Traub & Whittington; Cortical Oscillations
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Traub; Cortical Oscillations 5 Recent Developments in Cortical Oscillations
Traub; Cortical Oscillations 5 Earlier work (1999) was almost entirely concerned with gamma (30-70 Hz) and beta (10-30 Hz) oscillations evoked in hippocampal slices by tetanic stimulation, with a special emphasis on long-range synchrony of the oscillations. 0
Traub; Cortical Oscillations 6 Neurotransmitters/neuromodulatory substances act on a variety of receptors, both ionotropic (phasic) and metabotropic (slower, or tonic). 1
Traub; Cortical Oscillations 6 Large, slow, excitatory postsynaptic potentials (EPSPs) develop in pyramidal neurons as well as in interneurons, mediated in large part by metabotropic glutamate receptors. 0
Traub; Cortical Oscillations 6 Superimposed on the slow EPSPs are trains of fast inhibitory postsynaptic potentials (IPSPs). 0
Traub; Cortical Oscillations 6 Locally synchronized network oscillations develop after a latent period of 50 to several hundred milliseconds, at gamma frequencies, and lasting for hundreds of milliseconds. 0
Traub; Cortical Oscillations 6 Both the latent period and the duration of the electrically invoked gamma oscillations are similar to those observed in visual-neocortical gamma oscillations in vivo evoked by a stimulus such as a moving grating at appropriate orientation. 0
Traub; Cortical Oscillations 8 Long-range synchrony of gamma oscillations and interneuron doublets in a rat dorsal hippocampal slice (diagram) 2
Traub; Cortical Oscillations 12 There are at least three reasons to study cortical oscillations: (1) they may play a role in normal brain functions, cognition, and especially sleep; (2) they play a role in neuropsychiatric disorders such as epilepsy, schizophrenia, Parkinson's disease, and cerebellar ataxia; (3) study of oscillations has enriched cellular neurobiology with respect to gap junctions, synaptic mechanisms, and intrinsic neuronal membrane physiology. 4
Traub; Cortical Oscillations 12 Very fast oscillations (70-80 Hz) can be generated in conditions of chemical synaptic blockade, but also occur in other conditions as well. 0
Traub; Cortical Oscillations 12 Persistent gamma oscillations, which could be related to abnormal epileptiform activity. 0
Traub; Cortical Oscillations 12 Beta-2 oscillations, at about 25 Hz, are generated in large tufted pyramidal neurons of layer 5 of the cerebral cortex. 0
Traub; Cortical Oscillations 12 Mixtures of oscillations occur during epileptogenesis. 0
Traub; Cortical Oscillations 13 What all the diverse types of oscillations have in common is electrical coupling via gap junctions. 1
Traub; Cortical Oscillations 13 Most or all of the somatic action potentials originate in axons and then propagate antidromically (as well as orthodromically). 0
Traub; Cortical Oscillations 13 Fast oscillations are generated by axonal action potentials occurring either spontaneously (ectopically), or as a result of action potentials in electrically coupled axons -- and not as a result of synaptic input to the soma and dendrites. 0
Traub; Cortical Oscillations 13 Synaptic integration -- the postulate that neuronal firing is a consequence of synaptic inputs to cells, is a classic (and very deeply ingrained) concept that pervades all of neuroscience. 0
Traub; Cortical Oscillations 13 In epilepsy, why so many sorts of oscillations -- at widely different frequencies -- are associated with the epoch before a seizure, as well as during the seizure itself. 0
Traub; Cortical Oscillations 13 For schizophrenia, sensory stimulation evokes gamma followed by beta oscillations in the intact human brain, but the "habituation" properties of the beta portion are different in schizophrenics as compared with nonschizophrenics. 0
Traub; Cortical Oscillations 13 In Parkinson's disease, the symptomatic disease is correlated with enhanced beta oscillations (15-30 Hz) in a number of locations within the basal ganglia, and L-DOPA treatment, which elevates dopamine concentration within the brain, attenuates the beta activity as it relieves symptoms. 0
