135 research outputs found
Loss of synchrony in an inhibitory network of type-I oscillators
Synchronization of excitable cells coupled by reciprocal inhibition is a topic of significant interest due to the important role that inhibitory synaptic interaction plays in the generation and regulation of coherent rhythmic activity in a variety of neural systems. While recent work revealed the synchronizing influence of inhibitory coupling on the dynamics of many networks, it is known that strong coupling can destabilize phase-locked firing. Here we examine the loss of synchrony caused by an increase in inhibitory coupling in networks of type-I Morris-Lecar model oscillators, which is characterized by a period-doubling cascade and leads to mode-locked states with alternation in the firing order of the two cells, as reported recently by Maran and Canavier (2007) for a network of Wang-Buzsáki model neurons. Although alternating- order firing has been previously reported as a near-synchronous state, we show that the stable phase difference between the spikes of the two Morris-Lecar cells can constitute as much as 70% of the unperturbed oscillation period. Further, we examine the generality of this phenomenon for a class of type-I oscillators that are close to their excitation thresholds, and provide an intuitive geometric description of such leap-frog dynamics. In the Morris-Lecar model network, the alternation in the firing order arises under the condition of fast closing of K+ channels at hyperpolarized potentials, which leads to slow dynamics of membrane potential upon synaptic inhibition, allowing the presynaptic cell to advance past the postsynaptic cell in each cycle of the oscillation. Further, we show that non-zero synaptic decay time is crucial for the existence of leap-frog firing in networks of phase oscillators. However, we demonstrate that leap-frog spiking can also be obtained in pulse-coupled inhibitory networks of one-dimensional oscillators with a multi-branched phase domain, for instance in a network of quadratic integrate-and-fire model cells. Also, we show that the entire bifurcation structure of the network can be explained by a simple scaling of the STRC (spike- time response curve) amplitude, using a simplified quadratic STRC as an example, and derive the general conditions on the shape of the STRC function that leads to leap-frog firing. Further, for the case of a homogeneous network, we establish quantitative conditions on the phase resetting properties of each cell necessary for stable alternating-order spiking, complementing the analysis of Goel and Ermentrout (2002) of the order-preserving phase transition map. We show that the extension of STRC to negative values of phase is necessary to predict the response of a model cell to several close non-weak perturbations. This allows us for instance to accurately describe the dynamics of non-weakly coupled network of three model cells. Finally, the phase return map is also extended to the heterogenous network, and is used to analyze both the order-alternating firing and the order-preserving non-zero phase locked state in this case
Synaptic shot noise and conductance fluctuations affect the membrane voltage with equal significance
The subthresholdmembranevoltage of a neuron in active cortical tissue is
a fluctuating quantity with a distribution that reflects the firing statistics
of the presynaptic population. It was recently found that conductancebased
synaptic drive can lead to distributions with a significant skew.
Here it is demonstrated that the underlying shot noise caused by Poissonian
spike arrival also skews the membrane distribution, but in the opposite
sense. Using a perturbative method, we analyze the effects of shot
noise on the distribution of synaptic conductances and calculate the consequent
voltage distribution. To first order in the perturbation theory, the
voltage distribution is a gaussian modulated by a prefactor that captures
the skew. The gaussian component is identical to distributions derived
using current-based models with an effective membrane time constant.
The well-known effective-time-constant approximation can therefore be
identified as the leading-order solution to the full conductance-based
model. The higher-order modulatory prefactor containing the skew comprises
terms due to both shot noise and conductance fluctuations. The
diffusion approximation misses these shot-noise effects implying that
analytical approaches such as the Fokker-Planck equation or simulation
with filtered white noise cannot be used to improve on the gaussian approximation.
