All events, All years

The role of TrpC2 channel in mediating social behavior of male mice within a group

Lecture
Date:
Wednesday, August 1, 2018
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Yefim Pen (PhD Thesis Defense)
|
Tali Kimchi Lab, Dept of Neurobiology, WIS

Neural circuits for skilled forelimb movement

Lecture
Date:
Thursday, July 26, 2018
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eiman Azim
|
Molecular Neurobiology Laboratory Salk Institute for Biological Studies, La Jolla, CA

Movement shapes our interactions with the world, providing a means to translate intent into action. Among the wide repertoire of mammalian motor behaviors, the precise coordination of limb muscles to propel arms, hands and digits through space with speed and precision represents one of the more impressive achievements of the motor system. Skilled forelimb movements emerge from interactions between feedforward command pathways that induce muscle contraction and feedback systems that report and refine movement. Two broad classes of feedback modify motor output: one that originates in the periphery, and a second that is generated within the central nervous system itself. Yet the mechanisms by which these feedback pathways influence forelimb movement remain poorly understood. We take advantage of the genetic tractability of mice to examine the organization of motor circuits and define the ways in which these pathways enable dexterous behaviors. First, I will discuss recent studies that explore the transmission of proprioceptive and cutaneous signals from the forelimb into the spinal cord and brainstem, describing neural circuits that modulate the strength of this peripheral feedback and the implications of this sensory gain control for limb movement. Second, I will describe work exploring a diverse class of spinal interneurons that we hypothesize convey copies of forelimb motor commands as internal feedback to the cerebellum, enabling online predictions of motor outcome and reducing dependence on delayed sensory information. Through a complementary set of molecular, anatomical, electrophysiological and behavioral approaches, these findings are yielding insight into the organizational and functional logic of peripheral and internal feedback, and revealing how the circuits that convey feedback information help to orchestrate skilled behavior.

Human physiological and behavioral responses to olfactory stimuli in health and disease

Lecture
Date:
Tuesday, July 17, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Liron Rozenkrantz (PhD Thesis Defense)
|
Noam Sobel Lab, Dept of Neurobiology, WIS

In my PhD I led three projects probing human behavioral and physiological responses to olfactory stimuli in health and disease. In these projects I used every-day olfactory occurrences in order to infer on biological underpinnings of human behavior. In my main project I tested olfactory processing in autism, using the sniff response, a ten-minute non-verbal measure of respiratory response to odors. I found this objective measure to be profoundly altered in children with autism, and furthermore, to be highly correlated with autism severity. Using computational methods, I demonstrated 81% correct ASD classification based on differences in olfactory processing alone. These results provide proof-of-concept for a potential biomarker for autism (Rozenkrantz et al, Curr Bio, 2015). In a second and soon-to-be-submitted project, I investigated olfactory social communication in recurrent pregnancy loss (RPL), resting on a phenomenon in rodents in which females miscarry following exposure to bodily odors of non-stud males. I found that women with RPL display heightened social olfactory abilities, which were significantly correlated with number of miscarriages. Additionally, women with RPL showed significantly altered hormonal, physiological and neural responses to body odors of unfamiliar men. This project provides novel evidence for altered olfactory processing in human recurrent miscarriages. The third project is also my first foothold in placebo effect research, which I will pursue in my postdoc. Taking advantage of the non-invasive nature of olfactory stimuli, I used an odor as the placebo carrier, and tested two groups of subjects for different creativity tests. Both groups smelled the odor, but only the placebo group was told that it increases creativity (placebo manipulation). I found that following this simple manipulation, the placebo group displayed significantly enhanced creativity (Rozenkrantz et al., PLoS one, 2017). Taken together, these projects convey my deep interest in the interplay between human behavior and physiology.