Traub; Cortical Oscillations 14 For cerebellar ataxia, it is premature to draw firm conclusions about the importance of brain oscillations for ataxia, even though there must be some connection. 1
Traub; Cortical Oscillations 14 The best-known cerebellar oscillations consists of localized regions of 4-10 Hz rhythms that are generated in the inferior olive and projected to the cerebellum via the climbing fibers. 0
Traub; Cortical Oscillations 14 Faster oscillations occur in the cerebellum, and have some degree of coherence with oscillations in other parts of the motor system (portions of the thalamus, basal ganglia, and cerebral cortex). 0
Traub; Cortical Oscillations 14 Both gamma and very fast oscillations have been generated in cerebellar cortex slices, with very fast oscillations occurring at 100 to 200 Hz, being produced by electrical coupling. 0
Traub; Cortical Oscillations 14 Table of frequency ranges of various oscillations (table) 0
Traub; Cortical Oscillations 15 Do not use the term "gamma" for oscillations above 80 Hz because these are presumed not gated primarily by IPSPs. 1
Traub; Cortical Oscillations 15 The term "gamma" should be reserved for oscillations gated by inhibitory postsynaptic potentials (IPSPs). 0
Traub; Cortical Oscillations 56 Working memory (in prefrontal, parietal, and inferior temporal cortex) is apparently associated with the activation of selected brain regions; and within these regions, there appears to be an additional selection of some neurons that fire at high rates. 41
Traub; Cortical Oscillations 56 In addition to localized cortical activation, there are global cortical activated epochs (each lasting hundreds of milliseconds, and with hundreds-of-milliseconds to seconds separation between epochs), that occur during the slow (~1 Hz) oscillation of sleep. 0
Traub; Cortical Oscillations 57 Absence of firing in the hyperpolarized state ("downstate"). 1
Traub; Cortical Oscillations 58 Fast oscillations are coherent between thalamus and cortex. 1
Traub; Cortical Oscillations 58 Fast oscillations during slow wave sleep as spatially limited coherence. 0
Traub; Cortical Oscillations 60 "Standard" models of neuronal networks are based on the assumption that timing is determined by membrane depolarization and the pattern of synaptic inputs. 2
Traub; Cortical Oscillations 60 Action potentials can be generated in axons, influenced in large part by action potentials in electrically coupled axons. 0
Traub; Cortical Oscillations 60 The slow oscillation of sleep correlates with the occurrence of certain EEG patterns (delta waves). 0
Traub; Cortical Oscillations 60 During slow wave sleep, we do not see rapid eye movements, skeletal muscular paralysis, or continuous EEG fast rhythms. 0
Traub; Cortical Oscillations 63 Very Fast Oscillations Superimposed on Sensory Evoked Potentials 3
Traub; Cortical Oscillations 63 Free sensory stimulation, and any modality, evokes a series of neural responses in cortical structures, and early (<~150 ms) and it longer (<~500 ms) latencies, typically consisting of waves that last on the order of tens of milliseconds. 0
Traub; Cortical Oscillations 63 Neural responses to brief sensory stimulation are produced as neural "traffic" proceeds along axons, causing cell firing and then synaptic currents, and in turn influenced successive pools of neurons. 0
Traub; Cortical Oscillations 63 Synchronized epileptiform bursts can be regarded as a type of internally generated evoked response. 0
Traub; Cortical Oscillations 63 Neuronal population responses lasting tens of milliseconds often have very fast oscillations superimposed upon them. 0
Traub; Cortical Oscillations 63 In vivo hippocampal physiological sharp waves contain superimposed "ripples" at about 200 Hz. 0
Traub; Cortical Oscillations 63 It is critical to understand the relation between the slower spontaneous or evoked responses -- which are attributed to synchronized synaptic currents -- and the very fast oscillations that are superimposed. 0
Traub; Cortical Oscillations 64 Very fast oscillations (~390 Hz in this instance) occur superimposed on somatosensory evoked response in rat barrel cortex. (diagram) 1
Traub; Cortical Oscillations 66 Temporal Interactions between Cortical Oscillations in Different Frequencies 2
