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Biomedical subjects

L Bonasera

Publications and source records attributed to L Bonasera.

At least 19 recordsLinked to original sources
PubMed1996

Peripheral administration of NMDA, AMPA or KA results in pain behaviors in rats.

The present study investigated the role of N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptor subtypes in peripheral pain transmission. Activation of NMDA, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate acid (KA) receptors in glabrous skin of the rat hindpaw resulted in mechanical allodynia and mechanical hyperalgesia. These agonist-induced pain behaviors were attenuated following peripheral injection of appropriate antagonists (MK-801 and CNQX). Thus, activation of NMDA, AMPA or KA receptors at the level of the peripheral nerve terminal can produce nociceptive behavior. These data suggest that topical application of glutamate receptor antagonists may be useful in treating pain disorders. Since all three receptor subtypes are involved in peripheral pain transmission, however, it will be necessary to antagonize multiple glutamate receptor subtypes to achieve effective pain relief.

Animals↗
PubMed1980

Calcium binding to mastocyte plasma membrane.

Rat mastocyte plasma membrane possess two major classes of calcium binding sites which have widely different affinity. At pH 7.5 the low affinity sites can bind about 88 nmol of Ca2+ per milligram of membrane protein and are half-saturated at 125 micro M Ca2+, whereas the high-affinity sites bind about 12 nmol of Ca2+ per milligram of membrane protein and are half-saturated at 5.5 micro M Ca2+. Membrane phospholipids and neuraminic acid residues account for approximately 87% of calcium binding.

Animals↗
PubMed1979

Hydrocortisone increases the responsiveness of mast cells to beta-adrenergic agonists by an action distal to the beta-adrenoreceptors.

Hydrocortisone in pharmacologically attainable concentrations potentiates beta-adrenergic-stimulated cyclic AMP accumulation in rat peritoneal mast cells. Direct binding studies using 3H-dihydroalprenolol indicated no significant changes in the number of beta-adrenoreceptors or in the kinetics of the interaction of the radio-ligand with receptors after treatment of mast cells with the corticosteroid. Competition binding studies with epinephrine revealed no hydrocortisone-induced change in Kd values for this agonist. It is concluded that hydrocortisone-induced stimulation of cyclic AMP synthesis results from an effect that occurs beyond the interaction of the beta-adrenergic agonist with its receptor.

Adrenergic beta-Agonists↗
PubMed1978

Biosynthesis and release of prostaglandins by mast cells.

Rat mast cells, isolated from peritoneal fluids, were found to release substantial amounts of immunoreactive E-type prostaglandin when stimulated in vitro by foetal calf serum or incubated in the presence of arachidonic acid. Extracellular accumulation of iPGE reflected synthesis, rather than release of preformed material, since it was abolished by indomethacin, a potent and relatively specific inhibitor of prostaglandin synthetase. Hydrocortisone and Compound 48/80, in such experimental conditions, did not affect PGE release.

Animals↗
PubMed1978

Influence of hydrocortisone on the modulation of the inflammatory response.

In vitro hydrocortisone, in pharmacologically attainable concentrations, binds nonspecifically to rat peritoneal mast cells and amplifies the stimulating effects of PGE1 on membrane-bound adenylate cyclase. As a consequence, the intracellular concentration of cyclic AMP in the target cells increases and histamine release is markedly reduced. Deoxycorticosterone, at the same concentrations, has no effect. These findings may in part explain the mechanism of action of anti-inflammatory steroids, possibly related to the modulating effects of E-type prostaglandins.

Animals↗