Sensory processing across behavioral and neuromodulatory states

Lecture
Date:
Tuesday, July 3, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Yuval Nir
|
Sagol School of Neuroscience & Sackler School of Medicine Tel-Aviv University

"Sensory disconnection" – conditions when the same sensory stimulus does not reliably affect behavior or subjective experience - is a defining feature of sleep, and similar processes may occur during light anesthesia or during cognitive lapses in wakefulness. What are the changes in brain activity that mediate sensory disconnection? In a series of studies in humans and rodents, we investigate how "disconnected" states affect sensory processing. The first set of studies reveals differences in neuronal responses to identical sensory stimuli across states. We find that in humans, cognitive lapses after sleep deprivation involve attenuated and delayed single-neuron responses in MTL co-occurring with local slow/theta waves. In the auditory domain, we show in both rodents and humans that responses in sleep and light anesthesia are preserved up to A1, challenging the classic "thalamic gating" notion, but robust attenuation occurs later in high-level cortical regions. In addition, sleep affects more strongly responses that require integration over long time intervals, and responses to high-frequency content. The second set of studies investigates the underlying mechanisms, testing the potential role of locus coeruleus-noradrenaline (LC-NE) neuromodulation. In rats, we test how NE signaling affects the probability to wake up from sleep in response to sounds. We establish a new approach for selective in-vivo LC optogenetics by showing effects on spiking activity, evoked sleep-wake transitions, and pupil dilation. Combined LC and auditory stimulation synergistically increases the probability of awakenings beyond independent effects of sound and laser alone, supporting a role for LC-NE activity in mediating sensory responses. We also tested the effects of NE levels on sensory perception and sensory-evoked activity (EEG, fMRI) in awake humans. Pharmacologically manipulating NE levels in double-blind placebo-controlled experiments, we found that NE modulates sensitivity and accuracy of visual perception without significant effects on decision bias (criterion). In addition, NE increased the fidelity of late EEG visual responses, and selectively modulated BOLD fMRI responses in high-order visual cortex, suggesting that NE plays an enabling causal role in visual awareness by affecting late visual processing.

Neural networks mapping actions to their sensory consequences

Lecture
Date:
Tuesday, June 26, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Roy Mukamel
|
School of Psychological Sciences and Sagol School of Neuroscience Tel-Aviv University

A specific motor action can lead to different sensory consequences, and a particular sensory consequence can be achieved by different motor actions. This non-unique mapping between actions and sensory consequences is context dependent and requires learning in order to optimize behavior. During my talk, I will describe behavioral and neuroimaging studies in humans, in which we examined how actions modulate perception and how perception can lead to motor skill learning even in the absence of voluntary movement. Manipulating the link between actions and their sensory consequences by using virtual reality, we explore various training techniques to facilitate learning in healthy subjects and rehabilitation in patients with hemiparesis due to neurological origin.

What the nose tells the brain

Lecture
Date:
Thursday, June 21, 2018
Hour: 12:30 - 13:30
Location:
Prof. Dmitry Rinberg
|
Dept of Neuroscience & Physiology NYU Neuroscience Institute

All living organisms extract chemical information from the surrounding world. We know a lot about the genetic, cellular, and anatomical organization of our sense of smell, which has similar organization from insects to mammals. However, we still do not know basic principles of odor coding, organization of the odor parameter space, and how odors are represented in the brain. In humans, odors are sensed by millions of receptor cells using ~350 types of receptor cells. Flies have 60 and mice ~1000 receptor types. An odor evokes a concentration-dependent spatial-temporal pattern of receptor cell activity. We are presented with an immensely complex combinatorial computation. And the central question of my research is to understand how these patterns are read by the brain. In this talk I will present our recent results on testing a novel model for concentration-invariant odor coding based on temporal ranking of receptor. And then I will discuss our attempt to build a theory of odor space representation in the brain based on this model.