It is further demonstrated that quantities used for fitting
theory to experiment, such as the voltage mean and variance, are robust
against these non-Gaussian effects. The effective-time-constant approximation
is therefore relevant to experiment and provides a simple analytic
base on which other pertinent biological details may be added
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)
A Complex-Valued Firing-Rate Model That Approximates the Dynamics of Spiking Networks
Firing-rate models provide an attractive approach for studying large neural networks because they can be simulated rapidly and are amenable to mathematical analysis. Traditional firing-rate models assume a simple form in which the dynamics are governed by a single time constant. These models fail to replicate certain dynamic features of populations of spiking neurons, especially those involving synchronization. We present a complex-valued firing-rate model derived from an eigenfunction expansion of the Fokker-Planck equation and apply it to the linear, quadratic and exponential integrate-and-fire models. Despite being almost as simple as a traditional firing-rate description, this model can reproduce firing-rate dynamics due to partial synchronization of the action potentials in a spiking model, and it successfully predicts the transition to spike synchronization in networks of coupled excitatory and inhibitory neurons
Noise Suppression and Surplus Synchrony by Coincidence Detection
The functional significance of correlations between action potentials of
neurons is still a matter of vivid debates. In particular it is presently
unclear how much synchrony is caused by afferent synchronized events and how
much is intrinsic due to the connectivity structure of cortex. The available
analytical approaches based on the diffusion approximation do not allow to
model spike synchrony, preventing a thorough analysis. Here we theoretically
investigate to what extent common synaptic afferents and synchronized inputs
each contribute to closely time-locked spiking activity of pairs of neurons. We
employ direct simulation and extend earlier analytical methods based on the
diffusion approximation to pulse-coupling, allowing us to introduce precisely
timed correlations in the spiking activity of the synaptic afferents. We
investigate the transmission of correlated synaptic input currents by pairs of
integrate-and-fire model neurons, so that the same input covariance can be
realized by common inputs or by spiking synchrony. We identify two distinct
regimes: In the limit of low correlation linear perturbation theory accurately
determines the correlation transmission coefficient, which is typically smaller
than unity, but increases sensitively even for weakly synchronous inputs. In
the limit of high afferent correlation, in the presence of synchrony a
qualitatively new picture arises. As the non-linear neuronal response becomes
dominant, the output correlation becomes higher than the total correlation in
the input. This transmission coefficient larger unity is a direct consequence
of non-linear neural processing in the presence of noise, elucidating how
synchrony-coded signals benefit from these generic properties present in
cortical networks
Amplification of asynchronous inhibition-mediated synchronization by feedback in recurrent networks
Synchronization of 30-80 Hz oscillatory activity of the principle neurons in the olfactory bulb (mitral cells) is believed to be important for odor discrimination. Previous theoretical studies of these fast rhythms in other brain areas have proposed that principle neuron synchrony can be mediated by short-latency, rapidly decaying inhibition. This phasic inhibition provides a narrow time window for the principle neurons to fire, thus promoting synchrony. However, in the olfactory bulb, the inhibitory granule cells produce long lasting, small amplitude, asynchronous and aperiodic inhibitory input and thus the narrow time window that is required to synchronize spiking does not exist. Instead, it has been suggested that correlated output of the granule cells could serve to synchronize uncoupled mitral cells through a mechanism called "stochastic synchronization", wherein the synchronization arises through correlation of inputs to two neural oscillators. Almost all work on synchrony due to correlations presumes that the correlation is imposed and fixed. Building on theory and experiments that we and others have developed, we show that increased synchrony in the mitral cells could produce an increase in granule cell activity for those granule cells that share a synchronous group of mitral cells. Common granule cell input increases the input correlation to the mitral cells and hence their synchrony by providing a positive feedback loop in correlation. Thus we demonstrate the emergence and temporal evolution of input correlation in recurrent networks with feedback. We explore several theoretical models of this idea, ranging from spiking models to an analytically tractable model. © 2010 Marella, Ermentrout
A Model of Stimulus-Specific Neural Assemblies in the Insect Antennal Lobe
