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PubMed1992

A specific form of cognitive rigidity following excitotoxic lesions of the basal forebrain in marmosets.

The effects of N-methyl-D-aspartate-induced lesions of the basal forebrain were studied on performance of a series of visual discrimination tests that examined a range of cognitive functions in the marmoset. These included the ability to attend to the various dimensional properties of stimuli and to use just one of these properties in order to solve a discrimination (intra-dimensional shift); to switch attention from one dimension to another (extra-dimensional shift); to learn the reinforcement value of specific exemplars within a dimension (new learning); and to relearn their reinforcement value following reversal of the reward contingencies (serial reversals). Lesions of the basal forebrain did not impair the ability either to attend selectively to the dimensional properties of the stimuli or to switch attention from one dimension to the other. However, the lesion did affect various aspects of associative learning including a transient impairment of new learning and a marked disruption of serial reversal learning. The reversal deficit could be characterised as a tendency to perseverate on the previously correct stimulus and as a failure to to show the formation of a reversal learning set. In addition, the lesion prevented disruption of performance of a well-learned discrimination when novel exemplars from the irrelevant dimension were introduced (probe test). It is suggested that the functional effects of the basal forebrain lesion reflect impaired learning of stimulus-reward associations and behavioural rigidity. The finding, however, that there was no effect of the lesion on attentional set-shifting suggests that any loss of inhibitory control was specific to the level of stimulus-response or stimulus-reward associations, inhibitory control at the level of attentional selection remaining intact. The similarity of the effects of damage to the basal forebrain to those seen following damage to the orbitofrontal cortex and the amygdala are discussed in the context of the close anatomical and functional relationships that exist among these three structures.

Animals↗
PubMed1992

Restoration of learning ability in fornix-transected monkeys after fetal basal forebrain but not fetal hippocampal tissue transplantation.

Monkeys with bilateral transection of the fornix were severely but selectively impaired on learning and retention of visuospatial conditional discriminations, visual conditional discriminations and non-conditional spatial-response tasks. Bilateral transplantation of cholinergic-rich fetal basal forebrain tissue into the hippocampus abolished significant learning impairments on all those tasks impaired by fornix lesions when tested three to nine months after transplantation whereas bilateral transplants of non-cholinergic fetal hippocampal tissue into hippocampus showed no such beneficial effect. Acetylcholinesterase staining was severely depleted throughout the dentate gyrus and hippocampus in fornix-transected monkeys compared with animals with control corpus callosum ablations. Staining was largely restored to normal in the host hippocampus and dentate gyrus in monkeys with cholinergic transplants, whereas acetylcholinesterase staining was abnormal in those with non-cholinergic grafts. These experiments suggest that where a "higher order" cognitive function, in this case the acquisition of specific types of information into long-term memory, is disturbed by a neuropharmacologically simple lesion, cognitive function can be restored by transplantation of neurons containing appropriate neurotransmitters.

Analysis of Variance↗
PubMed1993

Regional distribution of sulfonylurea receptors in the brain of rodent and primate.

Glibenclamide, one of the most potent antidiabetic sulfonylureas, inhibits the activity of ATP-sensitive K+ channels in the pancreas as well as in the brain through its binding to specific receptors. Quantitative autoradiography was used to localize such receptors in the brain of rat, mouse, guinea-pig and marmoset, using [3H]glibenclamide as radioligand. In all four species, specific glibenclamide binding sites were found to be heterogeneously distributed. The highest densities were in the cerebral cortex, the molecular layer of the cerebellar cortex, the thalamus and the caudate-putamen. The globus pallidus and the substantia nigra were highly labelled in rat and mouse but poorly labelled in guinea-pig and marmoset. The distribution of glibenclamide binding sites in the hippocampus was different between the rodents and marmoset; in rodents, most binding sites were distributed in the fascia dentata and the CA3-CA4 fields of Ammon's horn, contrasting with a very homogeneous distribution in all subfields of the marmoset hippocampus. In conclusion, we demonstrate that primate brain contains specific binding sites for [3H]glibenclamide with a distribution not exactly similar to that in rodent brain.

