| 1. |
- Froriep, Ulrich P, et al.
(författare)
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Altered theta coupling between medial entorhinal cortex and dentate gyrus in temporal lobe epilepsy
- 2012
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Ingår i: Epilepsia. - : Wiley. - 0013-9580 .- 1528-1167. ; 53:11, s. 1937-1947
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Temporal lobe epilepsy is often accompanied by neuron loss and rewiring in the hippocampus. We hypothesized that the interaction of subnetworks of the entorhinalhippocampal loop between epileptic events should show significant signatures of these pathologic changes.Methods: We combined simultaneous recording of local field potentials in entorhinal cortex (EC) and dentate gyrus (DG) in freely behaving kainate-injected mice with histologic analyses and computational modeling.Key Findings: In healthy mice, theta band activity was synchronized between EC and DG. In contrast, in epileptic mice, theta activity in the EC was delayed with respect to the DG. A computational neural mass model suggests that hippocampal cell loss imbalances the coupling of subnetworks, introducing the shift.Significance: We show that pathologic dynamics in epilepsy encompass ongoing activity in the entorhinal-hippocampal loop beyond acute epileptiform activity. This predominantly affects theta band activity, which links this shift in entorhinal-hippocampal interaction to behavioral aspects in epilepsy.
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| 2. |
- Grah, Gunnar, et al.
(författare)
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Wettstreit der Metaphern
- 2014
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Ingår i: Geist und Gehirn. - 1618-8519. ; :7, s. 60-65
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Forskningsöversikt (populärvet., debatt m.m.)
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| 3. |
- Grah, Gunnar, et al.
(författare)
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Zittern in zahlen
- 2013
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Ingår i: Geist und Gehirn. - 1618-8519. ; :5, s. 68-73
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Forskningsöversikt (populärvet., debatt m.m.)
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| 4. |
- Hahn, Gerald, et al.
(författare)
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Communication through resonance in spiking neuronal networks
- 2014
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Ingår i: PloS Computational Biology. - : Public Library of Science (PLoS). - 1553-734X .- 1553-7358. ; 10:8
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Tidskriftsartikel (refereegranskat)abstract
- The cortex processes stimuli through a distributed network of specialized brain areas. This processing requires mechanisms that can route neuronal activity across weakly connected cortical regions. Routing models proposed thus far are either limited to propagation of spiking activity across strongly connected networks or require distinct mechanisms that create local oscillations and establish their coherence between distant cortical areas. Here, we propose a novel mechanism which explains how synchronous spiking activity propagates across weakly connected brain areas supported by oscillations. In our model, oscillatory activity unleashes network resonance that amplifies feeble synchronous signals and promotes their propagation along weak connections ("communication through resonance''). The emergence of coherent oscillations is a natural consequence of synchronous activity propagation and therefore the assumption of different mechanisms that create oscillations and provide coherence is not necessary. Moreover, the phase-locking of oscillations is a side effect of communication rather than its requirement. Finally, we show how the state of ongoing activity could affect the communication through resonance and propose that modulations of the ongoing activity state could influence information processing in distributed cortical networks.
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| 5. |
- Kremkow, Jens, et al.
(författare)
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Gating of signal propagation in spiking neural networks by balanced and correlated excitation and inhibition
- 2010
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Ingår i: Journal of Neuroscience. - 0270-6474 .- 1529-2401. ; 30:47, s. 15760-8
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Tidskriftsartikel (refereegranskat)abstract
- Both ongoing and natural stimulus driven neuronal activity are dominated by transients. Selective gating of these transients is mandatory for proper brain function and may, in fact, form the basis of millisecond-fast decision making and action selection. Here we propose that neuronal networks may exploit timing differences between correlated excitation and inhibition (temporal gating) to control the propagation of spiking activity transients. When combined with excitation-inhibition balance, temporal gating constitutes a powerful mechanism to control the propagation of mixtures of transient and tonic neural activity components.
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| 6. |
- Kumar, Arvind, et al.
(författare)
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Challenges of understanding brain function by selective modulation of neuronal subpopulations
- 2013
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Ingår i: TINS - Trends in Neurosciences. - : Elsevier BV. - 0166-2236 .- 1878-108X. ; 36:10, s. 579-586
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Forskningsöversikt (refereegranskat)abstract
- Neuronal networks confront researchers with an overwhelming complexity of interactions between their elements. A common approach to understanding neuronal processing is to reduce complexity by defining subunits and infer their functional role by selectively modulating them. However, this seemingly straightforward approach may lead to confusing results if the network exhibits parallel pathways leading to recurrent connectivity. We demonstrate limits of the selective modulation approach and argue that, even though highly successful in some instances, the approach fails in networks with complex connectivity. We argue to refine experimental techniques by carefully considering the structural features of the neuronal networks involved. Such methods could dramatically increase the effectiveness of selective modulation and may lead to a mechanistic understanding of principles underlying brain function.
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| 7. |
- Kumar, Arvind, et al.
