2,800 research outputs found
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
Characterizing synaptic conductance fluctuations in cortical neurons and their influence on spike generation
Cortical neurons are subject to sustained and irregular synaptic activity
which causes important fluctuations of the membrane potential (Vm). We review
here different methods to characterize this activity and its impact on spike
generation. The simplified, fluctuating point-conductance model of synaptic
activity provides the starting point of a variety of methods for the analysis
of intracellular Vm recordings. In this model, the synaptic excitatory and
inhibitory conductances are described by Gaussian-distributed stochastic
variables, or colored conductance noise. The matching of experimentally
recorded Vm distributions to an invertible theoretical expression derived from
the model allows the extraction of parameters characterizing the synaptic
conductance distributions. This analysis can be complemented by the matching of
experimental Vm power spectral densities (PSDs) to a theoretical template, even
though the unexpected scaling properties of experimental PSDs limit the
precision of this latter approach. Building on this stochastic characterization
of synaptic activity, we also propose methods to qualitatively and
quantitatively evaluate spike-triggered averages of synaptic time-courses
preceding spikes. This analysis points to an essential role for synaptic
conductance variance in determining spike times. The presented methods are
evaluated using controlled conductance injection in cortical neurons in vitro
with the dynamic-clamp technique. We review their applications to the analysis
of in vivo intracellular recordings in cat association cortex, which suggest a
predominant role for inhibition in determining both sub- and supra-threshold
dynamics of cortical neurons embedded in active networks.Comment: 9 figures, Journal of Neuroscience Methods (in press, 2008
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)
Fundamental activity constraints lead to specific interpretations of the connectome
The continuous integration of experimental data into coherent models of the
brain is an increasing challenge of modern neuroscience. Such models provide a
bridge between structure and activity, and identify the mechanisms giving rise
to experimental observations. Nevertheless, structurally realistic network
models of spiking neurons are necessarily underconstrained even if experimental
data on brain connectivity are incorporated to the best of our knowledge.
Guided by physiological observations, any model must therefore explore the
parameter ranges within the uncertainty of the data. Based on simulation
results alone, however, the mechanisms underlying stable and physiologically
realistic activity often remain obscure. We here employ a mean-field reduction
of the dynamics, which allows us to include activity constraints into the
process of model construction. We shape the phase space of a multi-scale
network model of the vision-related areas of macaque cortex by systematically
refining its connectivity. Fundamental constraints on the activity, i.e.,
prohibiting quiescence and requiring global stability, prove sufficient to
obtain realistic layer- and area-specific activity. Only small adaptations of
the structure are required, showing that the network operates close to an
instability. The procedure identifies components of the network critical to its
collective dynamics and creates hypotheses for structural data and future
experiments. The method can be applied to networks involving any neuron model
with a known gain function.Comment: J. Schuecker and M. Schmidt contributed equally to this wor
The correlation structure of local cortical networks intrinsically results from recurrent dynamics
The co-occurrence of action potentials of pairs of neurons within short time
intervals is known since long. Such synchronous events can appear time-locked
to the behavior of an animal and also theoretical considerations argue for a
functional role of synchrony. Early theoretical work tried to explain
correlated activity by neurons transmitting common fluctuations due to shared
inputs. This, however, overestimates correlations. Recently the recurrent
connectivity of cortical networks was shown responsible for the observed low
baseline correlations. Two different explanations were given: One argues that
excitatory and inhibitory population activities closely follow the external
inputs to the network, so that their effects on a pair of cells mutually
cancel. Another explanation relies on negative recurrent feedback to suppress
fluctuations in the population activity, equivalent to small correlations. In a
biological neuronal network one expects both, external inputs and recurrence,
to affect correlated activity. The present work extends the theoretical
framework of correlations to include both contributions and explains their
qualitative differences. Moreover the study shows that the arguments of fast
tracking and recurrent feedback are not equivalent, only the latter correctly
predicts the cell-type specific correlations
The Spatial Structure of Stimuli Shapes the Timescale of Correlations in Population Spiking Activity
Throughout the central nervous system, the timescale over which pairs of neural spike trains are correlated is shaped by stimulus structure and behavioral context. Such shaping is thought to underlie important changes in the neural code, but the neural circuitry responsible is largely unknown. In this study, we investigate a stimulus-induced shaping of pairwise spike train correlations in the electrosensory system of weakly electric fish. Simultaneous single unit recordings of principal electrosensory cells show that an increase in the spatial extent of stimuli increases correlations at short (~10 ms) timescales while simultaneously reducing correlations at long (~100 ms) timescales. A spiking network model of the first two stages of electrosensory processing replicates this correlation shaping, under the assumptions that spatially broad stimuli both saturate feedforward afferent input and recruit an open-loop inhibitory feedback pathway. Our model predictions are experimentally verified using both the natural heterogeneity of the electrosensory system and pharmacological blockade of descending feedback projections. For weak stimuli, linear response analysis of the spiking network shows that the reduction of long timescale correlation for spatially broad stimuli is similar to correlation cancellation mechanisms previously suggested to be operative in mammalian cortex. The mechanism for correlation shaping supports population-level filtering of irrelevant distractor stimuli, thereby enhancing the population response to relevant prey and conspecific communication inputs. © 2012 Litwin-Kumar et al
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