Animals↗
PubMed1993

Stimulus-bound perseveration after frontal ablations in marmosets.

Marmosets with bilateral ablations of either the lateral or ventral surface of the frontal lobes were found to perseverate on object but not spatial serial reversal. They also perseverated on reversal of a visuospatial task where different stimuli required different spatial responses. No differences were found between the two lesion groups. Since the control animals showed mild perseveration on spatial but not object serial reversal it is argued that frontal ablations do not lead to perseveration of a natural tendency but rather that object and visuospatial perseveration are forms of stimulus-bound behaviour which do not occur when the animal is performing a spatial task in which stimulus position is irrelevant. Perseveration was reduced by pretreatment with a dopamine-blocking drug (haloperidol). It is suggested that information from temporal lobe mechanisms, involved in long-term memory, and from frontal lobe mechanisms, which exert shorter acting influences on behaviour, compete within the basal ganglia to determine stimulus choice. The ascending dopaminergic pathway may modulate the balance between these competing factors.

Animals↗
PubMed1993

Protective effects of SR 57746A in central and peripheral models of neurodegenerative disorders in rodents and primates.

Compounds possessing neurotrophic properties may represent a possible treatment for neurodegenerative disorders such as Alzheimer's disease. SR 57746A, 1-[2-(naphth-2-yl)ethyl]-4-(3-trifluoromethylphenyl)-1,2,5,6- tetrahydropyridine hydrochloride, is a new compound with neurotrophic activity in a number of in vitro preparations. The neurotrophic effects of this compound have been evaluated in vivo using four distinct rat models of neurodegeneration: transient global ischaemia produced by a four-vessel occlusion; septohippocampal lesion produced by injection of vincristine sulphate into the medial septum; sciatic nerve crushing; and acrylamide-induced peripheral neuropathy. Rats were administered vehicle or 2.5-10 mg/kg p.o. SR 57746A, after initiation of the degenerative process, then once daily for 10 days in the first two models, 16 days in the third and 26 days in the fourth model. Median scores for ischaemia-induced neuronal damage were reduced by 30-40% by SR 57746A treatment in hippocampal CA1, CA2, and CA3 regions, and in the dorsal striatum. Twelve days after intraseptal vincristine administration, there was a marked loss of septohippocampal cholinergic neurons, as indicated by reduced choline acetyltransferase activity in both the septum and hippocampus. SR 57746A dose-dependently reversed this reduction in both areas. These results were confirmed by histoenzymological evaluation of hippocampal acetylcholinesterase content. SR 57746A also reversed the loss of hippocampal choline acetyltransferase induced by intraseptal vincristine in marmosets. Behavioral deficits in these models (exploratory behaviour in the former and short-term social memory in the latter) were also significantly reduced by SR 57746A treatment. In the sciatic crush model, sensorimotor function improved more rapidly in rats treated with 10 mg/kg SR 57746A. In this same model, SR 57746A (10 mg/kg/day) also significantly increased the length of regenerated nerve eight days after the crush, as measured using the pinch test. Finally, SR 57746A retarded the onset, reduced the amplitude and accelerated the recovery of acrylamide-induced peripheral neuropathy. Thus, SR 57746A possesses notable neurotrophic activity in a variety of neurodegenerative models in vivo, suggesting that the compound may possess therapeutic potential for the treatment of neurodegenerative diseases.

Acetylcholinesterase↗
PubMed1993

Chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to monkeys: behavioural, morphological and biochemical correlates.

