Malséance : la mort et l'image dans le (méta)théâtre de Samuel Beckett et de Jean Genet

Both ludic and macabre, the theatrical works of Samuel Beckett and Jean Genet are a paradox to behold. Indeed, as this thesis seeks to illustrate, despite their vastly differing aesthetics, at the core of each playwright’s stage productions is a tension between the characters’ yearning for silence and invisibility, and the continual creation of an often humorous, chaotic, exaggerated or theatrical image that depicts this very longing. Seeking an impossible intersection between their image and their death, they are trapped in a double bind that guarantees aesthetic failure. In order to grasp the close, yet delicate, relationship between the image of death and the death of the image, as presented in the plays of Beckett and Genet, we will explore how the characters’ creative processes deflate the very images — both visual and auditory — that they create. More specifically, we will examine how mimesis both liberates and confines the characters; while the symbolic realm provides the only means of self-representation, it is also a source of profound alienation and powerlessness, for it never adequately conveys meaning. Thus, body, gesture, language and voice are each the site of simultaneous and ceaseless reappearance and disappearance, for which death remains the only (aporetic) cure. Struggling against theatrical form, which demands the actors’ and the audience’s physical presence, both playwrights make shrewd use of metatheatre to slowly empty the stage and thereby suggest the impending, yet impossible, erasure of their characters.

Cold acclimation of chill coma mechanisms in the locust CNS

Temperature has profound effects on the neural function and behaviour of insects. When exposed to low temperature, migratory locusts (Locusta migratoria) enter chill coma (neuromuscular paralysis) and can resume normal body functions after returning to normal temperature. Our laboratory has studied phenomena underlying environmental stress-induced comas in locusts and found that they are associated with a sudden loss of K+ homeostasis and also a temporary electrical silence in the central nervous system (CNS). However, the mechanisms underlying chill coma entry and recovery are not well understood, particularly the role of the CNS has not been determined. Here, I investigated neural function during chill coma in the locust by measuring electrical activity in the CNS. As pre-exposure to moderately low temperatures, either chronically (cold acclimation) or acutely (rapid cold hardening; RCH), has been found to improve the insect’s cold tolerance, I also determined cold acclimation and RCH protocols that will improve the locust's cold tolerance and whether these protocols affect neural shutdown during chill coma in the locust. With an implanted thermocouple in the thorax, I determined the temperature associated with a loss of responsiveness (CTmin) in intact male adult locusts. In parallel experiments, I recorded field potential (FP) in the metathoracic ganglion (MTG) in semi-intact preparations to determine the temperature that would induce neural shutdown. I found that acclimation at 10 ˚C and RCH at 4 ˚C reduced chill coma recovery time (CCRT) in intact animal preparations and RCH at 4 ˚C for 4 hours reduced the temperature at neural shutdown in semi-intact preparations. These results suggest that pre-exposure to cold can improve the locust's resistance to chill coma and support the notion that the CNS has a role in determining entry into and exit from chill coma in locusts.