לוח שנה משולב

Chromatin architectural proteins bind to nucleosome without specificity for the underlying DNA sequence, alter the architecture of their cognate binding sites, leading to changes in chromatin structure and in the epigenetic marks in the tails of core histones. Competitive FRAP analysis of live cells and global ChIP sequence analysis reveal that the proteins function within a dynamic network of competitive interactions which play a functional role in the plasticity of the chromatin fiber. I will discuss the molecular mechanisms whereby architectural proteins alter the structure and function of chromatin and their role in transcriptional regulation and in establishing the cellular phenotype.

Are we our brains?
This question has troubled Western society for centuries, and still does today. Philosophers, psychologists, psychiatrists and neuroscientists - as much as the lay public - battle with the question of whether our personality, sense of self and states of mind can truly be explained through a scientific study of the brain, and whether one can at least correlate these with brain activity and structure. With the recent hyperbolic advances made in neuroscience, these questions arise in the form of intensive and broad debates on whether one may be able, at some point in the future, to fully account for what we cherish more than all, our sense that we are more than a lump of flesh.
This "more" however, does not belong to the realm of science: in the laboratory, one must deal with observable and operalizationable phenomena – everything core subjectivity ('qualia'- e.g. the experience of pain, of seeing the color red) is not. How can neuroscience approach the mind without losing its brain? How well has it done thus far, and what may we expect in the future?
This talk will suggest one – among many – approaches to this quandary, by looking at the history and current practices of brain localization. By introducing the mind-body conundrum into the study of this enterprise, we will consider the extent to which localization and classification of brain/mind functions serve as a way to materialize what is/was believed to be beyond 'matter'. The following debate will allow a discussion of an issue that concerns us all.

Understanding the neural mechanisms of visual object recognition is a difficult task in part, because for any given object it is not clear, which exact part of the brain to study. Yet evolution has presented us with a unique model system to decipher these mechanisms. The temporal lobes of macaque monkeys contain neural machinery to support face recognition consisting of six discrete patches of face-selective cortex. The two main organizing features of this system – concentration of cells encoding the same complex object category into modules and spatial separation of modules – make it possible to break down the process of face recognition into its components. In my talk I will present anatomical results supporting the notion that the distributed face patches really are part of an integrated face-processing machine, and electrophysiological results showing that each patch subserves a distinct computational function. In the second part of my talk I will turn to something completely different, attention. Using fMRI in macaque monkeys, we found a network of areas to be modulated by attention in motion-discrimination task, included a hitherto unsuspected region within inferotemporal cortex, PITd. We then targeted PITd for electrophysiological recordings and electrical microstimulation in different tasks to learn about its role in sensory information processing and spatial attention. I will discuss the somewhat radical conclusion we arrived at, namely that PITd may constitute a region for attentional control.

In order to function adaptively in a complex environment, individuals must both react to environmental threats and modify their reactions as circumstances change. A large body of work employing Pavlovian conditioning paradigms has generated a detailed neuroscientific understanding of how fear responses are acquired. More recent research has begun to probe the various means by which learned fear can be diminished. The vast majority of this research focuses on the mechanisms that underlie typical responding in an idealized “average” individual. A robust model of fear learning must also account for the substantial variability in fear reactivity and regulation that exists between individuals. The experiments presented here explore neurobiological and experiential factors that are associated with individual variation in the expression and regulation of conditioned fear using psychophysiology, neuroimaging, and behavioral genetics.