Traub; Cortical Oscillations 66 Oscillations can be superimposed on transient neuronal population events, and also on particular phases of another, slower, oscillation. 0
Traub; Cortical Oscillations 66 Perhaps the best-known example of one oscillation superimposed on, and amplitude modulated, by another is the case of gamma oscillations superimposed on the hippocampal theta rhythm. 0
Traub; Cortical Oscillations 66 Understanding how interactions take place between oscillations at different frequencies may be important for unraveling the functional importance of each frequency, and how the respective distinct functions might be interrelated. 0
Traub; Cortical Oscillations 66 The cortical beta-1 (~15 Hz) oscillation appears to be produced by fitting together (rather than phase-resetting or amplitude-modulating) two simpler oscillations. 0
Traub; Cortical Oscillations 67 Cerebellar Oscillations 1
Traub; Cortical Oscillations 67 The cellular mechanisms of cerebellar oscillations provide interesting contrasts with mechanisms of neocortical oscillations at comparable frequencies, because the synaptic architecture of cerebral and cerebellar cortices is so different. 0
Traub; Cortical Oscillations 67 Oscillations at theta and alpha frequencies are generated among the electrically coupled pool of inferior olivary neurons, and transmitted to the deep cerebellar nuclei in cerebellar cortex via climbing fibers. 0
Traub; Cortical Oscillations 67 Auditory evoked activity contains fast oscillations. (diagram) 0
Traub; Cortical Oscillations 68 Example of one oscillation (delta) modulating the amplitude of another (theta). 1
Traub; Cortical Oscillations 69 Beta and gamma (as well as lower frequency) oscillations are generated within the cerebellar cortex. 1
Traub; Cortical Oscillations 70 Epilepsy 1
Traub; Cortical Oscillations 105 Parkinson's Disease 35
Traub; Cortical Oscillations 105 The most critical discovery about Parkinson's disease concerned elucidation of the role of dopamine deficiency in causing many of the signs and symptoms. 0
Traub; Cortical Oscillations 105 The discovery of dopamine deficiency in Parkinson's disease led to a range of related pharmacological treatments that are close to miraculous, but ultimately frustrating, because of disease progression, failure to maintain desired clinical actions, and the emergence of troubling side effects. 0
Traub; Cortical Oscillations 105 Parkinson's Disease therapy via implanted device intended for long-term "deep brain stimulation" (DBS). 0
Traub; Cortical Oscillations 106 "Parkinsonism," a clinical constellation of signs and symptoms, with "Parkinson's Disease" referring to a characteristic clinical syndrome with a characteristic underlying neuropathology. 1
Traub; Cortical Oscillations 106 The most characteristic clinical features of Parkinson's disease include a rest tremor (that may initially be voluntarily suppressable, and tends to diminish with intentional movement), muscle rigidity, slowing of movement (bradykinesia -- in its extreme form, akinesia), and a characteristically impaired gait. 0
Traub; Cortical Oscillations 106 Later in Parkinson's disease, postural instability, freezing, and falls can constitute major problems. 0
Traub; Cortical Oscillations 106 In Parkinson's disease, immobility eventually results in confinement to chair and then to bed, as well as difficulty swallowing and clearing secretions. 0
Traub; Cortical Oscillations 107 Dopamine was discovered in the brain (1957) 1
Traub; Cortical Oscillations 109 Organizational Principles of the Basal Ganglia 2
Traub; Cortical Oscillations 110 Some Effects of Dopamine in the Brain 1
Traub; Cortical Oscillations 115 Dopamine and Gap Junctions 5
Traub; Cortical Oscillations 116 Experimental Models of Parkinson's Disease 1
Traub; Cortical Oscillations 116 How is it that dopamine depletion in the brain leads to so many of the signs and symptoms of Parkinson's disease. 0
Traub; Cortical Oscillations 117 Parkinson's disease in humans is associated with a loss of norepinephrine neurons (e.g. in locus coeruleus) as well as dopaminergic neurons. 1
Traub; Cortical Oscillations 117 The Subthalamic Nucleus 0
