4,734 research outputs found
Spiking Dynamics during Perceptual Grouping in the Laminar Circuits of Visual Cortex
Grouping of collinear boundary contours is a fundamental process during visual perception. Illusory contour completion vividly illustrates how stable perceptual boundaries interpolate between pairs of contour inducers, but do not extrapolate from a single inducer. Neural models have simulated how perceptual grouping occurs in laminar visual cortical circuits. These models predicted the existence of grouping cells that obey a bipole property whereby grouping can occur inwardly between pairs or greater numbers of similarly oriented and co-axial inducers, but not outwardly from individual inducers. These models have not, however, incorporated spiking dynamics. Perceptual grouping is a challenge for spiking cells because its properties of collinear facilitation and analog sensitivity to inducer configurations occur despite irregularities in spike timing across all the interacting cells. Other models have demonstrated spiking dynamics in laminar neocortical circuits, but not how perceptual grouping occurs. The current model begins to unify these two modeling streams by implementing a laminar cortical network of spiking cells whose intracellular temporal dynamics interact with recurrent intercellular spiking interactions to quantitatively simulate data from neurophysiological experiments about perceptual grouping, the structure of non-classical visual receptive fields, and gamma oscillations.CELEST, an NSF Science of Learning Center (SBE-0354378); SyNAPSE program of the Defense Advanced Research Project Agency (HR001109-03-0001); Defense Advanced Research Project Agency (HR001-09-C-0011
Learning intrinsic excitability in medium spiny neurons
We present an unsupervised, local activation-dependent learning rule for
intrinsic plasticity (IP) which affects the composition of ion channel
conductances for single neurons in a use-dependent way. We use a
single-compartment conductance-based model for medium spiny striatal neurons in
order to show the effects of parametrization of individual ion channels on the
neuronal activation function. We show that parameter changes within the
physiological ranges are sufficient to create an ensemble of neurons with
significantly different activation functions. We emphasize that the effects of
intrinsic neuronal variability on spiking behavior require a distributed mode
of synaptic input and can be eliminated by strongly correlated input. We show
how variability and adaptivity in ion channel conductances can be utilized to
store patterns without an additional contribution by synaptic plasticity (SP).
The adaptation of the spike response may result in either "positive" or
"negative" pattern learning. However, read-out of stored information depends on
a distributed pattern of synaptic activity to let intrinsic variability
determine spike response. We briefly discuss the implications of this
conditional memory on learning and addiction.Comment: 20 pages, 8 figure
Functional effects of schizophrenia-linked genetic variants on intrinsic single-neuron excitability: A modeling study
Background: Recent genome-wide association studies (GWAS) have identified a
large number of genetic risk factors for schizophrenia (SCZ) featuring ion
channels and calcium transporters. For some of these risk factors, independent
prior investigations have examined the effects of genetic alterations on the
cellular electrical excitability and calcium homeostasis. In the present
proof-of-concept study, we harnessed these experimental results for modeling of
computational properties on layer V cortical pyramidal cell and identify
possible common alterations in behavior across SCZ-related genes.
Methods: We applied a biophysically detailed multi-compartmental model to
study the excitability of a layer V pyramidal cell. We reviewed the literature
on functional genomics for variants of genes associated with SCZ, and used
changes in neuron model parameters to represent the effects of these variants.
Results: We present and apply a framework for examining the effects of subtle
single nucleotide polymorphisms in ion channel and Ca2+ transporter-encoding
genes on neuron excitability. Our analysis indicates that most of the
considered SCZ- related genetic variants affect the spiking behavior and
intracellular calcium dynamics resulting from summation of inputs across the
dendritic tree.
