4,840 research outputs found
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)
Intrinsically-generated fluctuating activity in excitatory-inhibitory networks
Recurrent networks of non-linear units display a variety of dynamical regimes
depending on the structure of their synaptic connectivity. A particularly
remarkable phenomenon is the appearance of strongly fluctuating, chaotic
activity in networks of deterministic, but randomly connected rate units. How
this type of intrinsi- cally generated fluctuations appears in more realistic
networks of spiking neurons has been a long standing question. To ease the
comparison between rate and spiking networks, recent works investigated the
dynami- cal regimes of randomly-connected rate networks with segregated
excitatory and inhibitory populations, and firing rates constrained to be
positive. These works derived general dynamical mean field (DMF) equations
describing the fluctuating dynamics, but solved these equations only in the
case of purely inhibitory networks. Using a simplified excitatory-inhibitory
architecture in which DMF equations are more easily tractable, here we show
that the presence of excitation qualitatively modifies the fluctuating activity
compared to purely inhibitory networks. In presence of excitation,
intrinsically generated fluctuations induce a strong increase in mean firing
rates, a phenomenon that is much weaker in purely inhibitory networks.
Excitation moreover induces two different fluctuating regimes: for moderate
overall coupling, recurrent inhibition is sufficient to stabilize fluctuations,
for strong coupling, firing rates are stabilized solely by the upper bound
imposed on activity, even if inhibition is stronger than excitation. These
results extend to more general network architectures, and to rate networks
receiving noisy inputs mimicking spiking activity. Finally, we show that
signatures of the second dynamical regime appear in networks of
integrate-and-fire neurons
Locking of correlated neural activity to ongoing oscillations
Population-wide oscillations are ubiquitously observed in mesoscopic signals
of cortical activity. In these network states a global oscillatory cycle
modulates the propensity of neurons to fire. Synchronous activation of neurons
has been hypothesized to be a separate channel of signal processing information
in the brain. A salient question is therefore if and how oscillations interact
with spike synchrony and in how far these channels can be considered separate.
Experiments indeed showed that correlated spiking co-modulates with the static
firing rate and is also tightly locked to the phase of beta-oscillations. While
the dependence of correlations on the mean rate is well understood in
feed-forward networks, it remains unclear why and by which mechanisms
correlations tightly lock to an oscillatory cycle. We here demonstrate that
such correlated activation of pairs of neurons is qualitatively explained by
periodically-driven random networks. We identify the mechanisms by which
covariances depend on a driving periodic stimulus. Mean-field theory combined
with linear response theory yields closed-form expressions for the
cyclostationary mean activities and pairwise zero-time-lag covariances of
binary recurrent random networks. Two distinct mechanisms cause time-dependent
covariances: the modulation of the susceptibility of single neurons (via the
external input and network feedback) and the time-varying variances of single
unit activities. For some parameters, the effectively inhibitory recurrent
feedback leads to resonant covariances even if mean activities show
non-resonant behavior. Our analytical results open the question of
time-modulated synchronous activity to a quantitative analysis.Comment: 57 pages, 12 figures, published versio
The effect of heterogeneity on decorrelation mechanisms in spiking neural networks: a neuromorphic-hardware study
High-level brain function such as memory, classification or reasoning can be
realized by means of recurrent networks of simplified model neurons. Analog
neuromorphic hardware constitutes a fast and energy efficient substrate for the
implementation of such neural computing architectures in technical applications
and neuroscientific research. The functional performance of neural networks is
often critically dependent on the level of correlations in the neural activity.