The behavioural, biochemical and morphological effects of a chronic administration of low doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were studied in the common marmoset. Monkeys received the toxin (1 mg/kg i.p.) twice a week for four months. Group A monkeys were studied one week after the last injection of MPTP; group B monkeys were studied eight months after the last toxic injection. The monkey behaviour was observed throughout the experiment; the biochemical and morphological correlates were studied post mortem in the neostriatum and in the substantia nigra, respectively. Data collected from MPTP-treated marmosets were compared to those obtained from sham-injected control monkeys. The results can be summarized as follows. (1) In all MPTP-treated marmosets a progressive Parkinsonism occurred. In group B monkeys, a gradual behavioural recovery was observed after MPTP was discontinued. (2) Biochemical analysis of group A marmosets showed a depletion of dopamine, of 3,4-hydroxyphenylacetic acid and of homovanillic acid, and no variations in dopamine turnover in the neostriatum of MPTP-treated marmosets. In group B, biochemical analysis showed no differences between controls and MPTP-treated animals. (3) Morphological analysis showed that the density of midbrain dopaminergic neurons located in the substantia nigra was unchanged in group A monkeys, but was reduced by 6.8% in MPTP-treated monkeys of group B. The measurement of cross-sectional area showed that midbrain dopaminergic neurons were swollen in MPTP-treated monkeys of group A, with a 11.0% increase of cell size as compared to controls. In group A the nuclei were also swollen, being 304.8% larger in MPTP-treated monkeys, with a nucleus-to-cytoplasm ratio of 65.9% (as compared to 34.0% of controls). In group B monkeys cell size was increased by 18.4% in MPTP-treated marmosets, but the nuclei were of comparable size. The present data show that a chronic administration of low doses of MPTP brings about biochemical and morphological abnormalities. The first occur acutely in terminals and are reverted early after discontinuance of exposure to the toxin; the latter occur in dopaminergic perikarya, last longer than biochemical abnormalities and, at variance with them, increase in severity after MPTP is discontinued. Morphological abnormalities include early events, such as a transient swelling of nuclei or a long-lasting swelling of neurons, and late events, such as a decrease in the number of tyrosine hydroxylase-positive perikarya.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

Restoration of cognitive abilities by cholinergic grafts in cortex of monkeys with lesions of the basal nucleus of Meynert.

Three groups of marmosets were trained to perform a series of visual discrimination tasks in a Wisconsin General Test Apparatus. Two groups then received bilateral lesions of the basal nucleus of Meynert using the excitotoxin N-methyl-D-aspartate and were found to be severely impaired on relearning a visual discrimination first learnt prior to surgery. One lesioned group then received grafts of acetylcholine-rich tissue dissected from the basal forebrain of fetal marmosets. Three months later the marmosets with lesion alone remained impaired on a number of retention and reversal tasks whereas the transplanted animals were no longer significantly impaired. Histological examination of the brains indicated that all lesioned animals had sustained substantial loss of the cholinergic neurons of the basal nucleus of Meynert (assessed by nerve growth factor receptor immunoreactivity) and that the lesion-alone animals showed marked loss of the cholinergic marker acetylcholinesterase in the dorsolateral frontal and parietal cortex. All transplanted animals had surviving graft tissue (visualized by Cresyl Violet staining, dense acetylcholinesterase staining and the presence of a limited number of nerve growth factor receptor-immunoreactive neurons) in the neocortex and 5/6 transplanted animals showed near complete restitution of acetylcholinesterase staining in frontal and parietal cortex. Examination of individual animal data showed that the animal without this restitution performed very poorly. The performance of the remaining transplanted animals was significantly better than that of the animals with lesion alone. There was a significant positive correlation between the degree of acetylcholinesterase staining and good performance on tasks sensitive to frontal lobe damage. These results demonstrate that acetylcholine-rich tissue transplanted into the neocortex of primates with damage to the cholinergic projections to the neocortex can produce substantial restitution of function provided that an appropriate level of interaction between graft and host tissue is achieved.

Acetylcholine↗
PubMed1994

Death of neurons in the neonatal rodent and primate globus pallidus occurs by a mechanism of apoptosis.