Mechanisms of sparse coding in the dentate gyrus

Lecture
Date:
Tuesday, June 19, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Dr. Heinz Beck
|
Institute of Experimental Epileptology and Cognition Research Life and Brain Center, University of Bonn Medical Center

Pluripotent models for neurodegenerative diseases

Lecture
Date:
Tuesday, June 12, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eran Meshorer
|
Department of Genetics, The Institute of Life Sciences and The Edmond and Lily Safra Centre for Brain Sciences The Hebrew University of Jerusalem

Enhanced capacity and dynamic gating in a model of context-dependent associative memory

Lecture
Date:
Thursday, May 31, 2018
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Bill Podlaski
|
Centre for Neural Circuits and Behaviour University of Oxford

An increasing amount of evidence suggests that memory formation and retrieval are modulated by contextual signals, such as behavioral or emotional state. However, typical models of associative memory do not incorporate this dependency. Here we propose an extension to the Hopfield network which takes into account contextual modulation. The network is divided into a set of overlapping subnetworks, each representing a different context with a separate set of memory patterns. Only one subnetwork is active at any given time, thereby reducing interference from memories found in other contexts, which remain dormant through inhibitory control. Using theoretical and numerical methods, we show that these context-modular Hopfield networks have substantially increased memory capacity, as well as robustness to noise and to memory overloading. Their performance depends on two parameters—the number of subnetworks, and their relative size—and when chosen optimally, the capacity is up to ten times greater than the standard Hopfield model. We then show that adding context-dependent dendritic pruning further enhances the performance of the model. Improved performance comes at the cost of limited retrieval, because only memories stored in the active subnetwork can be recalled. To address this, we propose a system in which a controller network dynamically switches the memory network to a desired contextual state before storage or retrieval. Through simulations, we successfully show that this system is able to bias memory retrieval based on context. Overall, our work illustrates the benefits of context-dependent memory, and may have implications for our understanding of cortical memories and their interaction with contextual signals in the prefrontal cortex and hippocampus.

Synaptic and extrasynaptic neuron-glia interactions

Lecture
Date:
Tuesday, May 29, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Alexey Semyanov
|
Institute of Neuroscience University of Nizhny Novgorod, Russia

Brain is often viewed as large neuronal connectome where the information is encoded in the patterns of action potentials and stored in the changes of synaptic strength or appearance of new wiring routes. However, recent studies have demonstrated that astrocytes also possess complex patterns of calcium signals influenced by neuronal activity. Astrocytic calcium signals regulate various functions of these cells including release of gliotransmitters and morphological changes in the astrocytic processes (Tanaka et al., 2013). It has been tempting to suggest that information in astrocytes is encoded in the frequency of calcium events, similar to patters of neuronal action potentials. Synaptically released neurotransmitters thought to trigger new calcium events in perisynaptic astrocytic processes (PAPs) though activation of metabotropic glutamate receptors (mGluRs). In contrast, our recent findings suggest that PAPs are devoid of calcium stores that are required for mGluR-mediated calcium signaling (Patrushev et al., 2013). This makes unlikely any significant role of mGluRs in triggering calcium events in PAPs. Instead, we show that activation of ‘extrasynaptic’ astrocytic mGluRs increases proportion of spatially extended calcium events in the power-law based distribution of calcium event sizes (Wu et al., 2014). This effect takes place without any significant increase in the frequency of calcium events. These findings suggest that astrocytic response to surrounding neuronal activity is rather encoded in spatial characteristics of their calcium events and fundamentally different from temporal information coding in neurons (e.g. coincidence detection, action potentials sequences etc). Nevertheless, we cannot exclude local ionic changes in PAPs in response to synaptic activity. For example, potassium ions accumulate in the synaptic cleft of glutamatergic synapses during repetitive activity. We have demonstrated that the bulk of these ions is contributed by potassium efflux through postsynaptic NMDA receptors (Shih et al., 2013). Potassium mediated depolarization of presynaptic terminal increases glutamate release probability. Now we have found that accumulation of intracleft potassium during repetitive synaptic activity could also inhibit astrocytic glutamate uptake by depolarizing PAPs. This extends glutamate dwell-time in the synaptic cleft and boosts glutamate spillover effects.