Conclusions: Our results suggest that alteration in the ability of a single
neuron to integrate the inputs and scale its excitability may constitute a
fundamental mechanistic contributor to mental disease, alongside with the
previously proposed deficits in synaptic communication and network behavior
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
Electrical Compartmentalization in Neurons
The dendritic tree of neurons plays an important role in information processing in the brain. While it is thought that dendrites require independent subunits to perform most of their computations, it is still not understood how they compartmentalize into functional subunits. Here, we show how these subunits can be deduced from the properties of dendrites. We devised a formalism that links the dendritic arborization to an impedance-based tree graph and show how the topology of this graph reveals independent subunits. This analysis reveals that cooperativity between synapses decreases slowly with increasing electrical separation and thus that few independent subunits coexist. We nevertheless find that balanced inputs or shunting inhibition can modify this topology and increase the number and size of the subunits in a context-dependent manner. We also find that this dynamic recompartmentalization can enable branch-specific learning of stimulus features. Analysis of dendritic patch-clamp recording experiments confirmed our theoretical predictions.Peer reviewe
Dwelling Quietly in the Rich Club: Brain Network Determinants of Slow Cortical Fluctuations
For more than a century, cerebral cartography has been driven by
investigations of structural and morphological properties of the brain across
spatial scales and the temporal/functional phenomena that emerge from these
underlying features. The next era of brain mapping will be driven by studies
that consider both of these components of brain organization simultaneously --
elucidating their interactions and dependencies. Using this guiding principle,
we explored the origin of slowly fluctuating patterns of synchronization within
the topological core of brain regions known as the rich club, implicated in the
regulation of mood and introspection. We find that a constellation of densely
interconnected regions that constitute the rich club (including the anterior
insula, amygdala, and precuneus) play a central role in promoting a stable,
dynamical core of spontaneous activity in the primate cortex. The slow time
scales are well matched to the regulation of internal visceral states,
corresponding to the somatic correlates of mood and anxiety. In contrast, the
topology of the surrounding "feeder" cortical regions show unstable, rapidly
fluctuating dynamics likely crucial for fast perceptual processes. We discuss
these findings in relation to psychiatric disorders and the future of
connectomics.Comment: 35 pages, 6 figure
The Decade of the Dendritic NMDA Spike
In the field of cortical cellular physiology, much effort has been invested in understanding thick apical drites of pyramidal neurons and the regenerative sodium and calcium spikes that take place in the apical trunk. Here we focus on thin dendrites of pyramidal cells (basal, oblique, and tuft dendrites), and we discuss one relatively novel form of an electrical signal (“NMDA spike”) that is specific for these branches. Basal, oblique, and apical tuft dendrites receive a high density of glutamatergic synaptic contacts. Synchronous activation of 10–50 neighboring glutamatergic synapses triggers a local dendritic regenerative potential, NMDA spike/plateau, which is characterized by significant local amplitude (40–50 mV) and an extraordinary duration (up to several hundred milliseconds). The NMDA plateau potential, when it is initiated in an apical tuft dendrite, is able to maintain a good portion of that tuft in a sustained depolarized state. However, if NMDA-dominated plateau potentials originate in proximal segments of basal dendrites, they regularly bring the neuronal cell body into a sustained depolarized state, which resembles a cortical up state. At each dendritic initiation site (basal, oblique, and tuft) an NMDA spike creates favorable conditions for causal interactions of active synaptic inputs, including the spatial or temporal binding of information, as well as processes of short-term and long-term synaptic modifications (e.g., long-term potentiation or long-term depression). Because of their strong amplitudes and durations, local dendritic NMDA spikes make up the cellular substrate for multisite independent subunit computations that enrich the computational power and repertoire of cortical pyramidal cells. We propose that NMDA spikes are likely to play significant roles in cortical information processing in awake animals (spatiotemporal binding, working memory) and during slow-wave sleep (neuronal up states, consolidation of memories
The role of ongoing dendritic oscillations in single-neuron dynamics
The dendritic tree contributes significantly to the elementary computations a neuron performs while converting its synaptic inputs into action potential output. Traditionally, these computations have been characterized as temporally local, near-instantaneous mappings from the current input of the cell to its current output, brought about by somatic summation of dendritic contributions that are generated in spatially localized functional compartments. However, recent evidence about the presence of oscillations in dendrites suggests a qualitatively different mode of operation: the instantaneous phase of such oscillations can depend on a long history of inputs, and under appropriate conditions, even dendritic oscillators that are remote may interact through synchronization. Here, we develop a mathematical framework to analyze the interactions of local dendritic oscillations, and the way these interactions influence single cell computations. Combining weakly coupled oscillator methods with cable theoretic arguments, we derive phase-locking states for multiple oscillating dendritic compartments. We characterize how the phase-locking properties depend on key parameters of the oscillating dendrite: the electrotonic properties of the (active) dendritic segment, and the intrinsic properties of the dendritic oscillators. As a direct consequence, we show how input to the dendrites can modulate phase-locking behavior and hence global dendritic coherence. In turn, dendritic coherence is able to gate the integration and propagation of synaptic signals to the soma, ultimately leading to an effective control of somatic spike generation. Our results suggest that dendritic oscillations enable the dendritic tree to operate on more global temporal and spatial scales than previously thought
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