(författare)
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Frequency dependent changes in NMDAR-dependent synaptic plasticity
- 2011
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Ingår i: Frontiers in Computational Neuroscience. - : Frontiers Media SA. - 1662-5188. ; 5:38
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Tidskriftsartikel (refereegranskat)abstract
- The NMDAR-dependent synaptic plasticity is thought to mediate several forms of learning, and can be induced by spike trains containing a small number of spikes occurring with varying rates and timing, as well as with oscillations. We computed the influence of these variables on the plasticity induced at a single NMDAR containing synapse using a reduced model that was analytically tractable, and these findings were confirmed using detailed, multi-compartment model. In addition to explaining diverse experimental results about the rate and timing dependence of synaptic plasticity, the model made several novel and testable predictions. We found that there was a preferred frequency for inducing long-term potentiation (LTP) such that higher frequency stimuli induced lesser LTP, decreasing as 1/f when the number of spikes in the stimulus was kept fixed. Among other things, the preferred frequency for inducing LTP varied as a function of the distance of the synapse from the soma. In fact, same stimulation frequencies could induce LTP or long-term depression depending on the dendritic location of the synapse. Next, we found that rhythmic stimuli induced greater plasticity then irregular stimuli. Furthermore, brief bursts of spikes significantly expanded the timing dependence of plasticity. Finally, we found that in the ~5-15-Hz frequency range both rate- and timing-dependent plasticity mechanisms work synergistically to render the synaptic plasticity most sensitive to spike timing. These findings provide computational evidence that oscillations can have a profound influence on the plasticity of an NMDAR-dependent synapse, and show a novel role for the dendritic morphology in this process.
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| 8. |
- Kumar, Arvind, et al.
(författare)
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Information homeostasis as a fundamental principle governing the cell division and death
- 2011
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Ingår i: Medical Hypotheses. - : Elsevier. - 0306-9877 .- 1532-2777. ; 77:3, s. 318-322
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Tidskriftsartikel (refereegranskat)abstract
- To express the genetic information with minimal error is one of the key functions of a cell. Here we propose an information theory based, phenomenological model for the expression of genetic information. Based on the model we propose the concept of 'information homeostasis' which ensures that genetic information is expressed with minimal error. We suggest that together with energy homeostasis, information homeostasis is a fundamental working principle of a biological cell. This model proposes a novel explanation of why a cell divides and why it stops to divide and, thus, provides novel insights into oncogenesis and various neuro-degenerative diseases. Moreover, the model suggests a theoretical framework to understand cell division and death, beyond specific biochemical pathways.
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| 9. |
- Kumar, Arvind, et al.
(författare)
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Spiking activity propagation in neuronal networks : reconciling different perspectives on neural coding
- 2010
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Ingår i: Nature Reviews Neuroscience. - : Springer Science and Business Media LLC. - 1471-003X .- 1471-0048. ; 11:9, s. 615-627
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Tidskriftsartikel (refereegranskat)abstract
- The brain is a highly modular structure. To exploit modularity, it is necessary that spiking activity can propagate from one module to another while preserving the information it carries. Therefore, reliable propagation is one of the key properties of a candidate neural code. Surprisingly, the conditions under which spiking activity can be propagated have received comparatively little attention in the experimental literature. By contrast, several computational studies in the last decade have addressed this issue. Using feedforward networks (FFNs) as a generic network model, they have identified two dynamical activity modes that support the propagation of either asynchronous (rate code) or synchronous (temporal code) spiking. Here, we review the dichotomy of asynchronous and synchronous propagation in FFNs, propose their integration into a single extended conceptual framework and suggest experimental strategies to test our hypothesis.
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| 10. |
- Kumar, Arvind, et al.
(författare)
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The role of inhibition in generating and controlling Parkinson’s disease oscillations in the Basal Ganglia
- 2011
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Ingår i: Frontiers in Systems Neuroscience. - : Frontiers Media SA. - 1662-5137. ; OCTOBER 2011
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Tidskriftsartikel (refereegranskat)abstract
- Movement disorders in Parkinson’s disease (PD) are commonly associated with slow oscillations and increased synchrony of neuronal activity in the basal ganglia. The neural mechanisms underlying this dynamic network dysfunction, however, are only poorly understood. Here, we show that the strength of inhibitory inputs from striatum to globus pallidus external (GPe) is a key parameter controlling oscillations in the basal ganglia. Specifically, the increase in striatal activity observed in PD is sufficient to unleash the oscillations in the basal ganglia. This finding allows us to propose a unified explanation for different phenomena: absence of oscillation in the healthy state of the basal ganglia, oscillations in dopamine-depleted state and quenching of oscillations under deep-brain-stimulation (DBS). These novel insights help us to better understand and optimize the function of DBS protocols. Furthermore, studying the model behavior under transient increase of activity of the striatal neurons projecting to the indirect pathway, we are able to account for both motor impairment in PD patients and for reduced response inhibition in DBS implanted patients.
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