Pages

All events, All years

Human physiological and behavioral responses to olfactory stimuli in health and disease

Lecture
Date:
Tuesday, July 17, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Liron Rozenkrantz (PhD Thesis Defense)
|
Noam Sobel Lab, Dept of Neurobiology, WIS

In my PhD I led three projects probing human behavioral and physiological responses to olfactory stimuli in health and disease. In these projects I used every-day olfactory occurrences in order to infer on biological underpinnings of human behavior. In my main project I tested olfactory processing in autism, using the sniff response, a ten-minute non-verbal measure of respiratory response to odors. I found this objective measure to be profoundly altered in children with autism, and furthermore, to be highly correlated with autism severity. Using computational methods, I demonstrated 81% correct ASD classification based on differences in olfactory processing alone. These results provide proof-of-concept for a potential biomarker for autism (Rozenkrantz et al, Curr Bio, 2015). In a second and soon-to-be-submitted project, I investigated olfactory social communication in recurrent pregnancy loss (RPL), resting on a phenomenon in rodents in which females miscarry following exposure to bodily odors of non-stud males. I found that women with RPL display heightened social olfactory abilities, which were significantly correlated with number of miscarriages. Additionally, women with RPL showed significantly altered hormonal, physiological and neural responses to body odors of unfamiliar men. This project provides novel evidence for altered olfactory processing in human recurrent miscarriages. The third project is also my first foothold in placebo effect research, which I will pursue in my postdoc. Taking advantage of the non-invasive nature of olfactory stimuli, I used an odor as the placebo carrier, and tested two groups of subjects for different creativity tests. Both groups smelled the odor, but only the placebo group was told that it increases creativity (placebo manipulation). I found that following this simple manipulation, the placebo group displayed significantly enhanced creativity (Rozenkrantz et al., PLoS one, 2017). Taken together, these projects convey my deep interest in the interplay between human behavior and physiology.

Sensory processing across behavioral and neuromodulatory states

Lecture
Date:
Tuesday, July 3, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Yuval Nir
|
Sagol School of Neuroscience & Sackler School of Medicine Tel-Aviv University

"Sensory disconnection" – conditions when the same sensory stimulus does not reliably affect behavior or subjective experience - is a defining feature of sleep, and similar processes may occur during light anesthesia or during cognitive lapses in wakefulness. What are the changes in brain activity that mediate sensory disconnection? In a series of studies in humans and rodents, we investigate how "disconnected" states affect sensory processing. The first set of studies reveals differences in neuronal responses to identical sensory stimuli across states. We find that in humans, cognitive lapses after sleep deprivation involve attenuated and delayed single-neuron responses in MTL co-occurring with local slow/theta waves. In the auditory domain, we show in both rodents and humans that responses in sleep and light anesthesia are preserved up to A1, challenging the classic "thalamic gating" notion, but robust attenuation occurs later in high-level cortical regions. In addition, sleep affects more strongly responses that require integration over long time intervals, and responses to high-frequency content. The second set of studies investigates the underlying mechanisms, testing the potential role of locus coeruleus-noradrenaline (LC-NE) neuromodulation. In rats, we test how NE signaling affects the probability to wake up from sleep in response to sounds. We establish a new approach for selective in-vivo LC optogenetics by showing effects on spiking activity, evoked sleep-wake transitions, and pupil dilation. Combined LC and auditory stimulation synergistically increases the probability of awakenings beyond independent effects of sound and laser alone, supporting a role for LC-NE activity in mediating sensory responses. We also tested the effects of NE levels on sensory perception and sensory-evoked activity (EEG, fMRI) in awake humans. Pharmacologically manipulating NE levels in double-blind placebo-controlled experiments, we found that NE modulates sensitivity and accuracy of visual perception without significant effects on decision bias (criterion). In addition, NE increased the fidelity of late EEG visual responses, and selectively modulated BOLD fMRI responses in high-order visual cortex, suggesting that NE plays an enabling causal role in visual awareness by affecting late visual processing.

