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M Rodriguez

Publications and source records attributed to M Rodriguez.

At least 613 records · Page 34Linked to original sources

Lateralization in male rats and dopaminergic system: evidence of right-side population bias.

Recent studies have reported population right-biased lateralization in rats, although with low percentages (between 54-59%). The present study investigated the spatial preference of rats in an electrified T-maze during successive days and the influence of ascending dopaminergic systems using apomorphine, a dopamine agonist, as well as ipsilateral and contralateral lesions on the side preference. Results showed a marked right-biased lateralization at both individual and population levels (85.71% of the rats presented a behavioral asymmetry, being 80% right-biased and 20% left-biased within the lateralized group). Also, the results suggest that there is a presynaptic dominance in the contralateral dopaminergic system to the spatial preference in the T-maze and postsynaptic dominance in the ipsilateral side.

Animals↗

Behavioral lateralization in the T-maze and monoaminergic brain asymmetries.

Recently we have reported a marked rat lateralization in the T-maze choice. The present study examines the relationship between the ascending monoaminergic systems and the T-maze behavioral asymmetry. There were no significant differences for serotonin or norepinephrine between the T-maze preferred and non-preferred brain sides in the s. nigra, ventral tegmental area, striatum, acumbens, frontal lobe or hippocampus. Only in the hippocampus was dopamine concentration significantly greater for the brain site ipsilateral to the T-maze choice side. Previously, we reported that both apomorphine, a dopamine receptor agonist, and 6-hydroxydopamine lesion in the medial forebrain bundle of the catecholaminergic neurons affect the T-maze asymmetry; we therefore suggested that the T-maze choice could be related with the ascending dopaminergic systems. The present data strongly support this hypothesis and suggest that the DA cells involved in the spatial asymmetry in the T-maze are included in the dopaminergic mesohippocampal system.

Animals↗

Tyrosine administration to pregnant rats induces persistent behavioral modifications in the male offspring.

Pregnant rats were given, by stomach intubation, 1-tyrosine (20 or 500 mg/kg), beginning on day 11 post-coitus. Tyrosine or saline solution administrations were continued on a once-daily basis until day 20 of gestation. When male offspring were seventy days old, the spontaneous locomotor activity, open field test, swim test and motor ability test were performed. The offspring treated with large tyrosine doses showed a marked increase in both spontaneous locomotor activity and open field locomotion as adults. However, activity in the swim test decreased. The number of defecation boluses produced in the open field test and the motor ability in the rotating rod test diminished. The behavior of the rats treated with small doses of tyrosine was similar, in all tests performed, to that of rats treated with saline solution. These findings strongly suggest that a large increase in diet tyrosine during pregnancy modifies the behavior of male offspring.

Animals↗

Magnetic resonance imaging and clinical relationships in multiple sclerosis.

Magnetic resonance imaging (MRI) was done in 109 patients with suspected demyelinating disease (56 with clinical multiple sclerosis [MS] and 53 without). Of those with clinical MS, 43 (77%) had multifocal lesions of the white matter detected on MRI; 12 of the 43 also had confluent periventricular signaling. Nine patients (17%) without clinical MS had similar findings. Of the 56 patients with MS, 35 underwent both computed tomography (CT) and MRI. In this group, 80% of MRI scans showed multiple demyelinating lesions compatible with MS, as compared with 29% of the CT scans. A CT scan was "positive" more often if obtained within 1 month after an attack of MS than later. In contrast, the sensitivity of MRI or the number of lesions detected by MRI did not increase in patients with recent exacerbations. MRI was "positive" in patients with clinical MS more often than was any single evoked response study. In statistical analyses, both the sensitivity of MRI and the number of lesions were associated with the duration of MS. A pattern of confluent periventricular signaling around the lateral ventricle was associated with greater duration of MS and patient disability.

Adult↗

Synthesis and biological activity of partially modified retro-inverso pseudopeptide derivatives of the C-terminal tetrapeptide of gastrin.

The effects of partial retro-inverso modifications of selected peptide bonds of the N-terminal tetrapeptide of gastrin have been studied. In some of the synthesized compounds, the phenylalanyl residue has been replaced by the (R,S)-2-benzylmalonyl, 3-phenylpropionyl, benzylcarbamoyl, or benzyloxycarbonyl moieties. All pseudopeptides showed affinity for the gastrin receptor, in vitro, with potencies varying from IC50 = 10(-7) to IC50 = 10(-4) M. These compounds exhibited little or no activity on acid secretion in the anesthetized rat but were able to antagonize the action of gastrin. Among the most potent were Boc-Trp-Leu-gAsp-CO-CH2CH2C6H5 (20) (ED50 = 0.15 microM/kg), Boc-Trp-Leu-gAsp-m(R,S)Phe-NH2 (3) (ED50 = 0.15 microM/kg), and Boc-Trp-gLeu-D-Asp-m(R,S)Phe-NH2 (7) (ED50 = 0.3 microM/kg).

Animals↗

Synthesis and biological activities of pseudopeptide analogues of the C-terminal heptapeptide of cholecystokinin. On the importance of the peptide bonds.

