CiteULike: nelmor's synchronization

Rate-specific synchrony: Using noisy oscillations to detect equally active neurons

David Markowitz — 2008-06-18T10:25:06-00:00

Proceedings of the National Academy of Sciences, Vol. 105, No. 24. (17 June 2008), pp. 8422-8427.

Although gamma frequency oscillations are common in the brain, their functional contributions to neural computation are not understood. Here we report in vitro electrophysiological recordings to evaluate how noisy gamma frequency oscillatory input interacts with the overall activation level of a neuron to determine the precise timing of its action potentials. The experiments were designed to evaluate spike synchrony in a neural circuit architecture in which a population of neurons receives a common noisy gamma oscillatory synaptic drive while the firing rate of each individual neuron is determined by a slowly varying independent input. We demonstrate that similarity of firing rate is a major determinant of synchrony under common noisy oscillatory input: Near coincidence of spikes at similar rates gives way to substantial desynchronization at larger firing rate differences. Analysis of this rate-specific synchrony phenomenon reveals distinct spike timing "fingerprints" at different firing rates that emerge through a combination of phase shifting and abrupt changes in spike patterns. We further demonstrate that rate-specific synchrony permits robust detection of rate similarity in a population of neurons through synchronous activation of a postsynaptic neuron, supporting the biological plausibility of a Many Are Equal computation. Our results reveal that spatially coherent noisy oscillations, which are common throughout the brain, can generate previously unknown relationships among neural rate codes, noisy interspike intervals, and precise spike synchrony codes. All of these can coexist in a self-consistent manner because of rate-specific synchrony. 10.1073/pnas.0803183105

Disrupted Dopamine Transmission and the Emergence of Exaggerated Beta Oscillations in Subthalamic Nucleus and Cerebral Cortex

Nicolas Mallet — 2008-05-02T08:52:58-00:00

J. Neurosci., Vol. 28, No. 18. (30 April 2008), pp. 4795-4806.

In the subthalamic nucleus (STN) of Parkinson's disease (PD) patients, a pronounced synchronization of oscillatory activity at beta frequencies (15-30 Hz) accompanies movement difficulties. Abnormal beta oscillations and motor symptoms are concomitantly and acutely suppressed by dopaminergic therapies, suggesting that these inappropriate rhythms might also emerge acutely from disrupted dopamine transmission. The neural basis of these abnormal beta oscillations is unclear, and how they might compromise information processing, or how they arise, is unknown. Using a 6-hydroxydopamine-lesioned rodent model of PD, we demonstrate that beta oscillations are inappropriately exaggerated, compared with controls, in a brain-state-dependent manner after chronic dopamine loss. Exaggerated beta oscillations are expressed at the levels of single neurons and small neuronal ensembles, and are focally present and spatially distributed within STN. They are also expressed in synchronous population activities, as evinced by oscillatory local field potentials, in STN and cortex. Excessively synchronized beta oscillations reduce the information coding capacity of STN neuronal ensembles, which may contribute to parkinsonian motor impairment. Acute disruption of dopamine transmission in control animals with antagonists of D1/D2 receptors did not exaggerate STN or cortical beta oscillations. Moreover, beta oscillations were not exaggerated until several days after 6-hydroxydopamine injections. Thus, contrary to predictions, abnormally amplified beta oscillations in cortico-STN circuits do not result simply from an acute absence of dopamine receptor stimulation, but are instead delayed sequelae of chronic dopamine depletion. Targeting the plastic processes underlying the delayed emergence of pathological beta oscillations after continuing dopaminergic dysfunction may offer considerable therapeutic promise. 10.1523/JNEUROSCI.0123-08.2008

Decoupling through Synchrony in Neuronal Circuits with Propagation Delays

Evgueniy Lubenov — 2008-04-10T12:05:30-00:00

Neuron, Vol. 58, No. 1. (10 April 2008), pp. 118-131.

Summary The level of synchronization in distributed systems is often controlled by the strength of the interactions between individual elements. In brain circuits the connection strengths between neurons are modified under the influence of spike-timing-dependent plasticity (STDP) rules. Here we show that when recurrent networks with conduction delays exhibit population bursts, STDP rules exert a strong decoupling force that desynchronizes activity. Conversely, when activity in the network is random, the same rules can have a coupling and synchronizing influence. The presence of these opposing forces promotes the self-organization of spontaneously active neuronal networks to a state at the border between randomness and synchrony. The decoupling force of STDP may be engaged by the synchronous bursts occurring in the hippocampus during slow-wave sleep, leading to the selective erasure of information from hippocampal circuits as memories are established in neocortical areas.

Neural correlations, population coding and computation

Bruno Averbeck — 2006-04-25T04:28:57-00:00

Nature Reviews Neuroscience, Vol. 7, No. 5., pp. 358-366.