It has been proposed that synchronized neural assemblies in the antennal lobe of insects encode the identity of olfactory stimuli. In response to an odor, some projection neurons exhibit synchronous firing, phase-locked to the oscillations of the field potential, whereas others do not. Experimental data indicate that neural synchronization and field oscillations are induced by fast GABAA-type inhibition, but it remains unclear how desynchronization occurs. We hypothesize that slow inhibition plays a key role in desynchronizing projection neurons. Because synaptic noise is believed to be the dominant factor that limits neuronal reliability, we consider a computational model of the antennal lobe in which a population of oscillatory neurons interact through unreliable GABAA and GABAB inhibitory synapses. From theoretical analysis and extensive computer simulations, we show that transmission failures at slow GABAB synapses make the neural response unpredictable. Depending on the balance between GABAA and GABAB inputs, particular neurons may either synchronize or desynchronize. These findings suggest a wiring scheme that triggers stimulus-specific synchronized assemblies. Inhibitory connections are set by Hebbian learning and selectively activated by stimulus patterns to form a spiking associative memory whose storage capacity is comparable to that of classical binary-coded models. We conclude that fast inhibition acts in concert with slow inhibition to reformat the glomerular input into odor-specific synchronized neural assemblies
Analysis and Modeling of Ensemble Recordings from Respiratory Pre-Motor Neurons Indicate Changes in Functional Network Architecture after Acute Hypoxia
We have combined neurophysiologic recording, statistical analysis, and computational modeling to investigate the dynamics of the respiratory network in the brainstem. Using a multielectrode array, we recorded ensembles of respiratory neurons in perfused in situ rat preparations that produce spontaneous breathing patterns, focusing on inspiratory pre-motor neurons. We compared firing rates and neuronal synchronization among these neurons before and after a brief hypoxic stimulus. We observed a significant decrease in the number of spikes after stimulation, in part due to a transient slowing of the respiratory pattern. However, the median interspike interval did not change, suggesting that the firing threshold of the neurons was not affected but rather the synaptic input was. A bootstrap analysis of synchrony between spike trains revealed that both before and after brief hypoxia, up to 45% (but typically less than 5%) of coincident spikes across neuronal pairs was not explained by chance. Most likely, this synchrony resulted from common synaptic input to the pre-motor population, an example of stochastic synchronization. After brief hypoxia most pairs were less synchronized, although some were more, suggesting that the respiratory network was transiently “rewired” after the stimulus. To investigate this hypothesis, we created a simple computational model with feed-forward divergent connections along the inspiratory pathway. Assuming that (1) the number of divergent projections was not the same for all presynaptic cells, but rather spanned a wide range and (2) that the stimulus increased inhibition at the top of the network; this model reproduced the reduction in firing rate and bootstrap-corrected synchrony subsequent to hypoxic stimulation observed in our experimental data
The role of short term synamptic plasticity in temporal coding of neuronal networks
Short term synaptic plasticity is a phenomenon which is commonly found in the central nervous system. It could contribute to functions of signal processing namely, temporal integration and coincidence detection by modulating the input synaptic strength. This dissertation has two parts. First we study the effects of short term synaptic plasticity in enhancing coincidence detecting ability of neurons in the avian auditory brainstem. Coincidence detection means a target neuron has a higher firing rate when it receives simultaneous inputs from different neurons as opposed to inputs with large phase delays. This property is used by birds in sound localization. When there is no plasticity from the inputs, the firing rate of the neuron, depends more on input frequencies and less on phase delays between inputs. This leads to ambiguity in localizing the sound source. We derive a mathematical model of a reduced avian brainstem network and show that inputs with synaptic plasticity, to the coincidence detector neuron, play a vital role in enhancing coincidence detecting ability of the bird. We present comparisons to experiments. In the second part of the thesis, we prove the existence and stability of a ncluster solution in a m-cell network, in the presence of synaptic depression. The model used to represent a single neuron is based on the Hodgkin-Huxley model for the spiking neurons and we use techniques from geometric singular perturbation theory to show that any n-cluster solution must satisfy a set of consistency conditions that can be geometrically derived. The results of both problems are validated using numerical simulations
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