Yael Amitai
Ben-Gurion University of the Negev
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Yael Amitai.
Neuron | 1997
Ziv Gil; Barry W. Connors; Yael Amitai
Synapses are continually regulated by chemical modulators and by their own activity. We tested the specificity of regulation in two excitatory pathways of the neocortex: thalamocortical (TC) synapses, which mediate specific inputs, and intracortical (IC) synapses, which mediate the recombination of cortical information. Frequency-sensitive depression was much stronger in TC synapses than in IC synapses. The two synapse types were differentially sensitive to presynaptic neuromodulators: only IC synapses were suppressed by activation of GABA(B) receptors, only TC synapses were enhanced by nicotinic acetylcholine receptors, and muscarinic acetylcholine receptors suppressed both synapse types. Modulators also differentially altered the frequency sensitivity of the synapses. Our results suggest a mechanism by which the relative strength and dynamics of input and associational pathways of neocortex are regulated during changes in behavioral state.
Neuron | 1999
Ziv Gil; Barry W. Connors; Yael Amitai
Thalamocortical (TC) synapses carry information into the neocortex, but they are far outnumbered by excitatory intracortical (IC) synapses. We measured the synaptic properties that determine the efficacy of TC and IC axons converging onto spiny neurons of layer 4 in the mouse somatosensory cortex. Quantal events from TC and IC synapses were indistinguishable. However, TC axons had, on average, about 3 times more release sites than IC axons, and the mean release probability at TC synapses was about 1.5 times higher than that at IC synapses. Differences of innervation ratio and release probability make the average TC connection several times more effective than the average IC connection, and may allow small numbers of TC axons to dominate the activity of cortical layer 4 cells during sensory inflow.
Proceedings of the National Academy of Sciences of the United States of America | 2008
Wei-Chung Allen Lee; Jerry L. Chen; Hayden Huang; Jennifer H. Leslie; Yael Amitai; Peter T. C. So; Elly Nedivi
The contribution of structural remodeling to long-term adult brain plasticity is unclear. Here, we investigate features of GABAergic interneuron dendrite dynamics and extract clues regarding its potential role in cortical function and circuit plasticity. We show that remodeling interneurons are contained within a “dynamic zone” corresponding to a superficial strip of layers 2/3, and remodeling dendrites respect the lower border of this zone. Remodeling occurs primarily at the periphery of dendritic fields with addition and retraction of new branch tips. We further show that dendrite remodeling is not intrinsic to a specific interneuron class. These data suggest that interneuron remodeling is not a feature predetermined by genetic lineage, but rather, it is imposed by cortical laminar circuitry. Our findings are consistent with dynamic GABAergic modulation of feedforward and recurrent connections in response to top-down feedback and suggest a structural component to functional plasticity of supragranular neocortical laminae.
Archive | 1995
Yael Amitai; Barry W. Connors
Neocortical neurons are eclectic in function, shape, and chemistry. Here we review a relatively neglected topic of neocortical biology, its cellular neurophysiology. Our central premise is that neurons of the neocortex display variations in membrane properties, and that these are correlated with other characteristics of the cells. Current methods allow specification of neuronal morphology, synaptology, biochemistry, intrinsic physiology, and gene expression, and each measurement has reinforced the view that neocortex is comprised of many neuron types. Within distinct classes there may also be wide variations in certain properties. Variability may represent either adaption, developmental noise, pathology, or technical artifact, and the challenge is to recognize the differences. We will discuss the interesting, but still tenuous, hypothesis that biophysical diversity of neurons in neocortex is an adaptation to specific functions within cortical circuits.
