Demonstrating Hybrid Learning in a Flexible Neuromorphic Hardware System.

We present results from a new approach to learning and plasticity in neuromorphic hardware systems: to enable flexibility in implementable learning mechanisms while keeping high efficiency associated with neuromorphic implementations, we combine a general-purpose processor with full-custom analog elements. This processor is operating in parallel with a fully parallel neuromorphic system consisting of an array of synapses connected to analog, continuous time neuron circuits. Novel analog correlation sensor circuits process spike events for each synapse in parallel and in real-time. The processor uses this pre-processing to compute new weights possibly using additional information following its program. Therefore, to a certain extent, learning rules can be defined in software giving a large degree of flexibility. Synapses realize correlation detection geared towards Spike-Timing Dependent Plasticity (STDP) as central computational primitive in the analog domain. Operating at a speed-up factor of 1000 compared to biological time-scale, we measure time-constants from tens to hundreds of micro-seconds. We analyze variability across multiple chips and demonstrate learning using a multiplicative STDP rule. We conclude that the presented approach will enable flexible and efficient learning as a platform for neuroscientific research and technological applications.

NFATc1 induction in peripheral T and B lymphocytes.

NFAT transcription factors control the proliferation and survival of peripheral lymphocytes. We have reported previously that the short isoform NFATc1/αA whose generation is induced by immune receptor stimulation supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cells. We will show in this study that in novel bacterial artificial chromosome transgenic mice that express EGFP under the control of entire Nfatc1 locus the Nfatc1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripheral T and B cells. Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated in B, Th1, and Th2 cells, but only weakly in T regulatory, Th9, and Th17 cells in vitro whose generation is affected by TGFß. In naive lymphocytes, persistent immune receptor signals led to a 3-5 increase in NFATc1/αA RNA levels during primary and secondary stimulation, but a much stronger induction was observed at the protein level. Whereas anti-CD3(+)CD28 stimulation of primary T cells induces both NFATc1/αA and their proliferation and survival, anti-IgM stimulation of B cells induces NFATc1/αA and proliferation, but activation-induced cell death after 3-d incubation in vitro. The anti-IgM-mediated activation-induced cell death induction of B cells in vitro is suppressed by anti-CD40-, LPS-, and CpG-mediated signals. In addition to inducing NF-κB factors, together with anti-IgM, these signals also support the generation of NFATc1/αA. According to these data and the architecture of its promoter region, the Nfatc1 gene resembles a primary response gene whose induction is affected at the posttranscriptional level.