A series of pseudopeptide analogues of the C-terminal heptapeptide of cholecystokinin in which each peptide bond, one at a time, has been replaced by a CH2NH bond were synthesized: Z-Tyr(SO3-)-Nle-Gly-Trp-Nle-Asp psi-(CH2NH)Phe-NH2 (1), Z-Tyr(SO3-)-Nle-Gly-Trp-Nle psi (CH2NH)Asp-Phe-NH2 (2), Z-Tyr(SO3-)-Nle-Gly-Trp psi-(CH2NH)Nle-Asp-Phe-NH2 (3), Z-Tyr(SO3-)-Nle-Gly psi(CH2NH)Trp-Nle-Asp-Phe-NH2 (4), Z-Tyr(SO3-)-Nle psi-(CH2NH)Gly-Trp-Nle-Asp-Phe-NH2 (5), Z-Tyr(SO3-)-Met-Gly-Trp-Nle-Asp psi (CH2NH)Phe-NH2 (6), Z-Tyr-(SO3-)-Met-Gly-Trp-Nle psi (CH2NH)Asp-Phe-NH2 (7), Z-Tyr(SO3-)-Met-Gly-Trp psi (CH2NH)Nle-Asp-Phe-NH2 (8). These derivatives were studied for their ability to stimulate amylase release from rat pancreatic acini and to inhibit the binding of labeled CCK-9 to rat pancreatic acini and to guinea pig brain membrane CCK receptors. They were compared to the potent CCK-8 analogue Boc-Asp-Tyr(SO3-)-Nle-Gly-Trp-Nle-Asp-Phe-NH2. All of these pseudopeptides were able to stimulate amylase secretion with the same efficacy as CCK-8 but with varying potencies. These compounds were also potent in inhibiting the binding of labeled CCK-9 to CCK receptors from rat pancreatic acini and from guinea pig brain membranes.

Amylases↗

The role of aluminum in the development of hypercalcemia in the rat.

The present study evaluates the effect of an intravenous (i.v.) aluminum infusion on total and ionized calcium. Seven groups of rats were studied, and it was found that the magnitude of hypercalcemia was dose dependent. During a two hour i.v. infusion containing 0.4 mg aluminum per 100 grams of body weight, the total plasma calcium increased from 9.7 +/- 0.2 to 12.7 +/- 0.7 mg/dl (X +/- SE, P less than 0.02) while the ionized calcium decreased from 5.1 +/- 0.12 to 4.05 +/- 0.24 mg/dl (P less than 0.001). The increase in plasma calcium occurred in intact and parathyroidectomized rats, and the hypercalcemia could not be attributed to changes in PTH, arterial pH, plasma protein, or plasma phosphate. In vitro studies indicate that the addition of aluminum to rat plasma results in decreased ionized calcium concentration. Similarly, ultrafilterable calcium declined from 5.4 +/- 0.17 to 4.53 +/- 0.12 mg/dl (P less than 0.001) after the addition of aluminum to rat plasma. In summary, high levels of intravenous aluminum increase total plasma calcium and decrease ionized calcium. As also supported by in vitro data, the most probable mechanism is increased binding of calcium in the plasma which decreases ionized calcium. As a result of the decreased concentration of ionized calcium, movement of bone and interstitial calcium into the vascular space may occur, thus increasing total plasma calcium.

Aluminum↗

Remyelination by oligodendrocytes stimulated by antiserum to spinal cord.

The new synthesis of myelin and the proliferation of oligodendrocytes was stimulated by serum from syngeneic mice immunized with homogenized spinal cord (SCH). Treatment with this antiserum produced a 10-fold increase in the area of remyelination in spinal cords that had become demyelinated previously as a result of infection by Theiler's murine encephalomyelitis virus. Inflammation was decreased in regions of white matter that showed remyelination. Oligodendrocytes exposed to anti-SCH in vitro incorporated three to five times more [3H]thymidine than resting cells did and expressed more myelin basic protein in their cytoplasm, suggesting stimulation of myelinogenesis. Thus, there is a factor present in anti-SCH antiserum that stimulates central nervous system-type remyelination. This finding may provide clues for the therapy of patients with demyelinating disorders such as multiple sclerosis.

Animals↗

1H and 13C n.m.r. studies of pseudo-peptide analogues of the C-terminal tetrapeptide of gastrin.

1H and 13C n.m.r. study of pseudo-peptide analogues of the C-terminal tetrapeptide of gastrin, obtained by replacing each peptide bond by a "reduced peptide bond", one at a time, e.g. Boc-Trp psi (CH2NH)Leu-Asp-Phe-NH2 2, Boc-Trp-Leu psi (CH2NH) Asp-Phe-NH2 3, Boc-Trp-Leu-Asp psi (CH2NH)Phe-NH2 4, were reported. The CH2NH bond was completely characterized. 1H and 13C spectroscopic data were reported. It appeared from the present work that the modifications produced by the replacement of a peptide bond by a CH2NH bond were localized around the CH2NH.

