57 research outputs found
Signal processing in local neuronal circuits based on activity-dependent noise and competition
We study the characteristics of weak signal detection by a recurrent neuronal
network with plastic synaptic coupling. It is shown that in the presence of an
asynchronous component in synaptic transmission, the network acquires
selectivity with respect to the frequency of weak periodic stimuli. For
non-periodic frequency-modulated stimuli, the response is quantified by the
mutual information between input (signal) and output (network's activity), and
is optimized by synaptic depression. Introducing correlations in signal
structure resulted in the decrease of input-output mutual information. Our
results suggest that in neural systems with plastic connectivity, information
is not merely carried passively by the signal; rather, the information content
of the signal itself might determine the mode of its processing by a local
neuronal circuit.Comment: 15 pages, 4 pages, in press for "Chaos
Coexistence of amplitude and frequency modulations in intracellular calcium dynamics
The complex dynamics of intracellular calcium regulates cellular responses to
information encoded in extracellular signals. Here, we study the encoding of
these external signals in the context of the Li-Rinzel model. We show that by
control of biophysical parameters the information can be encoded in amplitude
modulation, frequency modulation or mixed (AM and FM) modulation. We briefly
discuss the possible implications of this new role of information encoding for
astrocytes.Comment: 4 pages, 4 figure
On the determinants of calcium wave propagation distance in astrocyte networks: nonlinear gap junctions and oscillatory modes
A new paradigm has recently emerged in brain science whereby glial cells should be considered on a par with neurons to understand higher brain functions. In particular, astrocytes, the main type of glial cells in the cortex, are thought to form a gap-junction-coupled syncytium supporting cell-cell communication via propagating calcium (Ca2+) waves. The propagation properties of these waves and their relations to intracellular signalling dynamics are however poorly understood. Here, we propose a novel model of the gap-junctional route for intercellular Ca2+ wave propagation in astrocytes that yields two major predictions. First, we show that long-distance regenerative signalling requires gap junctions with nonlinear transport properties. Second, we show that even with nonlinear gap junctions, long-distance regenerative signalling is favoured when internal Ca2+ dynamics implements frequency modulation-encoding oscillations with pulsating dynamics, while amplitude modulation-encoding dynamics tends to restrict the propagation range. As a result, spatially heterogeneous molecular properties and/or weak couplings give rise to rich spatiotemporal dynamics and support complex propagation behaviours. These results suggest that the large variability of the wave propagation range that is consistently reported by experimental studies, is a result of the association of nonlinear gap junctions with heterogeneous astrocyte populations and/or low coupling
Gap Junctions and Epileptic Seizures – Two Sides of the Same Coin?
Electrical synapses (gap junctions) play a pivotal role in the synchronization of
neuronal ensembles which also makes them likely agonists of pathological brain
activity. Although large body of experimental data and theoretical
considerations indicate that coupling neurons by electrical synapses promotes
synchronous activity (and thus is potentially epileptogenic), some recent
evidence questions the hypothesis of gap junctions being among purely
epileptogenic factors. In particular, an expression of inter-neuronal gap
junctions is often found to be higher after the experimentally induced seizures
than before. Here we used a computational modeling approach to address the role
of neuronal gap junctions in shaping the stability of a network to perturbations
that are often associated with the onset of epileptic seizures. We show that
under some circumstances, the addition of gap junctions can increase the
dynamical stability of a network and thus suppress the collective electrical
activity associated with seizures. This implies that the experimentally observed
post-seizure additions of gap junctions could serve to prevent further
escalations, suggesting furthermore that they are a consequence of an adaptive
response of the neuronal network to the pathological activity. However, if the
seizures are strong and persistent, our model predicts the existence of a
critical tipping point after which additional gap junctions no longer suppress
but strongly facilitate the escalation of epileptic seizures. Our results thus
reveal a complex role of electrical coupling in relation to epileptiform events.