We have examined the developing rat, mouse and marmoset globus pallidus for evidence of cells dying by a process of "naturally occurring" or programmed cell death. We have demonstrated that cells in the developing mammalian globus pallidus die by a process of apoptosis and that by day 7 after birth many of the apoptotic cells possess a neuronal phenotype. Light microscopic and ultrastructural evidence of apoptotic cell death included cell shrinkage, blebbing of the extracellular membrane and condensation of the nuclear chromatin. Additionally we used an in situ nick translation method to assess the integrity of the DNA within the dying cells. This revealed that cells with the morphological characteristics of apoptosis also possessed fragmented DNA typical of cells undergoing Type 1 programmed or apoptotic cell death. The lack of lysosomal enzyme activity within the dying cells and the frequent observations of phagocytosis by neighbouring cells also suggest that the form of programmed cell death is apoptosis and not Type 2 autophagic degeneration. We found no evidence for cells dying by Type 3 non-lysosomal degeneration since all dying cells examined under the electron microscope possessed intact intracellular organelles and cell membranes. We developed a sensitive silver stain which detected balls of condensed chromatin within the apoptotic cells. This enabled identification of apoptotic cells in the developing globus pallidus at low magnification and so allowed us to map the numbers and distribution of dying cells with time. The incidence of apoptotic cells in the neonatal globus pallidus was greatest at birth and then declined such that few cells were detected at one week and none was seen in the adult rat. Although the loss of large numbers of cells in the developing nervous system is a well documented phenomenon, there are only a limited number of reports of the mechanism by which neuronal cells die, and few of these are in the developing mammalian brain. There are at least four different morphological categories of neuronal cell death which are discriminated on morphological and biochemical criteria. Our analysis suggests that apoptotic or Type 1 cell death is the major form of programmed cell death occurring in the mammalian globus pallidus in the first week of life. This report also describes the use of two methods for the ready identification of apoptotic cells at the light microscope level. Because these methods are suitable for use on tissue sections they provide a means to assess the incidence of apoptotic cell death, in parallel with other analyses of the expression of gene products which control cell fate.

Acid Phosphatase↗
PubMed1995

Conditional learning and memory impairments following neurotoxic lesion of the CA1 field of the hippocampus.

Monkeys with bilateral lesions of the CA1 field of the hippocampus produced by the injection of neurotoxin diagonally along the length of the hippocampus were found to have a severe impairment on the retention of a conditional task learnt prior to surgery and on the new acquisition of several types of this task. They were equally impaired on conditional tasks that required a spatial response or an object choice in response to either visual or spatial cues. They were not impaired on simple visual discrimination tasks, simple spatial discrimination tasks or reversal learning of these tasks. This patterns of impairment resembles that seen in the same species with neurotoxic lesions within the vertical limb of the diagonal band of Broca or transection of the fornix. Monkeys with subtotal lesions of the adjacent medial temporal area were not consistently impaired on any of these tasks. The results suggest that hippocampal lesions produce anterograde and retrograde amnesia for information other than reward association.

Animals↗
PubMed1995

Behavioral and neurochemical consequences of ibotenic acid lesion in the subthalamic nucleus of the common marmoset.

Five marmosets were unilaterally lesioned within the subthalamic nucleus (STN) by injection of 10 micrograms ibotenic acid. Seven marmosets served as saline injected controls. The lesioned marmosets showed an increased locomotor activity, occasional tongue protrusions, posture asymmetry, and abnormal movements of the contralateral legs and arms. The animals were sacrificed 21 days after the ibotenic acid injection and markers of gamma-aminobutyric acid (GABA), dopamine (DA), and acetylcholine were studied in a variety brain regions. There was a bilateral increase in the activity of glutamic acid decarboxylase (GAD) in the caudate, putamen, globus pallidus, superior colliculus, and the ventral anterior/ventral lateral (VA/VL) thalamus, whereas GABA concentrations were only increased ipsilaterally in the ventral posterior medial/centromedial/parafasciculus (VPM/CM/Pf) complex of the thalamus. Tyrosine hydroxylase (TH) activity was bilaterally increased in the medial segment of globus pallidus and nucleus accumbens. However, there were also changes restricted to the side contralateral to the lesion. TH activity and DA concentrations were increased contralateral to the lesion in the putamen. Choline acetyltransferase (CAT) activity was bilaterally increased in the medial segment of globus pallidus and hypothalamus. The ibotenic acid induced STN-lesion in the marmoset, thus, seemed to cause a widespread bilateral activation of neurons within the basal ganglia.

Acetylcholine↗
PubMed1996

Effects of lesions of different parts of the septo-hippocampal system in primates on learning and retention of information acquired before or after surgery.