Traub; Cortical Oscillations 117 One of the most effective nonpharmacological treatments of Parkinson's disease consists of chronic high-frequency stimulation, via an implanted device, of one or both subthalamic nuclei: a so-called deep brain stimulation (DBS) technique. 0
Traub; Cortical Oscillations 117 This subthalamic nucleus consists of glutamatergic cells with rather complex properties, which are able to fire in at least four different modes: a silent hyperpolarized mode, a depolarized plateau, tonic firing of single spikes, and rhythmic slow bursts. 0
Traub; Cortical Oscillations 117 It is not clear if subthalamic neurons interact with each other directly, either through chemical synapses or through gap junctions. 0
Traub; Cortical Oscillations 117 Gamma oscillations at 46 to 70 Hz have been recorded in subthalamus. 0
Traub; Cortical Oscillations 123 Schizophrenia 6
Traub; Cortical Oscillations 123 Schizophrenia is diagnosed by clinical presentation and evolution; it is particularly important to recognize a clear sensorium in the patient and to exclude psychotic states induced by drugs and by neurological disorders, especially disorders that may have specific treatments (such as encephalitis). 0
Traub; Cortical Oscillations 123 No particular laboratory tests -- including imaging, CSF analysis, EEG, and molecular genetic tests -- clenches the diagnosis. 0
Traub; Cortical Oscillations 123 Schizophrenia is defined predominantly by how patients behave, particularly about what they say and write, and how they seem to think. 0
Traub; Cortical Oscillations 124 Schizophrenia is associated with a decline in many aspects of cognitive functions. Perceptual disorganization and working memory deficits figure prominently. 1
Traub; Cortical Oscillations 125 Hallucinations and thought disorder in schizophrenic patients are complemented by examples revealing more specific aspects of disrupted Gestalt processes: limitations in perceptions of a whole sensory object through combination of a set of smaller, simpler features. 1
Traub; Cortical Oscillations 125 Only in the early 20th century did Alois Alzheimer (1964-1915), using staining techniques, define the characteristic neuropathology of the dementing disease: neuronal loss, senile (amyloid) plaques, and neurofibrillary tangles. 0
Traub; Cortical Oscillations 126 Schizophrenia was previously called dementia praecox, emphasizing what was considered to be the usual course of a progressive mental disability. 1
126 "Schizophrenia" derives from the Greek, meaning "splitting of the mind" -- not in the sense of split personality (generally a manifestation of hysteria), but in what was considered a fragmentation of the psyche, a concept difficult to nail down precisely. 0
Traub; Cortical Oscillations 126 The cardinal clinical manifestations of schizophrenia include delusions, that may be grandiose or persecution; abnormal perceptions, including auditory hallucinations in the form of internal voices speaking to the patient, perhaps commenting on him or her; formal thought disorder, in which the patient's trains of thought are difficult or impossible to follow; motor, volitional, and behavioral disorders, including catatonia (immobility and mutism, perhaps with automatic following of commands), mannerisms and stereotypic repeated behaviors; and emotional disorders, including flattened or inappropriate affect, and withdrawal. 0
Traub; Cortical Oscillations 126 Schizophrenia has acute and chronic presentations and courses. 0
Traub; Cortical Oscillations 126 Schizophrenia exhibits positive symptoms, such as hallucinations, and negative symptoms, such as apathy, muteness, and social withdrawal. 0
Traub; Cortical Oscillations 127 Estimates of the prevalence of schizophrenia vary, but one careful review suggests 0.4%, similar to the prevalence of epilepsy. 1
Traub; Cortical Oscillations 127 Schizophrenia most often (certainly not always) strikes in adolescence and young adulthood, and can be relapsing/remitting or progressive -- characteristics shared with multiple sclerosis. 0
Traub; Cortical Oscillations 128 Schizophrenia is a genetic disorder, in large part. 1
Traub; Cortical Oscillations 152 Cerebellar Ataxia 24