Neural networks mapping actions to their sensory consequences

Lecture
Date:
Tuesday, June 26, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Roy Mukamel
|
School of Psychological Sciences and Sagol School of Neuroscience Tel-Aviv University

A specific motor action can lead to different sensory consequences, and a particular sensory consequence can be achieved by different motor actions. This non-unique mapping between actions and sensory consequences is context dependent and requires learning in order to optimize behavior. During my talk, I will describe behavioral and neuroimaging studies in humans, in which we examined how actions modulate perception and how perception can lead to motor skill learning even in the absence of voluntary movement. Manipulating the link between actions and their sensory consequences by using virtual reality, we explore various training techniques to facilitate learning in healthy subjects and rehabilitation in patients with hemiparesis due to neurological origin.

What the nose tells the brain

Lecture
Date:
Thursday, June 21, 2018
Hour: 12:30 - 13:30
Location:
Prof. Dmitry Rinberg
|
Dept of Neuroscience & Physiology NYU Neuroscience Institute

All living organisms extract chemical information from the surrounding world. We know a lot about the genetic, cellular, and anatomical organization of our sense of smell, which has similar organization from insects to mammals. However, we still do not know basic principles of odor coding, organization of the odor parameter space, and how odors are represented in the brain. In humans, odors are sensed by millions of receptor cells using ~350 types of receptor cells. Flies have 60 and mice ~1000 receptor types. An odor evokes a concentration-dependent spatial-temporal pattern of receptor cell activity. We are presented with an immensely complex combinatorial computation. And the central question of my research is to understand how these patterns are read by the brain. In this talk I will present our recent results on testing a novel model for concentration-invariant odor coding based on temporal ranking of receptor. And then I will discuss our attempt to build a theory of odor space representation in the brain based on this model.

Mechanisms of sparse coding in the dentate gyrus

Lecture
Date:
Tuesday, June 19, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Dr. Heinz Beck
|
Institute of Experimental Epileptology and Cognition Research Life and Brain Center, University of Bonn Medical Center

Pluripotent models for neurodegenerative diseases

Lecture
Date:
Tuesday, June 12, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eran Meshorer
|
Department of Genetics, The Institute of Life Sciences and The Edmond and Lily Safra Centre for Brain Sciences The Hebrew University of Jerusalem

Enhanced capacity and dynamic gating in a model of context-dependent associative memory

Lecture
Date:
Thursday, May 31, 2018
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Bill Podlaski
|
Centre for Neural Circuits and Behaviour University of Oxford

An increasing amount of evidence suggests that memory formation and retrieval are modulated by contextual signals, such as behavioral or emotional state. However, typical models of associative memory do not incorporate this dependency. Here we propose an extension to the Hopfield network which takes into account contextual modulation. The network is divided into a set of overlapping subnetworks, each representing a different context with a separate set of memory patterns. Only one subnetwork is active at any given time, thereby reducing interference from memories found in other contexts, which remain dormant through inhibitory control. Using theoretical and numerical methods, we show that these context-modular Hopfield networks have substantially increased memory capacity, as well as robustness to noise and to memory overloading. Their performance depends on two parameters—the number of subnetworks, and their relative size—and when chosen optimally, the capacity is up to ten times greater than the standard Hopfield model. We then show that adding context-dependent dendritic pruning further enhances the performance of the model. Improved performance comes at the cost of limited retrieval, because only memories stored in the active subnetwork can be recalled. To address this, we propose a system in which a controller network dynamically switches the memory network to a desired contextual state before storage or retrieval. Through simulations, we successfully show that this system is able to bias memory retrieval based on context. Overall, our work illustrates the benefits of context-dependent memory, and may have implications for our understanding of cortical memories and their interaction with contextual signals in the prefrontal cortex and hippocampus.