Data from a large series of experiments on marmosets with lesions of the septal/diagonal band area (DB), fornix or CA1 area of the hippocampus are analysed in terms of retention of information learned before surgery, acquisition of new information and retention of information acquired after surgery. It is shown that although all three lesions impair acquisition of a specific type of new information, lesions of CA1 result in a severe retrograde amnesia but no forgetting of that type of information adequately acquired after surgery, whereas lesions of the DB do not cause retrograde amnesia but do result in significant forgetting. Monkeys with fornix transection occupied an intermediate position in their pattern of learning impairments; some animals showed evidence of forgetting, whereas the great majority showed retrograde amnesia. These data may be relevant to an understanding of the different extent of amnesia in patients with different pathology within the medial temporal lobe and associated subcortical structures.

Animals↗
PubMed1992

Gibbon and marmoset c-myc nucleotide sequences.

The nucleotide sequences of the gibbon and marmoset myc loci have been determined by the dideoxy ribomethod. The number of mutations which occurred during evolution and the branches affected were deduced according to the principle of maximum parsimony, from a comparison with known mammal sequences. As previously observed for the human and chimpanzee myc genes, an Alu repeat belonging to subclass III was observed in the second intron of the gibbon myc gene. In contrast, no such element was found in the marmoset gene. Alignment of the Myc amino acid (aa) sequences provided clues for detecting which aa or which protein regions have been more heavily mutated. Conversely, some regions remained free of mutations and remained unchanged from mouse to human, most probably in connection with some important embedded property(ies). An intriguing feature of the human Myc protein is duplication of 50 aa out of 439. Strikingly, most of these aa remain unchanged in mouse, rat, cat, marmoset, gibbon, chimpanzee and human.

Amino Acid Sequence↗
PubMed1991

Use of dabsylation, column switching and chiral separation for the determination of a renin inhibitor in rat, marmoset and human plasma.

A high-performance liquid chromatographic method with column switching was developed for the determination of the renin inhibitor Ro 42-5892/001, (S)-alpha-[(S)-alpha-[(tert.-butylsulphonyl)methyl]hydrocinnama mido]-N- [(1S,2R,3S)-1-(cyclohexylmethyl)-3-cylcopropyl-2, 3-dihydroxypropyl]imidazole-4-propionamide methanesulphonate (1:1), in rat, marmoset and human plasma, using a Nucleosil C8 120 (3 microns) stationary phase. Since the analyte and the internal standard are optical isomers, beta-cyclodextrin was used as a mobile phase constituent for their chiral separation. The method took advantage of the characteristics of dabsyl chloride derivatives, namely sensitivity, specificity and, particularly, stability, providing a quantification limit of 5 ng/ml. The accuracy (range of inaccuracy 1-13%) and the inter-assay precision (coefficient of variation range 1.8-9.1%) were acceptable. The method was successfully applied to toxicokinetic studies in rats and marmosets.

Animals↗
PubMed1994

Quantitative determination of CGP 53,437, a new HIV protease inhibitor, in plasma by high-performance liquid chromatography and fluorescence detection.

A specific and sensitive liquid chromatographic assay for CGP 53,437 (I), a potent HIV protease inhibitor, is described. The method is based on a deproteinization step, followed by a liquid-liquid extraction with diisopropyl ether. Then a deprotection step of the primary amine and derivatization using fluorescamine is performed. Chromatography is achieved by isocratic elution with a mobile phase of 63 mM borax buffer (pH 9)-acetonitrile (58:42, v/v). The flow-rate of the mobile phase is 1 ml/min. The derivatives of compound I and its internal standard CGP 54,451, II, fluoresce at 480 nm on excitation at 395 nm. The limit of quantitation which is the lowest concentration of the analyte that can be measured with a coefficient of variation and a deviation from theory of less than 20%, was 5 nmol/l plasma. The analyte is stable for at least seven months in spiked human plasma samples. It is also stable after freezing and thawing cycles. Different human plasma sources and plasma samples from three different species (dog, marmoset, and rat) were tested and no interferences from plasma constituents was observed.

Animals↗
PubMed1991

High conservation of sequences involved in cystic fibrosis mutations in five mammalian species.

