לוח שנה משולב

I will discuss our efforts towards understanding synaptic and circuit dysfunction in Fragile X syndrome, the most common heritable cause of intellectual disability and the leading genetic cause of autism. I will describe our studies identifying major presynaptic defects in excitability and neurotransmitter release in Fragile X and the role of ion channel dysregulation in these deficits. Finally, I will present evidence for a direct link between presynaptic dysregulation and specific Fragile X phenotypes in a patient.

Speakers: Meirav Pinkas, Anat Daniel

It is a well-known result from Hermann Weyl that if alpha is an irrational number in [0,1) then the number of visits of successive multiples of alpha modulo one in an interval contained in [0,1) is proportional to the size of the interval. In this talk we will revisit this problem, now looking at finer joint asymptotics of visits to several intervals with rational end points. We observe that the visit distribution can be modelled using random affine transformations

Primates live in environments characterized by continuous, complex cycles of social interactions, where the actions of any group member necessarily influences those of the other members. This raises the question of the extent to which adaptive behavior in social encounters involves specialized mechanisms to represent others’ intentions and affective states. In my talk, I will explore this topic at the behavioral level - asking whether monkeys take into account the welfare of their conspecific when making decisions- and at the brain level - asking what type of information about a social partner is encoded by single neurons in the amygdala and anterior insula. I will try yo argue that these two structures carry neuronal mechanisms for empathy and perspective taking.

Gut IgA production plays important an role in both shaping the composition of the gut commensal microbiota and in the protection from pathogens entering through the mucosa. While many recent studies have addressed interactions between the microbiota and IgA, fewer has studied in induction of IgA response, in particular at an antigen-specific level. Using cholera toxin conjugated to the well-known B cell hapten NP as an antigen we have followed antigen-specific gut IgA responses in vivo and compared them to response against antigens distributed systemically. In this seminar I will discuss the initiation of the response in the small intestine that differ from systemic responses in that B cells in PP invade pre-existing germinal centres (GC) rather than forming new GC. Furthermore, I will discuss the presence of subtypes of activated B cells in the PP during the response, where some B cells appear to migrate from the germinal centre, and how this allows for synchronization of the response between distinct PP along the gut. Finally, I will discuss the formation of life long B cell memory following oral immunization.