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Biomedical subjects

E Costa

Publications and source records attributed to E Costa.

At least 523 records · Page 29Linked to original sources
PubMed1978

Modulation of acetylcholine metabolism in the hippocampal cholinergic pathway by intraseptally injected substance P.

Intraventricular injection of substance P induced a dose-dependent decrease of acetylcholine (ACh) turnover rate (TRACh) in the hippocampus of rats. The highest dose used (20 nmol) decreased the hippocampal TRACh to 40% of the control value. No changes in the ACh or choline content were detected in the various brain areas 40 minutes after injection, but after 70 minutes an increase in ACh content in diencephalon was significant. Local injection of substance P into the medial nuclei of the septum decreased significantly the hippocampal TRACh. Neither intraventricular injection nor injection into the periaqueductal grey of high doses of substance P (30 nmol) induced analgesia, whereas beta-endorphin (1 nmol) and morphine (15 nmol) were effective. No specific change in the electroencephalograph pattern recorded from either cortex or hippocampus could be detected within the first 2 hours after intraventricular injection of substance P.

Acetylcholine↗
PubMed1978

Patoc 1 and Rufino strains of Leptospira biflexa, as screening antigens in the diagnosis of leptospirosis.

Patoc 1 and Rufino from L. complexo bifexa strains employed as screening antigen in the serologic diagnosis of liptospirosis in human and in six different animal species in comparison with a battery of 1.9 L complexo interrogans antigens, Patoc strain showed a 98.8% accordance in the sera agglutination tests, in humans; in animal it showed a low percentage of accordance in the sera agglutination tests in humans and in animals.

Animals↗
PubMed1977

Endogenous protein kinase inhibitors. Purification, characterization, and distribution in different tissues.

A thermostable inhibition of ATP-protein phosphotransferase (EC 2.7.1.37) (protein kinase) which is present in crude tissue extracts has been resolved by gel chromatography (Sephadex G-100) into two molecular forms. These two forms will be referred to as type I and type II inhibitor. The type I inhibitor (Mr approximately or equal to 24,000) is specific for cAMP-dependent protein kinase and corresponds to the inhibitor described earlier (Walsh, D. A., Ashby, C. D., Gonzalez, C., Calkins, D., Fisher, E. H., and Krebs, E. G. (1971) J. Biol. Chem. 246, 1977-1985). The type II inhibitor (Mr approximately or equal to 15,000) competes for the enzyme with various substrate proteins (histone, alpha-casein, and Leu-Arg-Arg-Ala-Ser-Leu-Gly (kemptide). The type II inhibitor blocks protein phosphorylation catalyzed by several types of protein kinases (cAMP- and cGMP-dependent or cyclic nucleotide-independent protein kinases). The type II inhibitor from rat brain has been purified 1500-fold; this protein is thermostable, has acidic characteristics, and does not require Ca2+ ions for its activity. Different ratios and concentrations of type I and type II inhibitors of protein kinase are found in rat skeletal muscle, pancreas, cerebellum and corpus striatum, and in lobster tail muscle.

Animals↗
PubMed1977

Dopamine-sensitive adenylate cyclase: location in substantia nigra.

A dopamine-sensitive adenylate cyclase with characteristics similar to those measured in the striatum is present in the rat substantia nigra. Destruction of dopamine cell bodies by intranigral 6-hydroxydopamine application failed to abolish the response of nigral adenylate cyclase to dopamine. In contrast, brain hemitransection between the striatum and substantia nigra, or a more circumscribed lesion of striatonigral pathways, abolished the dopamine stimulation of adenylate cyclase in the substantia nigra. These results suggest that dopamine receptors within the substantia nigra are not located on dopamine cell bodies but are associated with a pathway, containing gamma-aminobutyric acid or substance P, which projects from forebrain structures to the substantia nigra.

Adenylyl Cyclases↗
PubMed1977

Inhibition of acetylcholine turnover in rat hippocampus by intraseptal injections of beta-endorphin and morphine.

Intraseptal administration of morphine (70 nmol) or beta-endorphin (0.7 nmol) reduced the rate of acetylcholine (ACh) turnover (TRACh) in rat hippocampus but not in striatum or cortex. These intraseptal injections failed to modify the ACh content and did not elicit analgesia. Naltrexone (15 mumol/kg, i.p.) completely antagonized the decrease of hippocampal TRACh elicited by the two opiate receptor agonists. Furthermore, intraseptal injections of naltrexone partially blocked the decrease in hippocampal TRACh induced by intraperitoneal administration of morphine (70 mumol/kg, i.p.). These data suggest that opiate agonists decrease hippocampal TRACh by regulating septal cholinergic neurons, and that this effect is not associated with analgesia.

Acetylcholine↗
PubMed1977

Correlation between drug-induced supersensitivity of dopamine dependent striatal mechanisms and the increase in striatal content of the Ca2+ regulated protein activator of cAMP phosphodiesterase.

Rats were injected daily with 1.3 mumol/kg of haloperidol s.c. for 10 days. From the second to the ninth day after haloperidol withdrawal the rats developed supersensitivity to the behavioral affects of apomorphine. Concomitantly, the Ka of dopamine for the activation of striatal adenylate cyclase was lowered and the striatal content of the Ca2+ dependent protein that activates cAMP phosphodiesterase was increased. This activator protein is stored in striatal membranes and can be released by membrane phosphorylation in cytosol. This protein increases the activity of the high Km phosphodiesterase (Uzunov et al., 1976) but when it is bound to striatal membranes it facilitates the activation of striatal adenylate cyclase by dopamine (Gnegy et al., 1976b). The increase in protein activator content of striatal membranes caused by haloperidol could be a primary factor in causing supersensitivity to the biochemical and behavioral effects of dopamine receptor agonists.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

Regulation of nerve growth factor content in C6 glioma cells by beta-adrenergic receptor stimulation.

The C6 glioma cell line contains nerve growth factor (NGF) which can be released into the medium. Treatment of the cells with beta-adrenoceptor agonists resulted in increased content of NGF in both the cells and the medium within a few hours, whereas alpha-adrenoceptor agonists were ineffective. The response was blocked by beta- but not alpha-adrenoceptor antagonists. The increase of the NGF content of glioma cells appeared to be mediated by an elevation of cyclic AMP or GMP. The addition to the cell cultures of other putative neurotransmitters failed to change the content of either NGF or cyclic AMP. These results are discussed with respect to a model for adrenergic neuron-glial interactions.

Adrenergic beta-Antagonists↗
PubMed1977

On the mechanism of the decrease in cerebellar cyclic GMP content elicited by opiate receptor agonists.

Morphine, dextromoramide (4 mumol/kg i.p.) and vimonol R2 (17 mumol/kg i.p.) in analgesic doses (28 to 112 mumol/kg i.p.) decreased 3',5'-cyclic guanosine monophosphate (cGMP) in rat cerebellar cortex; morphine also decreased the cGMP content in deep cerebellar nuclei. Intrastriatal but not intracerebellar injections of morphine (20 mug) decreased cerebellar cGMP content. Naltrexone, an opiate receptor antagonist, but only apomorphine, a dopaminergic receptor agonist, blocked the effect of morphine on cerebellar cGMP. Pretreatment with 3-acetylpyridine (3-AP) which destroys the climbing fibers, failed to antagonize the effect of morphine on cerebellar cGMP. These results suggest that activation of opiate receptors in striatum decreases cerebellar cGMP content presumably by reducing activity in the mossy fiber excitatory input to cerebellum.

Analgesics↗