Several mutations have been identified in the first nucleotide binding fold (NBF) of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) gene. We have analyzed the DNA sequences of exons 10 and 11 in five different mammalian species, marmoset, mouse, cow, pig, and sheep; the amino acid conservation studied for nine disease mutations; and two "benign" mutations. For exon 10, 87% homology at the DNA level and 93.5% at the amino acid level were found for these species. For exon 11, the lowest homology (70%) was found in mouse and the highest in marmoset (93%), whereas the amino acid sequence conservation ranged from 82.5 to 100%. All codons involved in CF mutations are highly conserved throughout evolution.

Amino Acid Sequence↗
PubMed1992

Effect of ultraviolet irradiation on selected host cell proteins including Ro/SS-A and Epstein-Barr virus in cultured lymphoblastoid cell lines.

Although systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS) are distinct collagen vascular illnesses, they share certain features. Both have clinical manifestations involving skin and mucous membranes and characteristically have high titers of circulating autoantibodies to the cellular components Ro/SS-A, calreticulin/Ro, 52 kDa Ro and La/SS-B. Viruses have been postulated to be involved in the pathogenesis of both diseases. Sensitivity to sun is a cardinal feature of SLE, and UV light may be involved in its pathogenesis. Using human B-lymphoblastoid cell lines, the effect of the resident Epstein-Barr virus on the expression of the above cellular components was investigated by flow cytometry. Sublethal irradiation with ultraviolet B light appeared to diminish EBV antigen expression (gp350/220) during the first 48 to 72 hours in culture, whereas there was no change in the expression of MHC class I or immunoglobulin host cell proteins, and an apparent increase in the expression of host cell autoantigens. The virus appeared to be more sensitive to UVB-induced damage yet did appear to be able to undergo repair. No direct correlation could be made between the presence of the virus and the increase in autoantigen expression. La/SS-B and/or 52 kDa Ro antigen(s) were found to be present in the cytoplasm of the B lymphoblastoid cells at a higher base level in EBV-infected cell lines than in the EBV-negative cell lines.

Amino Acid Sequence↗
PubMed1992

Neuropathological changes during generalized seizures in newborn monkeys.

The brains of four 2-week-old marmoset monkeys were perfusion-fixed immediately after bicuculline-induced seizures lasting 1.5-4.3 h and were later examined by light and electron microscopy. Mean arterial blood pressure and rectal temperature measurements during seizures did not differ significantly from baseline. Plasma glucose concentrations decreased to the 1.5 mM range at the end of seizures, and arterial pH and bicarbonate were lower than in control animals, although arterial pO2 and pCO2 were maintained. Neuropathological changes were minimal. Swollen astrocytic processes surrounded some capillaries and some neurons in cerebral cortex, hippocampus, putamen and thalamus. Almost all the neurons examined looked normal, but mitochondrial swelling was present in a few. All but the most severe mitochondrial swelling, which occurred very rarely in one of four animals, is potentially reversible. The virtual absence of neuronal necrosis in these neonatal monkeys is consistent with the resistance to seizure-induced brain damage found in immature rats, and stands in sharp contrast to the damage seen in older animals. Lack of neuronal damage, however, does not rule out potential adverse effects of prolonged seizure activity on subsequent brain growth and development.

Animals↗
PubMed1992

Bacteriocin-like activity of Bacteroides fragilis group isolated from marmosets.

The ability of strains of the B. fragilis group, isolated from the oral cavity and intestine of marmosets, to produce bacteriorin-like substances in solid medium, in terms of auto-, iso- and heteroantagonism, was evaluated. Antagonistic activity was exhibited by 52% of the intestinal strains, 3 of which showed autoantagonistic activity. Three out of 9 oral strains isolated, tested against themselves, showed simultaneous isoantagonism to 4 indicator strains; but not autoantagonism. The same 9 oral strains, when tested against 16 reference strains, revealed interspecific activity only against 2 Gram-positive microorganisms. Higher activity, evaluated by the size of the inhibition halo, was observed in BHI-S agar, and greatest inhibition was obtained after 72 h of incubation.

Animals↗