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Priesemann, V.

Publications and source records attributed to Priesemann, V..

2 recordsLinked to original sources

Inference, validation and predictions about statistics and propagation of cortical spiking in vivo

Electrophysiological recordings of spiking activity can only access a small fraction of all neurons simultaneously. This spatial subsampling has hindered characterizing even most basic properties of collective spiking in cortex. In particular, two contradictory hypotheses prevailed for over a decade: the first proposed an asynchronous irregular, the second a critical state. While distinguishing them is straightforward in models, we show that in experiments classical approaches fail to infer them correctly, because subsampling can bias measures as basic as the correlation strength. Deploying a novel, subsampling-invariant estimator, we find evidence that in vivo cortical dynamics clearly differs from asynchronous or critical dynamics, and instead occupies a narrow \"reverberating\" regime, consistently across multiple mammalian species and cortical areas. These results enabled us to predict cortical properties that are difficult or impossible to obtain experimentally, including responses to minimal perturbations, intrinsic network timescales, and the strength of external input compared to recurrent activation.

neuroscience

Homeostatic plasticity and external input shape neural network dynamics

In vitro and in vivo spiking activity clearly differ. Whereas networks in vitro develop strong bursts separated by periods of very little spiking activity, in vivo cortical networks show continuous activity. This is puzzling considering that both networks presumably share similar single-neuron dynamics and plasticity rules. We propose that the defining difference between in vitro and in vivo dynamics is the strength of external input. In vitro, networks are virtually isolated, whereas in vivo every brain area receives continuous input. We analyze a model of spiking neurons in which the input strength, mediated by spike rate homeostasis, determines the characteristics of the dynamical state. In more detail, our analytical and numerical results on various network topologies show consistently that under increasing input, homeostatic plasticity generates distinct dynamic states, from bursting, to close-to-critical, reverberating and irregular states. This implies that the dynamic state of a neural network is not fixed but can readily adapt to the input strengths. Indeed, our results match experimental spike recordings in vitro and in vivo: the in vitro bursting behavior is consistent with a state generated by very low network input (< 0.1%), whereas in vivo activity suggests that on the order of 1% recorded spikes are input-driven, resulting in reverberating dynamics. Importantly, this predicts that one can abolish the ubiquitous bursts of in vitro preparations, and instead impose dynamics comparable to in vivo activity by exposing the system to weak long-term stimulation, thereby opening new paths to establish an in vivo-like assay in vitro for basic as well as neurological studies.

neuroscience