Carbon Isotopes↗

Theiler's murine encephalomyelitis: a model of demyelination and persistence of virus.

Theiler's murine encephalomyelitis virus (TMEV) causes immune-mediated demyelination in susceptible mice which is similar to human demyelinating disorders such as multiple sclerosis. In addition, the picornavirus persists within the central nervous system throughout the course of the chronic demyelinating disease. This article reviews the neuropathology, virology, immunology, and molecular biology of the model system. We analyze the possible mechanisms by which this virus induces demyelination and persists in the nervous system. Finally, we provide a hypothesis that the specificity of primary white matter destruction in the TMEV model depends on immune-sensitized cells which interact with viral antigen plus major histocompatibility complex (MHC) antigens on the surfaces of oligodendrocytes or myelin sheaths.

Acute Disease↗

Degradation of a tetragastrin analogue by a membrane fraction from rat gastric mucosa.

Our previous work on the effect of modification of peptide bonds in gastrin-like peptides led us to speculate that cleavage of the bond between the Met and Asp residues occurs in gastric mucosal membranes, and that this cleavage may have functional significance. In agreement with this speculation, we now show that the tetragastrin analogue BOC-Trp-Leu-Asp-Phe-NH2 (1) is degraded by a membrane fraction from rat gastric mucosa, and that the main products are BOC-Trp-Leu and Asp-Phe-NH2. Pseudo-peptide analogues in which the peptide bonds are replaced by CH2NH had differing stabilities; BOC-Trp-Leu-Asp-psi (CH2NH)-Phe NH2 (4) and BOC-Trp-Leu-psi(CH2NH)-Asp-Phe-NH2 (3) were stable under the incubation conditions, whereas BOC-Trp-psi(CH2NH)-Leu-Asp-Phe-NH2 (2) was degraded. The peptide and pseudo-peptide which were degraded (1 and 2) have been shown to stimulate gastric acid secretion in rats, in vivo, whereas 3 and 4 (which were not hydrolyzed) were inactive in stimulating gastric acid secretion and were found to antagonize the action of gastrin.

Animals↗

Different roles of intrahypothalamic and nigrostriatal dopaminergic systems in thermoregulatory responses of the rat.

Classically, two neurotransmitters in the brain have been implicated in thermoregulation: 5-hydroxytryptamine and norepinephrine. A dopamine action is less well-known and usually has been studied by means of pharmacological rather than physiological procedures. In the present work using a physiological approach to the problem, the role of different central dopaminergic systems in the thermoregulatory response of rats exposed to cold (4 degrees C) or warm (45 degrees C) environments has been studied. Rostral incertohypothalamic neurons in the medial preoptic area synthesized and released more dopamine in response to a warm but not to a cold environment. On the other hand DA and DOPAC levels in nigrostriatal systems were decreased by cold but not warm environments. The dopaminergic neurons projecting to nucleus accumbens or hypothalamus do not appear to be related to the thermoregulatory response in the rat.

3,4-Dihydroxyphenylacetic Acid↗

Susceptibility to Theiler's virus-induced demyelination. Mapping of the gene within the H-2D region.

Demyelination induced by Theiler's virus was examined in mouse strains with congeneic recombinant haplotypes. Light and electron microscopy of spinal cord sections from mice with s, q, v, p, and f H-2D alleles showed perivascular inflammation and primary demyelination. The presence of susceptible haplotypes in the K or I region did not correlate with pathologic abnormalities. The Qa, Tla, PgK, and UpG genes did not appear to be critical in determining susceptibility to disease. However, mutation in the H-2D genes altered the susceptibility to virus-induced demyelination. B10.D2dm1 mice, which have deletions in the 3' end of Dd and the 5' end of Ld, showed prominent demyelination and clinical deficits. In contrast, BALB/c-dm2, which have a deletion of the entire L gene, showed no pathologic changes. Central nervous system virus titers correlated with susceptibility to demyelination; both resistant and susceptible strains had a strong humoral immune response to the virus. The findings in the congeneic recombinant mice and in mice mutant in the H-2D region strongly suggest that at least one of the genes critical for determining virus-induced demyelination maps to the 3' end of the H-2D gene.

Animals↗

Therapeutic effect of the antiviral agent ribavirin in Junín virus infection of primates.

In order to assess the effect of the antiviral Ribavirin on the course of Junín virus infection in Callithrix jacchus, seven inoculated monkeys were treated with 15 mg of the drug, twice a day, starting 6 days after infection when all animals were viremic. The three untreated controls showed typical signs of Junín virus infection at 14 days pi and their mean time of death was 18 days. In contrast, no signs of illness were detected in Ribavirin-treated animals until 24 days pi, when marmosets showed signs of neurological involvement: 5 of these animals died (mean day of death: 36) but the two remaining treated monkeys improved and survived infection without sequelae. The comparison of survival rates (0% vs 28%) and the delay of the mean day of death observed indicates that the Ribavirin treatment used has therapeutic effect on Junín virus infection in vivo.

Animals↗