In finite networks, correlations are typically inevitable due to shared
presynaptic input. Recent theoretical studies have shown that inhibitory
feedback, abundant in biological neural networks, can actively suppress these
shared-input correlations and thereby enable neurons to fire nearly
independently. For networks of spiking neurons, the decorrelating effect of
inhibitory feedback has so far been explicitly demonstrated only for
homogeneous networks of neurons with linear sub-threshold dynamics. Theory,
however, suggests that the effect is a general phenomenon, present in any
system with sufficient inhibitory feedback, irrespective of the details of the
network structure or the neuronal and synaptic properties. Here, we investigate
the effect of network heterogeneity on correlations in sparse, random networks
of inhibitory neurons with non-linear, conductance-based synapses. Emulations
of these networks on the analog neuromorphic hardware system Spikey allow us to
test the efficiency of decorrelation by inhibitory feedback in the presence of
hardware-specific heterogeneities. The configurability of the hardware
substrate enables us to modulate the extent of heterogeneity in a systematic
manner. We selectively study the effects of shared input and recurrent
connections on correlations in membrane potentials and spike trains. Our
results confirm ...Comment: 20 pages, 10 figures, supplement
Deterministic networks for probabilistic computing
Neural-network models of high-level brain functions such as memory recall and
reasoning often rely on the presence of stochasticity. The majority of these
models assumes that each neuron in the functional network is equipped with its
own private source of randomness, often in the form of uncorrelated external
noise. However, both in vivo and in silico, the number of noise sources is
limited due to space and bandwidth constraints. Hence, neurons in large
networks usually need to share noise sources. Here, we show that the resulting
shared-noise correlations can significantly impair the performance of
stochastic network models. We demonstrate that this problem can be overcome by
using deterministic recurrent neural networks as sources of uncorrelated noise,
exploiting the decorrelating effect of inhibitory feedback. Consequently, even
a single recurrent network of a few hundred neurons can serve as a natural
noise source for large ensembles of functional networks, each comprising
thousands of units. We successfully apply the proposed framework to a diverse
set of binary-unit networks with different dimensionalities and entropies, as
well as to a network reproducing handwritten digits with distinct predefined
frequencies. Finally, we show that the same design transfers to functional
networks of spiking neurons.Comment: 22 pages, 11 figure
Regulation of Irregular Neuronal Firing by Autaptic Transmission
The importance of self-feedback autaptic transmission in modulating
spike-time irregularity is still poorly understood. By using a biophysical
model that incorporates autaptic coupling, we here show that self-innervation
of neurons participates in the modulation of irregular neuronal firing,
primarily by regulating the occurrence frequency of burst firing. In
particular, we find that both excitatory and electrical autapses increase the
occurrence of burst firing, thus reducing neuronal firing regularity. In
contrast, inhibitory autapses suppress burst firing and therefore tend to
improve the regularity of neuronal firing. Importantly, we show that these
findings are independent of the firing properties of individual neurons, and as
such can be observed for neurons operating in different modes. Our results
provide an insightful mechanistic understanding of how different types of
autapses shape irregular firing at the single-neuron level, and they highlight
the functional importance of autaptic self-innervation in taming and modulating
neurodynamics.Comment: 27 pages, 8 figure
How adaptation currents change threshold, gain and variability of neuronal spiking
Many types of neurons exhibit spike rate adaptation, mediated by intrinsic
slow -currents, which effectively inhibit neuronal responses. How
these adaptation currents change the relationship between in-vivo like
fluctuating synaptic input, spike rate output and the spike train statistics,
however, is not well understood. In this computational study we show that an
adaptation current which primarily depends on the subthreshold membrane voltage
changes the neuronal input-output relationship (I-O curve) subtractively,
thereby increasing the response threshold. A spike-dependent adaptation current
alters the I-O curve divisively, thus reducing the response gain. Both types of
adaptation currents naturally increase the mean inter-spike interval (ISI), but
they can affect ISI variability in opposite ways. A subthreshold current always
causes an increase of variability while a spike-triggered current decreases
high variability caused by fluctuation-dominated inputs and increases low
variability when the average input is large. The effects on I-O curves match
those caused by synaptic inhibition in networks with asynchronous irregular
activity, for which we find subtractive and divisive changes caused by external
and recurrent inhibition, respectively. Synaptic inhibition, however, always
increases the ISI variability. We analytically derive expressions for the I-O
curve and ISI variability, which demonstrate the robustness of our results.
Furthermore, we show how the biophysical parameters of slow
-conductances contribute to the two different types of adaptation
currents and find that -activated -currents are
effectively captured by a simple spike-dependent description, while
muscarine-sensitive or -activated -currents show a
dominant subthreshold component.Comment: 20 pages, 8 figures; Journal of Neurophysiology (in press
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