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Tom Tetzlaff

Publications and source records attributed to Tom Tetzlaff.

21 records · Page 2Linked to original sources

Echoes in correlated neural systems

Correlations are employed in modern physics to explain microscopic and macroscopic phenomena, like the fractional quantum Hall effect and the Mott insulator state in high temperature superconductors and ultracold atoms. Simultaneously probed neurons in the intact brain reveal correlations between their activity, an important measure to study information processing in the brain that also influences macroscopic signals of neural activity, like the electro encephalogram (EEG). Networks of spiking neurons differ from most physical systems: The interaction between elements is directed, time delayed, mediated by short pulses, and each neuron receives events from thousands of neurons. Even the stationary state of the network cannot be described by equilibrium statistical mechanics. Here we develop a quantitative theory of pairwise correlations in finite sized random networks of spiking neurons. We derive explicit analytic expressions for the population averaged cross correlation functions. Our theory explains why the intuitive mean field description fails, how the echo of single action potentials causes an apparent lag of inhibition with respect to excitation, and how the size of the network can be scaled while maintaining its dynamical state. Finally, we derive a new criterion for the emergence of collective oscillations from the spectrum of the time-evolution propagator.

q-bio.NC↗

Frequency dependence of signal power and spatial reach of the local field potential

The first recording of electrical potential from brain activity was reported already in 1875, but still the interpretation of the signal is debated. To take full advantage of the new generation of microelectrodes with hundreds or even thousands of electrode contacts, an accurate quantitative link between what is measured and the underlying neural circuit activity is needed. Here we address the question of how the observed frequency dependence of recorded local field potentials (LFPs) should be interpreted. By use of a well-established biophysical modeling scheme, combined with detailed reconstructed neuronal morphologies, we find that correlations in the synaptic inputs onto a population of pyramidal cells may significantly boost the low-frequency components of the generated LFP. We further find that these low-frequency components may be less `local' than the high-frequency LFP components in the sense that (1) the size of signal-generation region of the LFP recorded at an electrode is larger and (2) that the LFP generated by a synaptically activated population spreads further outside the population edge due to volume conduction.

q-bio.NC↗

Decorrelation of neural-network activity by inhibitory feedback

Correlations in spike-train ensembles can seriously impair the encoding of information by their spatio-temporal structure. An inevitable source of correlation in finite neural networks is common presynaptic input to pairs of neurons. Recent theoretical and experimental studies demonstrate that spike correlations in recurrent neural networks are considerably smaller than expected based on the amount of shared presynaptic input. By means of a linear network model and simulations of networks of leaky integrate-and-fire neurons, we show that shared-input correlations are efficiently suppressed by inhibitory feedback. To elucidate the effect of feedback, we compare the responses of the intact recurrent network and systems where the statistics of the feedback channel is perturbed. The suppression of spike-train correlations and population-rate fluctuations by inhibitory feedback can be observed both in purely inhibitory and in excitatory-inhibitory networks. The effect is fully understood by a linear theory and becomes already apparent at the macroscopic level of the population averaged activity. At the microscopic level, shared-input correlations are suppressed by spike-train correlations: In purely inhibitory networks, they are canceled by negative spike-train correlations. In excitatory-inhibitory networks, spike-train correlations are typically positive. Here, the suppression of input correlations is not a result of the mere existence of correlations between excitatory (E) and inhibitory (I) neurons, but a consequence of a particular structure of correlations among the three possible pairings (EE, EI, II).

q-bio.NC↗