Neuron | 1997
Barry W. Connors; Yael Amitai
Our current understanding of cortical oscillators is decidedly weak. Their phenomenology needs closer study. For example, how much do the various specific subclasses of neurons participate during various oscillations, how do excitatory and inhibitory neurons interact, how large are synchronous rhythmic cell assemblies, and how and when do they alter their size? Studies of mechanisms are impeded by a classic experimental dilemma: even a local cortical network is too complex to analyze and understand fully when intact but reducing it also fundamentally changes it. Apparent insights from drugged models in vitro must somehow be tested in vivo and au naturel. Local neocortical oscillators also need to be understood within their larger context. In the thinking brain, they may rarely operate uncoupled from subcortical oscillators, in particular those of the thalamus, and it is clear that oscillations in connected regions interact (e.g.,17xNicolelis, M.A.L., Baccala, L.A., Lin, R.C.S., and Chapin, J.K. Science. 1995; 268: 1353–1358Crossref | PubMedSee all References, 7xContreras, D., Destexhe, A., Sejnowski, T.J., and Steriade, M. Science. 1996; 274: 771–774Crossref | PubMed | Scopus (279)See all References, 21xSteriade, M., Contreras, D., Amzica, F., and Timofeev, I. J. Neurosci. 1996; 16: 2788–2808PubMedSee all References). The age-old observation that cerebral rhythms vary with functional states of the brain (Adrian and Matthews 1934xAdrian, E.D. and Matthews, B.C. Brain. 1934; 57: 355–385Crossref | Scopus (468)See all ReferencesAdrian and Matthews 1934) implies that oscillators are dynamically regulated. Key mechanistic questions include: how do sets of local oscillators rapidly and specifically couple and uncouple within the cortex, and how are cortical oscillators controlled by the subcortical regulatory systems associated with arousal and sleep? Understanding the ultimate problem, the behavioral functions of neocortical oscillations, would benefit immensely from methods that disrupt synchronous oscillations while doing minimal damage to all other cortical processes. Pessimists will scoff that this can never be done selectively, but recent success with a remarkably analogous problem in the locust brain (MacLeod and Laurent 1996xMacLeod, K. and Laurent, G. Science. 1996; 274: 976–979Crossref | PubMed | Scopus (251)See all ReferencesMacLeod and Laurent 1996) should give hope to those who investigate waves in the cerebral cortex of vertebrates.
European Journal of Neuroscience | 1991
Karin Brener; Yael Amitai; John G. R. Jefferys; Michael J. Gutnick
Injection of 0.2–3.0 ng of tetanus toxin into rat parietal neocortex resulted in permanent (> 7 months) changes in the local circuit properties of this tissue. It caused excessive synchronization of neuronal activity. This was seen as spontaneous paroxysmal field potentials and/or evoked all‐or‐none population burst discharges. Such activity was recorded widely over the parietal and temporal areas of both the injected and the contralateral hemispheres from as little as 16 h after injection up to the maximum survival time of 7 months. Several observations suggest that the speed with which the hypersynchronous activity spread to the opposite hemisphere reflects transport of the toxin through corticocortical axons, and consequent blockade of synaptic inhibition. However, from what is known of the half life of the peptide in brain, it is unlikely that the persistent, widespread distribution of epileptiform discharge several months after injection was due to the continued presence of toxin. Thus, intracortical application of tetanus toxin provides a good experimental model of chronic focal epilepsies, and raises fundamental questions regarding the long term regulation of local circuit properties in the neocortex.
Glia | 2010
Yael Amitai
Nitric oxide (NO) has been long recognized as an atypical neuronal messenger affecting excitatory synaptic transmission, but its cellular source has remained unresolved as the neuronal isoform of NO synthase (nNOS) in many brain regions is expressed only by small subsets of inhibitory neurons. It is generally believed that the glial NO‐producing isoform (iNOS) is not expressed in the normal brain, but rather it undergoes a transcription‐mediated up‐regulation following an immunological challenge. Therefore, the involvement of iNOS in modulating normal neuronal functions has been largely ignored. Here I review evidence to the contrary: I summarize data pointing to the existence of a functioning iNOS in normal undisturbed mammalian brains, and experimental results tracing this expression to astrocytes. Finally, I review recent findings asserting that iNOS‐dependent NO modulates synaptic release from presynaptic terminals. Based on these data, I propose that astrocytes express basal levels of iNOS. Flanking synaptic elements, astrocytes are perfectly positioned to release NO and affect synaptic transmission.
