26 research outputs found

    Descartes’ Emotions: From the Body to the Body

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    Abstract: Emotions are currently at the center of a lively international and interdisciplinary debate. The first sections of this essay present a synthetic overview of its key features. The main sections provide a re-examination of one of the most historically significant developments in the field of affective studies. René Descartes’ approach to the study of emotions implies a positive assessment of the role of the body and a remarkable attenuation of his classical dualism that allows an innovative perspective on the subject. He inaugurated a new scientific style of research, which is one of the original sources of some key concepts of the current research.Keywords: Emotions; René Descartes; Embodied Cognition; Classification of Emotions; Philosophy of EmotionsLe emozioni di Descartes: dal corpo al corpoRiassunto: Le emozioni sono attualmente al centro di un dibattito internazionale e interdisciplinare molto vivace, di cui la prima sezione del saggio presenta una panoramica sintetica. La sezione principale propone un’analisi critica di uno dei passaggi storicamente più significativi nel campo dello studio dei fenomeni emotivi. L’approccio di Descartes al tema delle emozioni presuppone una considerazione positiva del ruolo del corpo e una notevole attenuazione del dualismo per cui è noto, consentendo così una prospettiva innovativa al tema. Descartes inaugura un nuovo stile di ricerca che è alle origini di alcuni concetti chiave della ricerca contemporanea.Parole chiave: Emozioni; René Descartes; Conoscenza incarnata; Classificazione delle emozioni; Filosofia delle emozion

    Effects of NSAIDs on the Release of Calcitonin Gene-Related Peptide and Prostaglandin E2 from Rat Trigeminal Ganglia

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    Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used to treat migraine, but the mechanisms of their effects in this pathology are not fully elucidated. The trigeminal ganglia and calcitonin gene-related peptide (CGRP) have been implicated in the pathophysiology of migraine. The release of CGRP and prostaglandin E 2 (PGE 2 ) from freshly isolated rat trigeminal ganglia was evaluated after oral administration of nimesulide, etoricoxib, and ketoprofen, NSAIDs with different pharmacological features. Thirty minutes after oral administration, nimesulide, 10 mg/Kg, decreased the GCRP release induced by an inflammatory soup, while the other NSAIDs were ineffective at this point in time. Two hours after oral nimesulide (5 and 10 mg/Kg) and ketoprofen (10 mg/Kg), but not of etoricoxib, a significant decrease in the CGRP release was observed. All drugs reduced PGE 2 , although with some differences in timing and doses, and the action on CGRP does not seem to be related to PGE 2 inhibition. The reduction of CGRP release from rat trigeminal ganglia after nimesulide and ketoprofen may help to explain the mechanism of action of NSAIDs in migraine. Since at 30 minutes only nimesulide was effective in reducing CGRP release, these results suggest that this NSAID may exert a particularly rapid effect in patients with migraine

    Nimesulide inhibits protein kinase C epsilon and substance P in sensory neurons – comparison with paracetamol

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    In this paper we describe new actions of nimesulide and paracetamol in cultured peripheral neurons isolated from rat dorsal root ganglia (DRG). Both drugs were able to decrease in a dose-dependent fashion the number of cultured DRG neurons showing translocation of protein kinase C epsilon (PKCÉ›) caused by exposure to 1 ÎĽM bradykinin or 100 nM thrombin. In addition, the level of substance P (SP) released by DRG neurons and the level of preprotachykinin mRNA expression were measured in basal conditions and after 70 minutes or 36 hours of stimulation with nerve growth factor (NGF) or with an inflammatory soup containing bradykinin, thrombin, endothelin-1, and KCl. Nimesulide (10 ÎĽM) significantly decreased the mRNA levels of the SP precursor preprotachykinin in basal and in stimulated conditions, and decreased the amount of SP released in the medium during stimulation of neurons with NGF or with the inflammatory soup. The effects of paracetamol (10 ÎĽM) on such response was lower. Nimesulide completely inhibited the release of prostaglandin E2 (PGE2) from DRG neurons, either basal or induced by NGF and by inflammatory soup, while paracetamol decreased PGE2 release only partially. Our data demonstrate, for the first time, a direct effect of two drugs largely used as analgesics on DRG neurons. The present results suggest that PKCÉ› might be a target for the effect of nimesulide and paracetamol, while inhibition of SP synthesis and release is clearly more relevant for nimesulide than for paracetamol mechanism of action
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