Intrinsic firing patterns of diverse neocortical neurons

Connors, Barry W.; Gutnick, Michael J.

doi:10.1016/0166-2236(90)90185-d

Cited by 1,314 publications

(958 citation statements)

References 20 publications

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“…Layer IV stellate cells make no external connections outside of their own minicolumn in the model, as guided by the sparser stellate connections demonstrated in the cortical wiring model of Douglas and Martin (Douglas and Martin 2004). They are configured as regular spiking cells as well ( Figure 1a) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 98%

“…Only sparse connections between layer II/III pyramidal cells and double bouquet cells are observed histologically (Lewis et al 2002). All of the layer II/III pyramidal cells or of the regular-spiking variety, and exhibit spike adaptation ( Figure 1a) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 99%

“…Contacts to external inhibitory cells are kept at 5% of the excitatory connections. These cells are kept as regular spiking cells (Figure 1a) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 99%

“…Double bouquet cells are also probably contacted by basket cells, with estimates of 30% of calbindin and calretinin positive interneurons being contacted by parvalbumin positive cells (Peters and Sethares 1997), we include a 30% contact probability for available cells in our model. These inhibitory cells are all considered fast spiking in our model ( Figure 1c) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 99%

“…It has been estimated that 30% of parvalbumin positive cells (most chandelier and basket cells) are innervated by calretinin positive cells (double bouquet cells), and a figure of 30% of available cells within the 100 μm connection radius is included (DeFelipe et al 1999). The double bouquet cells are treated as fast spiking interneurons (Figure 1c) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 99%

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Studies of stimulus parameters for seizure disruption using neural network simulations

et al. 2007

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A large scale neural network simulation with realistic cortical architecture has been undertaken to investigate the effects of external electrical stimulation on the propagation and evolution of ongoing seizure activity. This is an effort to explore the parameter space of stimulation variables to uncover promising avenues of research for this therapeutic modality. The model consists of an approximately 800 μm × 800 μm region of simulated cortex, and includes seven neuron classes organized by cortical layer, inhibitory or excitatory properties, and electrophysiological characteristics. The cell dynamics are governed by a modified version of the Hodgkin-Huxley equations in single compartment format. Axonal connections are patterned after histological data and published models of local cortical wiring. Stimulation induced action potentials take place at the axon initial segments, according to threshold requirements on the applied electric field distribution. Stimulation induced action potentials in horizontal axonal branches are also separately simulated. The calculations are performed on a 16 node distributed 32-bit processor system. Clear differences in seizure evolution are presented for stimulated versus the undisturbed rhythmic activity. Data is provided for frequency dependent stimulation effects demonstrating a plateau effect of stimulation efficacy as the applied frequency is increased from 60 Hz to 200 Hz. Timing of the stimulation with respect to the underlying rhythmic activity demonstrates a phase dependent sensitivity. Electrode height and position effects are also presented. Using a dipole stimulation electrode arrangement, clear orientation effects of the dipole with respect to the model connectivity is also demonstrated. A sensitivity analysis of these results as a function of the stimulation threshold is also provided.

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Section: Model Cell-typesmentioning

confidence: 98%

Section: Model Cell-typesmentioning

confidence: 99%

“…Contacts to external inhibitory cells are kept at 5% of the excitatory connections. These cells are kept as regular spiking cells (Figure 1a) (Connors and Gutnick 1990).…”

Section: Model Cell-typesmentioning

confidence: 99%

Section: Model Cell-typesmentioning

confidence: 99%

Section: Model Cell-typesmentioning

confidence: 99%

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Studies of stimulus parameters for seizure disruption using neural network simulations

et al. 2007

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Efferent projections of the anterior perirhinal cortex in the rat

1996

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Because convulsive seizures develop very rapidly from kindling sites in the anterior perirhinal cortex, we studied perirhinal efferents by using the anterograde tracer Phaseolus vulgaris leucoagglutinin (PhAL). PhAL injections into the anterior perirhinal cortex labelled a prominent network of fibers within the frontal cortex that was most dense within layers I and II and layer VI. As individual PhAL injection sites within the perirhinal cortex were restricted to one or two adjacent laminae, we were able to determine that layer V was the main source of the perirhinofrontal projection. This was confirmed by frontal cortex injections of the retrograde tracer Fluorogold (FG). Other cortical areas with densely labelled fibers following perirhinal PhAL injections included the agranular insular, infralimbic, orbital, parietal, and entorhinal cortices. Moderate to mild fiber labelling was also noted in the posterior piriform, temporal and occipital cortices, and the claustrum. Subcortical labelling was seen in the nucleus accumbens; fundus striati; basal and lateral amygdala nuclei; the "acoustic thalamus"; and the central grey. Several of these cortical and subcortical projections were bilateral. The different laminar origin of these perirhinal efferents is discussed. These results confirmed our prediction of extensive direct projections from the anterior perirhinal cortex to the frontal cortex in the rat. The significance of this projection is discussed with special reference to the anatomical basis of convulsive limbic seizures.

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Morphological properties of intracellularly labeled layer I neurons in rat neocortex

Zhou

Hablitz

1996

J. Comp. Neurol.

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The morphology of neurons in layer I of rat neocortex, including Cajal-Retzius (CR) cells, was studied by using intracellular biocytin staining in brain slices obtained from rats during the first 22 postnatal days. Within the first postnatal week, horizontal bipolar neurons or CR cells were prominent in layer I. Typically, CR cells had one main dendrite and one axon originating from opposite poles of the somata. Even though the main dendrites and axons could be quite long, complex dendritic or axonal arbors were not observed. Starting around postnatal day 6 (PN 6), CR cells were less frequently observed. From PN 10 to PN 21, nonpyramidal neurons with diverse morphologies became the main neuronal component in layer I. The somata of layer I nonpyramidal neurons were quite variable in size and shape. Dendrites were smooth or sparsely spiny, and the dendritic trees were mainly restricted to layer I, covering an area with a diameter of about 200 microns. Axon collaterals of these cells formed elaborate arbors with diameters of around 700 microns in layer I and extending, in many cases, to layer II/III and even layer IV. This extensive axonal plexus provides a rich anatomical base on which layer I neurons, functioning as local circuit elements, may interact with each other and with neurons in other layers.

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Intrinsic firing patterns of diverse neocortical neurons

Cited by 1,314 publications

References 20 publications

Studies of stimulus parameters for seizure disruption using neural network simulations

Studies of stimulus parameters for seizure disruption using neural network simulations

Efferent projections of the anterior perirhinal cortex in the rat

Morphological properties of intracellularly labeled layer I neurons in rat neocortex

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