Gregory Lynch

Gadamer claims that human beings are capable of understanding only ‘aspects’ of reality, yet he also holds that, through these aspects, we understand reality itself. In this sense he is an ‘aspectival realist.’ This paper considers two attempts to explain Gadamer’s aspectival realism: the ‘schematization’ reading defended by Charles Taylor, and the ‘holist’ reading of Brice Wachterhauser. I criticize these views on two fronts: that they are at odds with Gadamer’s texts, and that they fail to reconcile aspectivalism and realism into a consistent philosophical position. I articulate an alternative reading that I call the ‘presentational’ account. At the heart of this account is the claim that, on Gadamer’s view, the ‘occasionality’ that characterizes language also characterizes being itself. I argue both that this interpretation fits Gadamer’s texts better than the views currently on offer in the literature and that it avoids the philosophical difficulties those views encounter.

Stabilization of long-term potentiation depends on reorganization of the dendritic spine actin cytoskeleton. The present study tested whether this involves activity-driven effects on the actin-regulatory protein cortactin, and whether such effects are disturbed in the Fmr1 knock-out model of fragile X syndrome, in which stabilization of both actin filaments and LTP is impaired. LTP induced by theta burst stimulation in hippocampal slices from wild-type mice was associated with rapid, broadly distributed, and NMDA receptor-dependent decreases in synapse-associated cortactin. The reduction in cortactin content was blocked by blebbistatin, while basal levels were reduced by nocodazole, indicating that cortactin's movements into and away from synapses are regulated by microtubule and actomyosin motors, respectively. These results further suggest that synapse-specific LTP influences cytoskeletal elements at distant connections. The rapid effects of TBS on synaptic cortactin content were absent in Fmr1 KOs as was evidence for activity-driven phosphorylation of the protein or its upstream kinase, ERK1/2. Phosphorylation regulates cortactin's interactions with actin, and coprecipitation of the two proteins was reduced in the KOs. We propose that, in the KOs, excessive basal phosphorylation of ERK1/2 disrupts its interactions with cortactin, thereby blocking the latter protein's use of actomyosin transport systems. These impairments are predicted to compromise the response of the subsynaptic cytoskeleton to learning-related afferent activity, both locally and at distant sites. © 2012 the authors.