Which dynamic scenario (seizure suppression or seizure escalation) is ultimately
adopted by the network depends critically on the strength and duration of
seizures, in turn emphasizing the importance of temporal and causal aspects when
linking gap junctions with epilepsy
Shunting Inhibition Controls the Gain Modulation Mediated by Asynchronous Neurotransmitter Release in Early Development
The sensitivity of a neuron to its input can be modulated in several ways. Changes in the slope of the neuronal input-output curve depend on factors such as shunting inhibition, background noise, frequency-dependent synaptic excitation, and balanced excitation and inhibition. However, in early development GABAergic interneurons are excitatory and other mechanisms such as asynchronous transmitter release might contribute to regulating neuronal sensitivity. We modeled both phasic and asynchronous synaptic transmission in early development to study the impact of activity-dependent noise and short-term plasticity on the synaptic gain. Asynchronous release decreased or increased the gain depending on the membrane conductance. In the high shunt regime, excitatory input due to asynchronous release was divisive, whereas in the low shunt regime it had a nearly multiplicative effect on the firing rate. In addition, sensitivity to correlated inputs was influenced by shunting and asynchronous release in opposite ways. Thus, asynchronous release can regulate the information flow at synapses and its impact can be flexibly modulated by the membrane conductance
Nonlinear gap junctions enable long-distance propagation of pulsating calcium waves in astrocyte networks
A new paradigm has recently emerged in brain science whereby communications
between glial cells and neuron-glia interactions should be considered together
with neurons and their networks to understand higher brain functions. In
particular, astrocytes, the main type of glial cells in the cortex, have been
shown to communicate with neurons and with each other. They are thought to form
a gap-junction-coupled syncytium supporting cell-cell communication via
propagating Ca2+ waves. An identified mode of propagation is based on
cytoplasm-to-cytoplasm transport of inositol trisphosphate (IP3) through gap
junctions that locally trigger Ca2+ pulses via IP3-dependent Ca2+-induced Ca2+
release. It is, however, currently unknown whether this intracellular route is
able to support the propagation of long-distance regenerative Ca2+ waves or is
restricted to short-distance signaling. Furthermore, the influence of the
intracellular signaling dynamics on intercellular propagation remains to be
understood. In this work, we propose a model of the gap-junctional route for
intercellular Ca2+ wave propagation in astrocytes showing that: (1)
long-distance regenerative signaling requires nonlinear coupling in the gap
junctions, and (2) even with nonlinear gap junctions, long-distance
regenerative signaling is favored when the internal Ca2+ dynamics implements
frequency modulation-encoding oscillations with pulsating dynamics, while
amplitude modulation-encoding dynamics tends to restrict the propagation range.
As a result, spatially heterogeneous molecular properties and/or weak couplings
are shown to give rise to rich spatiotemporal dynamics that support complex
propagation behaviors. These results shed new light on the mechanisms
implicated in the propagation of Ca2+ waves across astrocytes and precise the
conditions under which glial cells may participate in information processing in
the brain.Comment: Article: 30 pages, 7 figures. Supplementary Material: 11 pages, 6
figure
A tale of two stories: astrocyte regulation of synaptic depression and facilitation
Short-term presynaptic plasticity designates variations of the amplitude of
synaptic information transfer whereby the amount of neurotransmitter released
upon presynaptic stimulation changes over seconds as a function of the neuronal
firing activity. While a consensus has emerged that changes of the synapse
strength are crucial to neuronal computations, their modes of expression in
vivo remain unclear. Recent experimental studies have reported that glial
cells, particularly astrocytes in the hippocampus, are able to modulate
short-term plasticity but the underlying mechanism is poorly understood. Here,
we investigate the characteristics of short-term plasticity modulation by
astrocytes using a biophysically realistic computational model. Mean-field
analysis of the model unravels that astrocytes may mediate counterintuitive
effects. Depending on the expressed presynaptic signaling pathways, astrocytes
may globally inhibit or potentiate the synapse: the amount of released
neurotransmitter in the presence of the astrocyte is transiently smaller or
larger than in its absence. But this global effect usually coexists with the
opposite local effect on paired pulses: with release-decreasing astrocytes most
paired pulses become facilitated, while paired-pulse depression becomes
prominent under release-increasing astrocytes. Moreover, we show that the
frequency of astrocytic intracellular Ca2+ oscillations controls the effects of
the astrocyte on short-term synaptic plasticity. Our model explains several
experimental observations yet unsolved, and uncovers astrocytic
gliotransmission as a possible transient switch between short-term paired-pulse
depression and facilitation. This possibility has deep implications on the
processing of neuronal spikes and resulting information transfer at synapses.Comment: 93 pages, manuscript+supplementary text, 10 main figures, 11
supplementary figures, 1 tabl
- …