical. The two amino acid exchanges between human and primate preproinsulins are restricted to the pre- and the C-peptide, respectively.

Amino Acid Sequence↗
PubMedDate not supplied

A nonhuman primate version of the open field test for use in behavioral toxicology and teratology.

As reviewed here, little work has been done on testing nonhuman primates individually in open field paradigms. Hence, normative data from three studies of rhesus monkeys are presented. Important criteria for describing the pattern of activity exhibited by monkeys in the open field are introduced and the effects of gender and differences in rearing are assessed. Differences between this nonhuman primate version of the open field and that typically used with rodents are discussed, including reasons for differences in the variability of behavior between monkeys and rodents and a comparison of coefficients of detection (as an index of the power of the test to detect group differences). Overall, the use of the nonhuman primate version of the open field in behavioral toxicology and teratology is feasible and may fill a significant niche not presently well represented.

Animals↗
PubMed2004

Serotonin innervation of the primate suprachiasmatic nucleus.

The suprachiasmatic nucleus (SCN) in rodents receives a dense innervation from serotonin neurons of the midbrain raphe. This projection overlaps the terminal field of the retinohypothalamic tract in the SCN core, the central part of the nucleus characterized by a population of vasoactive intestinal polypeptide (VIP)-containing neurons. To determine whether a similar pathway is present in primates, we carried out an immnunocytochemical investigation of the primate SCN using antisera against either serotonin (monkey) or the serotonin transporter (human). This demonstrated a dense serotonergic plexus over the SCN core in both species. As in rodents, the distribution of the serotonin innervation of the primate SCN overlaps that of the retinohypothalamic input and the VIP neuronal population. We also find a supraependymal plexus of serotonin axons in the third and lateral ventricles of the human and monkey brains that is similar in distribution, but less dense, than the one reported in rodents.

Aged↗
PubMed2005

Ephrin/Eph receptor expression in brain of adult nonhuman primates: implications for neuroadaptation.

In developing brain, Eph receptors and their ephrin ligands (Ephs/ephrins) are implicated in facilitating topographic guidance of a number of pathways, including the nigrostriatal and mesolimbic dopamine (DA) pathways. In adult rodent brain, these molecules are implicated in neuronal plasticity associated with learning and memory. Cocaine significantly alters the expression of select members of this family of axonal guidance molecules, implicating Ephs, ephrins in drug-induced neuroadaptation. The potential contribution of Ephs, ephrins to cocaine-induced reorganization of striatal circuitry brain in primates [Saka, E., Goodrich, C., Harlan, P., Madras, B.K., Graybiel, A.M., 2004. Repetitive behaviors in monkeys are linked to specific striatal activation patterns. J. Neurosci. 24, 7557-7565] is unknown because there are no documented reports of Eph/ephrin expression or function in adult primate brain. We now report that brains of adult old and new world monkeys express mRNA encoding EphA4 receptor and ephrin-B2 ligand, implicated in topographic guidance of dopamine and striatal neurons during development. Their encoded proteins distributed highly selectively in regions of adult monkey brain. EphA4 mRNA levels were prominent in the DA-rich caudate/putamen, nucleus accumbens and globus pallidus, as well as the medial and orbitofrontal cortices, hippocampus, amygdala, thalamus and cerebellum. Immunocytochemical localization of EphA4 protein revealed discrete expression in caudate/putamen, globus pallidus, substantia nigra, cerebellar Purkinje cells, pyramidal cells of frontal cortices (layers II, III and V) and the subgranular zone of the hippocampus. Evidence for EphA4 expression in dopamine neurons emerged from colocalization with tyrosine-hydroxylase-positive terminals in striatum and substantia nigra and ventral tegmental area cell bodies. The association of axonal guidance molecules with drug-induced reorganization of adult primate brain circuitry warrants investigation.

Acclimatization↗
PubMedDate not supplied

Ca2+-dependent proteases in ischemic neuronal death: a conserved 'calpain-cathepsin cascade' from nematodes to primates.

From rodents to primates, transient global brain ischemia is a well known cause of delayed neuronal death of the vulnerable neurons including cornu Ammonis 1 (CA1) pyramidal cells of the hippocampus. Previous reports using the rodent experimental paradigm indicated that apoptosis is a main contributor to such ischemic neuronal death. In primates, however, the detailed molecular mechanism of ischemic neuronal death still remains obscure. Recent data suggest that necrosis rather than apoptosis appear to be the crucial component of the damage to the nervous system during human ischemic injuries and neurodegenerative diseases. Currently, necrotic neuronal death mediated by Ca2+-dependent cysteine proteases, is becoming accepted to underlie the pathology of neurodegenerative conditions from the nematode Caenorhabditis elegans to primates. This paper reviews the role of cysteine proteases such as caspase, calpain and cathepsin in order to clarify the mechanism of ischemic neuronal death being triggered by the unspecific digestion of lysosomal proteases.

Alzheimer Disease↗
PubMed2005

Activation of c-Jun and ATF-2 in primate motor cranial nerve nuclei is not associated with apoptosis following axotomy.

Nerve transection induces complex changes in gene regulation and expression that can have profound phenotypic effects on the fate of axotomized neurons. The transcription factors c-Jun and ATF-2 (activating transcription factor-2) are components of a regulatory network that mediates survival, regeneration, and apoptosis following axotomy in rodents. The activation and function of c-Jun and ATF-2 after nerve injury have not been examined in primates. Using a novel model of cranial nerve injury in baboons, we have examined the temporality of c-Jun activation (phosphorylation) in cranial nerve (CN) III and CN VI neurons and ATF-2 activation in CN VI neurons at 2, 4, and 9 days post-injury by immunohistochemistry. Furthermore, we have addressed whether the activation of these factors is associated with apoptosis by the TUNEL assay. We report that activated c-Jun is present in CN III and CN VI neurons ipsilateral to axotomy at 2, 4, and 9 days post-injury, but not in neurons contralateral to injury. Additionally, CN VI neurons ipsilateral to injury at 4 and 9 days contain activated ATF-2. Furthermore, no evidence of TUNEL reactivity was observed in either nucleus, regardless of laterality, at any of the examined time points. These findings suggest that activation of both c-Jun and ATF-2 does not mediate apoptosis in axotomized primate CN III and CN VI neurons at time points up to 9 days. This report serves as a basic inquiry into the neuronal response to cranial nerve injury in primates.

Abducens Nerve↗