Synaptic and extrasynaptic neuron-glia interactions

Lecture
Date:
Tuesday, May 29, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Alexey Semyanov
|
Institute of Neuroscience University of Nizhny Novgorod, Russia

Brain is often viewed as large neuronal connectome where the information is encoded in the patterns of action potentials and stored in the changes of synaptic strength or appearance of new wiring routes. However, recent studies have demonstrated that astrocytes also possess complex patterns of calcium signals influenced by neuronal activity. Astrocytic calcium signals regulate various functions of these cells including release of gliotransmitters and morphological changes in the astrocytic processes (Tanaka et al., 2013). It has been tempting to suggest that information in astrocytes is encoded in the frequency of calcium events, similar to patters of neuronal action potentials. Synaptically released neurotransmitters thought to trigger new calcium events in perisynaptic astrocytic processes (PAPs) though activation of metabotropic glutamate receptors (mGluRs). In contrast, our recent findings suggest that PAPs are devoid of calcium stores that are required for mGluR-mediated calcium signaling (Patrushev et al., 2013). This makes unlikely any significant role of mGluRs in triggering calcium events in PAPs. Instead, we show that activation of ‘extrasynaptic’ astrocytic mGluRs increases proportion of spatially extended calcium events in the power-law based distribution of calcium event sizes (Wu et al., 2014). This effect takes place without any significant increase in the frequency of calcium events. These findings suggest that astrocytic response to surrounding neuronal activity is rather encoded in spatial characteristics of their calcium events and fundamentally different from temporal information coding in neurons (e.g. coincidence detection, action potentials sequences etc). Nevertheless, we cannot exclude local ionic changes in PAPs in response to synaptic activity. For example, potassium ions accumulate in the synaptic cleft of glutamatergic synapses during repetitive activity. We have demonstrated that the bulk of these ions is contributed by potassium efflux through postsynaptic NMDA receptors (Shih et al., 2013). Potassium mediated depolarization of presynaptic terminal increases glutamate release probability. Now we have found that accumulation of intracleft potassium during repetitive synaptic activity could also inhibit astrocytic glutamate uptake by depolarizing PAPs. This extends glutamate dwell-time in the synaptic cleft and boosts glutamate spillover effects.

From dragons’ sleep to sliders’ sight: reexamination of reptilian model systems

Lecture
Date:
Monday, May 28, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Mark Shein-Idelson
|
Dept of Neurobiology Faculty of Life Sciences Sagol School for Neuroscience Tel Aviv University

Throughout the history of neuroscience, a large set of model systems has been used for studying a large variety of questions. These model systems were frequently chosen for their unique experimental advantages, but studying them also provided a wider perspective on basic questions: By examining the manifestation of a given biological phenomenon across different species, one could separate the salient or fundamental from the transient or variable. In my talk I will focus on two of our studies in reptiles: sleep in bearded dragons and visual processing in red eared sliders. I will show how we can use turtles for understanding structure function relations in neural circuits and how we can use lizards for exploring the organization of collective activity during sleep. In addition, I will show that such studies provide a new u! nderstanding of the evolution of brain dynamics.

Synaptic dynamics in mouse visual cortex

Lecture
Date:
Tuesday, May 15, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Tara Keck
|
University College London

Homeostatic synaptic scaling is thought to occur cell-wide, but recent evidence suggests this form of stabilizing plasticity can be implemented more locally in reduced preparations. To investigate the spatial scales of plasticity in vivo, we used repeated two-photon imaging in mouse visual cortex after sensory deprivation to measure TNF-α dependent increases in spine size as a proxy for synaptic scaling in vivo in both excitatory and inhibitory neurons. We found that after sensory deprivation, increases in spine size are restricted to a subset of dendritic branches, which we confirmed using immunohistochemistry. We found that the dendritic branches that had individual spines that increased in size following deprivation, also underwent a decrease in spine density. Within a given dendritic branch, the degree of spine size increases is proportional to recent spine loss within that branch. Using computational simulations, we show that this compartmentalized form of synaptic scaling better retained the previously established input-output relationship in the cell, while restoring activity levels. We then investigated the relationship between new spines that form after this spine loss and strengthening and find that their spatial positioning facilitates strengthening of maintained synapses.

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