Glia | 2005
Yossi Buskila; Shai Farkash; Michal Hershfinkel; Yael Amitai
Nitric oxide (NO), a cellular signaling molecule, is produced in the brain by both neurons and astrocytes. While neurons are capable of rapid release of small amounts of NO serving as neurotransmitter, astrocytic NO production has been demonstrated mainly as a slow reaction to various stress stimuli. Little is known about the role of astrocyte‐produced NO. Using the NO indicator 4,5‐diaminofluorescein‐2 diacetate (DAF‐2DA) and acute slices from mouse brain, we distinguished neurons from astrocytes based on their different fluorescence kinetics and pattern, cellular morphology, electrophysiology, and responses to selective nitric oxide synthase (NOS) inhibitors. Typically, astrocytic fluorescence followed neuronal fluorescence with a delay of 1–2 min and was dependent on the inducible NOS isoform (iNOS) activity. Western blot analysis established the presence of functional iNOS in the neocortex. An assay for cell death revealed that most DAF‐2DA‐positive neurons, but not astrocytes, were damaged. Whole cell recordings from astrocytes confirmed that these cells maintained their membrane potential and passive properties during illumination and afterward. Induction of excitotoxicity by brief application of glutamate triggered an immediate and intense astrocytic response, while high‐frequency electrical stimulation failed to do so. The present study demonstrates, for the first time, rapid and massive iNOS‐dependent NO production by astrocytes in situ, which appears to be triggered by acute neuronal death. These data may bear important implications for our theoretical understanding and practical management of acute brain insults.
Reviews in The Neurosciences | 2001
Yael Amitai
The thalamic input to the neocortex is communicated by glutamatergic synapses. The properties and organization of these synapses determine the primary level of cortical processing. Similar to intracortical synapses, both AMPA and NMDA receptors in young and mature animals mediate thalamocortical transmission. Kainate receptors participate in thalamocortical transmission during early development. The shape of thalamocortical synaptic potentials is similar to the shape of intracortical potentials. On the other hand, thalamocortical synapses have on average a higher release probability than intracortical synapses, and a much higher number of release sites per axon. As a result, the transmission of each thalamocortical axon is significantly more reliable and efficient than most intracortical axons. Thalamic axons specifically innervate a subset of inhibitory cells, to create a strong and secure feed-forward inhibitory pathway. Thalamocortical connections display many forms of synaptic plasticity in the first postnatal week, but not afterwards. The implications of the functional organization of thalamocortical synapses for neocortical processing are discussed.
The Journal of Neuroscience | 2007
Yulia Bereshpolova; Yael Amitai; Alexander G. Gusev; Carl R. Stoelzel; Harvey A. Swadlow
The spread of somatic spikes into dendritic trees has become central to models of dendritic integrative properties and synaptic plasticity. However, backpropagating action potentials (BPAPs) have been studied mainly in slices, in which they are highly sensitive to multiple factors such as firing frequency and membrane conductance, raising doubts about their effectiveness in the awake behaving brain. Here, we examine the spatiotemporal characteristics of BPAPs in layer 5 pyramidal neurons in the visual cortex of adult, awake rabbits, in which EEG-defined brain states ranged from alert vigilance to drowsy/inattention, and, in some cases, to light sleep. To achieve this, we recorded extracellular spikes from layer 5 pyramidal neurons and field potentials above and below these neurons using a 16-channel linear probe, and applied methods of spike-triggered current source-density analysis to these records (Buzsáki and Kandel, 1998; Swadlow et al., 2002). Precise retinotopic alignment of superficial and deep cortical sites was used to optimize alignment of the recording probe with the axis of the apical dendrite. During the above network states, we studied BPAPs generated spontaneously, antidromically (from corticotectal neurons), or via intense synaptic drive caused by natural visual stimulation. Surprisingly, the invasion of BPAPs as far as 800 μm from the soma was little affected by the network state and only mildly attenuated by high firing frequencies. These data reveal that the BPAP is a robust and highly reliable property of neocortical apical dendrites. These events, therefore, are well suited to provide crucial signals for the control of synaptic plasticity during information-processing brain states.