Theory of coupled neuronal-synaptic dynamics

In neural circuits, synaptic strengths influence neuronal activity by shaping network dynamics, and neuronal activity influences synaptic strengths through activity-dependent plasticity. Motivated by this fact, we study a recurrent-network model in which neuronal units and synaptic couplings are interacting dynamic variables, with couplings subject to Hebbian modification with decay around quenched random strengths. Rather than assigning a specific role to the plasticity, we use dynamical mean-field theory and other techniques to systematically characterize the neuronal-synaptic dynamics, revealing a rich phase diagram. Adding Hebbian plasticity slows activity in chaotic networks and can induce chaos in otherwise quiescent networks. Anti-Hebbian plasticity quickens activity and produces an oscillatory component. Analysis of the Jacobian shows that Hebbian and anti-Hebbian plasticity push locally unstable modes toward the real and imaginary axes, explaining these behaviors. Both random-matrix and Lyapunov analysis show that strong Hebbian plasticity segregates network timescales into two bands with a slow, synapse-dominated band driving the dynamics, suggesting a flipped view of the network as synapses connected by neurons. For increasing strength, Hebbian plasticity initially raises the complexity of the dynamics, measured by the maximum Lyapunov exponent and attractor dimension, but then decreases these metrics, likely due to the proliferation of stable fixed points. We compute the marginally stable spectra of such fixed points as well as their number, showing exponential growth with network size. In chaotic states with strong Hebbian plasticity, a stable fixed point of neuronal dynamics is destabilized by synaptic dynamics, allowing any neuronal state to be stored as a stable fixed point by halting the plasticity. This phase of freezable chaos offers a new mechanism for working memory.Comment: 20 pages, 9 figure

Abnormal infant islet morphology precedes insulin resistance in PCOS-like monkeys.

Polycystic ovary syndrome (PCOS) is prevalent in reproductive-aged women and confounded by metabolic morbidities, including insulin resistance and type 2 diabetes. Although the etiology of PCOS is undefined, contribution of prenatal androgen (PA) exposure has been proposed in a rhesus monkey model as premenopausal PA female adults have PCOS-like phenotypes in addition to insulin resistance and decreased glucose tolerance. PA female infants exhibit relative hyperinsulinemia, suggesting prenatal sequelae of androgen excess on glucose metabolism and an antecedent to future metabolic disease. We assessed consequences of PA exposure on pancreatic islet morphology to identify evidence of programming on islet development. Islet counts and size were quantified and correlated with data from intravenous glucose tolerance tests (ivGTT) obtained from dams and their offspring. Average islet size was decreased in PA female infants along with corresponding increases in islet number, while islet fractional area was preserved. Infants also demonstrated an increase in both the proliferation marker Ki67 within islets and the beta to alpha cell ratio suggestive of enhanced beta cell expansion. PA adult females have reduced proportion of small islets without changes in proliferative or apoptotic markers, or in beta to alpha cell ratios. Together, these data suggest in utero androgen excess combined with mild maternal glucose intolerance alter infant and adult islet morphology, implicating deviant islet development. Marked infant, but subtle adult, morphological differences provide evidence of islet post-natal plasticity in adapting to changing physiologic demands: from insulin sensitivity and relative hypersecretion to insulin resistance and diminished insulin response to glucose in the mature PCOS-like phenotype

Increased Yield of ttbb at Hadron Colliders in Low-Energy Supersymmetry

Light bottom squarks and gluinos have been invoked to explain the b quark pair production excess at the Tevatron. We investigate the associated production of ttbb at hadron colliders in this scenario, and find that the rates for this process are enhanced over the Standard Model prediction. If light gluinos exist, it may be possible to detect them at the Tevatron, and they could easily be observed at the LHC.Comment: 5p, references added, version accepted to PR