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Biomedical subjects

G Palladini

Publications and source records attributed to G Palladini.

At least 73 records · Page 4Linked to original sources
PubMed1987

Immunocomplexes in rat and rabbit spinal cord after injury.

The possibility that, following a major lesion of the central nervous system, a humoral immune response could be evoked with formation of immune complexes "in situ" was investigated. For this purpose, an immunohistochemical study on rabbit and rat spinal cord at different times after surgical transection was carried out. The peroxidase-antiperoxidase method showed IgG decoration of the myelin sheaths starting a short time after surgery. The sera of intact and injured animals were then tested both by immunohistochemical methods on intact spinal cord sections and by immunoelectrophoresis on a protein extract of homologous spinal cord. The results showed in the rabbit the absence of antibodies to neural antigens before surgical injury and its appearance within a few days after surgery. On the other hand, in the rat, even before the injury, we found antibodies to neural tissue which decreased in the first few hours after injury, and returned to control values during successive days. The same experiments were conducted after a peripheral nerve lesion (sciatic nerve crush), but no immune response could be detected. The possible role of this immune response in the failure of axonal regeneration in mammalian spinal cord is briefly discussed.

Animals↗
PubMed1986

The response of ventral horn neurons to ricin. An experimental abiotrophy model.

The morphological alterations of anterior horn neurons of the spinal cord of rabbits produced by the administration of ricin conveyed via retrograde axonal flow are described. The differences with the primary response after axonal transection and the similarity with degenerative abiotrophic systemic lesions are discussed.

Animals↗
PubMed1986

Preliminary histochemical and electron microscopic observations on the nervous system of hydra.

The nervous system of a primitive Coelenterate (Chlorohydra viridissima) has been studied using ultrastructural and histochemical techniques. The authors confirm the ultrastructural pattern of nerve cells described by Lentz and coworkers. Reserpine treatment fails to induce any reduction of catechol- and indoleamine content visible to histochemical observation. In vivo treatment with tetanus toxin does not induce behavioural changes and no specific binding of toxin is revealed by immunocytological analysis. This suggests that neuron tetanus toxin receptor sites are absent in hydra. Hydra nerve cells must therefore be considered as extremely primitive elements, which the Authors consider to support the hypothesis of neurons having originated as a gradual differentiation of myoepithelial cells, as proposed by Pantin (1956) and by Passano (1963).

Animals↗
PubMed1984

Aminergic neurotransmitters and adenylate cyclase in hydra.

Serotonin, dopamine and, in lesser amounts, norepinephrine were detected in Chlorohydra viridissima with electrochemical detection coupled to liquid chromatography (LCED). Treatment with reserpine induces a significant decrease in amine levels. Adenylate cyclase was found in Hydra tissue; the enzyme is stimulated by Mg, Mn and F and sensitive to guanine nucleotide activation. Dopamine, serotonin, GSH and glutamate do not affect cyclase activity.

Adenylyl Cyclases↗
PubMed1983

Radioimmunological and immunocytochemical demonstration of Met-enkephalin in planaria.

1. An anti-Met-enkephalin serum has been used for radioimmunological and immunocyto-chemical demonstration of Met-enkephalin in planaria. 2. The serum showed a high degree of sensitivity and specificity. 3. Radioimmunoassay demonstrated in planaria extracts a considerable concentration of Met-enkephalin. 4. Met-enkephalin was localized by immunocytochemical methods in neurons and neuropil.

Animals↗
PubMed1983

Effects of dopaminergic agents on monoamine levels and motor behaviour in planaria.

1. Dopamine, serotonin and, in lesser amounts, norepinephrine were detected in Dugesia gonocephala using electrochemical detection coupled with liquid chromatography (LCED). 2. Treatment with L-dopa induced hyperkinesias, and a rise in dopamine, serotonin and norepinephrine content, whereas reserpine reduced motor activity and the concentrations of all three monoamines. 3. Haloperidol reduced motor activity and dopamine and norepinephrine levels. 4. Apomorphine induced hyperkinesias without altering monoamine levels.

Animals↗
PubMed1983

The cerebrum of Dugesia gonocephala s.1. Platyhelminthes, Turbellaria, Tricladida. Morphological and functional observations.

Investigation of the cerebrum of Dugesia gonocephala s.1. using modern techniques has shown that the neurons of these animals situated at the bottom of the phylogenetic scale are basically the same as those of Vertebrates from the ultrastructural and molecular standpoints (tetanus toxin binding). There is no evidence of any biochemical glio-neuronal relationship, nor do the so-called supporting cells appear similar to the glial cells of the higher Vertebrates from this point of view.

Animals↗
PubMed1981

Photosensitization and the nervous system in the planarian Dugesia gonocephala. A histochemical, ultrastructural and behavioral investigation.

Photosensitization phenomena may be induced in planarias by eosin and hematoporphyrin, and as a result, dopamine agonistic behavior ("screw-like hyperkinesia") is set up in the animal. Histochemical, ultrastructural and pharmacological investigations have shown that this hyperkinesia is of post-synaptic origin in eosin photosensitization, and of pre-synaptic origin in hematoporphyrin photosensitization. The authors suggest an hypothesis to explain the different activity of the two photosensitizers, and discuss the validity of the experiment with regard to human porphyria.

Animals↗
PubMed1979

The pigmentary system of planaria. I. Morphology.

The pigmentary system of the planaria, Dugesia gonocephala s.l. (Platyhelminthes, Turbellaria, Tricladida), has been studied by light and electron microscopy. The system consists of granules contained in chromatophore-like cells embedded in the parenchyma. The cell processes penetrate between the muscle layers and extend to the sub-epidermal basal lamina. The nature of the pigment and the comparative anatomical significance of the chromatophore structure is discussed.

Animals↗
PubMed1979

The pigmentary system of planaria. II. Physiology and functional morphology.

The pigmentary system of the planaria, Dugesia gonocephala s.l. (Platyhelminthes, Turbellaria, Tricladida), consists of granules contained in chromatophore cells distributed in the parenchyma tissue. The administration of MSH release-inhibiting Factor (M.I.F.) leads to an easily observable general decolouration of the animal due to the migration of the pigment granules towards the deeper-lying cell nucleus. In planarians bisected transversely through the pharyngeal region, the decolouration occurs only in the cephalic segment, and the caudal segment remains dark. When, however, the decapitated caudal segment regenerates a head region, a decolouration response occurs when exposed to M.I.F. The significance of these results is discussed, and an hypothesis on the hormonal regulation of the pigmentary system is proposed.

Animals↗
PubMed1977

[Copper and nervous system. An experimental study (author's transl)].

Sodium azide is known to produce alterations in mammalian copper proteins, thus rendering them unable to bind exogenous metal, which remains in the "labile pool" condition. Continuous administration of sodium azide at LD50 for 30 days causes copper accumulation in several tissues and even in the nervous system, with characteristic changes in neurones and glial cells, very much resembling the alterations observed in Wilson's disease. Dietary copper administration, on the contrary, though raising the level of tissue-bound metal, does not produce cellular damage. These findings allow us to suppose that sodium azide may alterate the coppper chelating proteins in the tissues, especially in the nervous system, thus causing the storage of cell-toxic "labile pool" metal. The pathogenesis of Wilson's disease and the problem of "pathoclisis" in the nervous system are debated.

Animals↗