Gamma oscillations dynamically couple hippocampal CA3 and CA1 regions during memory task performance

Sean Montgomery — 2007-08-29T08:22:58-00:00

PNAS (28 August 2007), 0701826104.

Edited by Fred H. Gage, The Salk Institute for Biological Sciences, San Diego, CA, and approved July 20, 2007 (received for review February 27, 2007)The hippocampal formation is believed to be critical for the encoding, consolidation, and retrieval of episodic memories. Yet, how these processes are supported by the anatomically diverse hippocampal networks is still unknown. To examine this issue, we tested rats in a hippocampus-dependent delayed spatial alternation task on a modified T maze while simultaneously recording local field potentials from dendritic and somatic layers of the dentate gyrus, CA3, and CA1 regions by using high-density, 96-site silicon probes. Both the power and coherence of gamma oscillations exhibited layer-specific changes during task performance. Peak increases in the gamma power and coherence were found in the CA3CA1 interface on the maze segment approaching the T junction, independent of motor aspects of task performance. These results show that hippocampal networks can be dynamically coupled by gamma oscillations according to specific behavioral demands. Based on these findings, we propose that gamma oscillations may serve as a physiological mechanism by which CA3 output can coordinate CA1 activity to support retrieval of hippocampus-dependent memories. 10.1073/pnas.0701826104

Measuring spike train synchrony

Thomas Kreuz — 2007-07-13T13:51:00-00:00

Journal of Neuroscience Methods, Vol. In Press, Corrected Proof

Estimating the degree of synchrony or reliability between two or more spike trains is a frequent task in both experimental and computational neuroscience. In recent years, many different methods have been proposed that typically compare the timing of spikes on a certain time scale to be optimized by the analyst. Here, we propose the ISI-distance, a simple complementary approach that extracts information from the interspike intervals by evaluating the ratio of the instantaneous firing rates. The method is parameter free, time scale independent and easy to visualize as illustrated by an application to real neuronal spike trains obtained in vitro from rat slices. In a comparison with existing approaches on spike trains extracted from a simulated Hindemarsh-Rose network, the ISI-distance performs as well as the best time-scale-optimized measure based on spike timing.

Correlation between neural spike trains increases with firing rate

de La — 2007-08-16T08:30:24-00:00

Nature, Vol. 448, No. 7155. (2007), pp. 802-806.

Pathological synchronization in Parkinson's disease: networks, models and treatments

Constance Hammond — 2007-07-03T08:13:20-00:00

Trends in Neurosciences, Vol. 30, No. 7. (July 2007), pp. 357-364.

Parkinson's disease is a common and disabling disorder of movement owing to dopaminergic denervation of the striatum. However, it is still unclear how this denervation perverts normal functioning to cause slowing of voluntary movements. Recent work using tissue slice preparations, animal models and in humans with Parkinson's disease has demonstrated abnormally synchronized oscillatory activity at multiple levels of the basal ganglia-cortical loop. This excessive synchronization correlates with motor deficit, and its suppression by dopaminergic therapies, ablative surgery or deep-brain stimulation might provide the basic mechanism whereby diverse therapeutic strategies ameliorate motor impairment in patients with Parkinson's disease. This review is part of the INMED/TINS special issue, Physiogenic and pathogenic oscillations: the beauty and the beast, based on presentations at the annual INMED/TINS symposium (http://inmednet.com/).

Neural Mechanisms of Visual Attention: How Top-Down Feedback Highlights Relevant Locations

Yuri Saalmann — 2007-06-15T08:59:06-00:00

Science, Vol. 316, No. 5831. (15 June 2007), pp. 1612-1615.

Attention helps us process potentially important objects by selectively increasing the activity of sensory neurons that represent the relevant locations and features of our environment. This selection process requires top-down feedback about what is important in our environment. We investigated how parietal cortical output influences neural activity in early sensory areas. Neural recordings were made simultaneously from the posterior parietal cortex and an earlier area in the visual pathway, the medial temporal area, of macaques performing a visual matching task. When the monkey selectively attended to a location, the timing of activities in the two regions became synchronized, with the parietal cortex leading the medial temporal area. Parietal neurons may thus selectively increase activity in earlier sensory areas to enable focused spatial attention. 10.1126/science.1139140

Modulation of Neuronal Interactions Through Neuronal Synchronization

Thilo Womelsdorf — 2007-06-15T08:56:16-00:00

Science, Vol. 316, No. 5831. (15 June 2007), pp. 1609-1612.

Brain processing depends on the interactions between neuronal groups. Those interactions are governed by the pattern of anatomical connections and by yet unknown mechanisms that modulate the effective strength of a given connection. We found that the mutual influence among neuronal groups depends on the phase relation between rhythmic activities within the groups. Phase relations supporting interactions between the groups preceded those interactions by a few milliseconds, consistent with a mechanistic role. These effects were specific in time, frequency, and space, and we therefore propose that the pattern of synchronization flexibly determines the pattern of neuronal interactions. 10.1126/science.1139597