examined uncinate and sternal length in birds. Uncinate length varies according to the specilisations to different modes of locomotion utilised by the bird. Walking birds have the shortest uncinate length, flying and swimming birds have intermediate lengths while diving birds have the longest processes. Sternal dimensions also vary according to mode of locomotion. Walking birds have the shortest while diving birds have the longest and widest sternum. The correlation between uncinate length and sternal morphology is indicative of a functional link. We suggest there may be fundamental differences in the breathing mechanics of birds associated with adaptations in accessory breathing structures linked to different forms of locomotion. doi:10.1016/j.cbpa.2007.01.371 A12.13 Apoptosis in salmonid cell lines: The importance of apoptotic volume decrease, chloride fluxes and potassium fluxes in staurosporine-induced cell death G. Krumschnabel, (University of Innsbruck); C. Manzl, (Innsbruck Medical University); P. Schwarzbaum (University of Buenos Aires) In numerous mammalian cell models apoptosis is associated with cell shrinkage. Inhibition of this apoptotic volume decrease by blockers of swelling-activated ion transporters has been repeatedly found to be cytoprotective, suggesting that cell shrinkage is an important early event in this mode of cell death. In hepatoma and gill cells from rainbow trout staurosporine induced apoptosis, as assessed by activation of effector caspases, nuclear condensation, and a decrease of mitochondrial membrane potential (MMP), and these changes were accompanied by cell shrinkage. The Cl - transport inhibitor DIDS and the K + channel inhibitor quinidine both prevented apoptotic volume decrease, but only DIDS also inhibited apoptosis. Other inhibitors of Cl - fluxes such as SITS and NPPB did not prevent cell shrinkage, but still prevented caspase activation. Furthermore, although cyclosporine A, a blocker of the mitochondrial permeability transition pore (PTP), also inhib- ited the decrease of MMP, it did not prevent activation of caspases. Taken together, these results indicate that the protective effect of DIDS is not due to inhibition of cell shrinkage, but due to the blockage of Cl - fluxes activated upon staurosporine-exposure. In addition, it appears that not the inhibition of PTP opening, but possibly inhibition of mitochondrial outer membrane permeabilization is critical for the protective effect of DIDS. Supported by “Aktion D. Swarowski” of the University of Innsbruck. P.J.S. was sponsored by UBA, CONICET and ANPCYT. doi:10.1016/j.cbpa.2007.01.372 A12.14 Role and function of the apoptosis-regulator PIDD C. Manzl, (Medical University Innsbruck); V. Labi, F. Baumgartner, G. Boeck, A. Villunger, (Medical University Innsbruck, Austria); J. Tschopp, (Universite de Lausanne, Switzerland) The p53-induced protein with a death domain (PIDD) is a gene activated in response to p53 activation in a wide variety of cells and tissues. Together with the adapter molecule RAIDD, PIDD is involved in the activation of caspase-2, triggering the formation of a pro- apoptotic complex called the “PIDDosome”. PIDD has recently also been implicated in DNA damage-induced NF-κB activa- tion, promoting the transcription of survival genes. The mechanism allowing PIDD to sequentially activate these two opposing signalling pathways involves auto-proteolytic clea- vage, leading to the generation of two fragments that can preferentially promote NF-κB or caspase-2 activation. In order to investigate the physiological role of PIDD in the DNA damage response, we have generated PIDD-deficient mice. The mice are viable and show no overt phenotypic abnormalities. However, the thymic cellularity is lower in female pidd -/- mice when compared to wild-type mice. To study the importance of PIDD for DNA damage-induced apoptosis, thymocytes were isolated from wt and pidd -/- mice and treated with ?-irradiation ex-vivo, but no difference in cell survival was observed. Activation of caspase-2 could readily be detected in primary thymocytes treated with ?-irradiation, etoposide, and after a prolonged recovery from heat-shock indicating that at least one additional pathway to caspase-2 activation exists. Staurosporine and heat-shock reduced mito- chondrial membrane potential in primary splenocytes but not in thymocytes of pidd -/- mice. Interestingly, pidd -/- mouse embryonic fibroblasts (MEFs) showed better survival after heat-shock treatment than wild-type MEF indicating that the net-effect of PIDD-deficiency may be decreased stress- tolerance due to impaired NF-Kb activation. doi:10.1016/j.cbpa.2007.01.373 A12.15 Dippu-allatostatin and proctolin are releasing factors in the locust, Locusta migratoria A. Lange, (University of Toronto); L. Clark, J. Zhang, S. Tobe (Toronto) The allatostatins are neuropeptides best known for their ability to inhibit juvenile hormone synthesis in the corpora allata (CA) of insects, especially the cockroach, Diploptera punctata. Evidence is presented through the use of immunohistochemistry that allatostatin-like immunoreactivity exists within lateral neurosecretory cells (LNCs) which project to the corpus cardiacum (CC) and CA of L. migratoria. Allatostatin-like S175 Abstracts / Comparative Biochemistry and Physiology, Part A 146 (2007) S171–S188