Traub; Cortical Oscillations 152 The principal cell type of the cerebellum, the Purkinje cell, is susceptible to anoxia and other biochemical and metabolic stresses, and once lost, these cells are not replaced. 0
Traub; Cortical Oscillations 152 Multiple sclerosis is a common neurological disease (prevalence ~1.0 cases per 1000 population), with ataxia and tremor. 0
Traub; Cortical Oscillations 152 Cerebellar ataxia and tremor are, in almost all cases, extremely difficult to treat. 0
Traub; Cortical Oscillations 152 Ataxia and tremor can be so disabling as to make a patient bedfast, unable to speak or swallow, and completely dependent on caregivers. 0
Traub; Cortical Oscillations 153 The phenomenology of cerebellar disorders has been described exhaustively, but the underlying pathophysiology remains largely mysterious. 1
Traub; Cortical Oscillations 153 Ataxia is notable in learned complex movements of the limbs and articulation, but gait and eye movements can also be ataxic. 0
Traub; Cortical Oscillations 153 Tremor, especially with movement such as reaching or grasping, but possibly also with holding posture, is a symptom of major focal cerebellar injury. 0
Traub; Cortical Oscillations 153 Most movements in humans involve smooth interaction of flexions and extensions (and sometimes rotations) across several joints, both within a given limb (e.g. shoulder, elbow, and wrist), and between limbs (swinging the arms and legs in proper relative phases during walking). 0
Traub; Cortical Oscillations 153 The decomposition of smooth interactions flexions and extensions in limbs and joints may fail with cerebellar disease, to be replaced but not by paralysis, but by a less elegant performance, so that one joint carries out its action, then the next, then the next . . . decomposition. 0
Traub; Cortical Oscillations 154 The cerebellum is not sufficient by itself to produce movements, but it is necessary for movements -- especially complicated ones, involving many joints or muscles -- to be executed smoothly and in coordinated fashion. 1
Traub; Cortical Oscillations 154 The cerebellum is particularly required when sensory input (visual, proprioceptive, vestibular, alone or in combination) is helping to guide the movement. 0
Traub; Cortical Oscillations 154 The cerebellum is intimately interconnected with a number of other important paired structures, including the inferior olive in the medulla, the red nucleus in the midbrain, the vestibular nuclei in the medulla, and perhaps most critically, the deep cerebellar nuclei. 0
Traub; Cortical Oscillations 155 Prominent existence of gap junctions in the inferior olive and vestibular nuclei, and a marked tendency of the inferior olive to generate its own oscillations, whose synchrony depends on gap junctions. 1
Traub; Cortical Oscillations 157 Purkinje cells, the principal neuron of the cerebellar cortex, receiving two distinct types of excitatory afferent, as well as GABAergic input from other cerebellar neurons. 2
Traub; Cortical Oscillations 157 Purkinje cells themselves are GABAergic (inhibitory). 0
Traub; Cortical Oscillations 157 The Purkinje cell has an extensive dendritic arborization, with a proximal smooth (nonspiny) portion, and innumerable spiny branchlets that receive, in total, more than 100,000 excitatory synapses (although many or most of the synapses are probably "silent"). 0
Traub; Cortical Oscillations 157 The dendrites of Purkinje cells are lie roughly in a plane, and the dendritic planes of nearby Purkinje cells are nearly parallel, and orthogonal to the axis of the local folium. 0
Traub; Cortical Oscillations 157 There are an estimated 340,000 Purkinje cells in rat cerebellum. Their somata lie in a single layer, the Purkinje cell layer. 0
Traub; Cortical Oscillations 157 The region inhabited by the Purkinje cell dendrites is called the "molecular layer", and the region just below the Purkinje stomata, through which the Purkinje axons pass, is call the "granular layer". 0
Traub; Cortical Oscillations 160 Lack of Recurrent Synaptic Excitation within This Cerebellar Cortex 3
Traub; Cortical Oscillations 160 Most of the synapses within the cerebral cortex are excitatory synapses lying on excitatory neurons. With suppression of synaptic inhibition, synchronized epileptiform discharges will develop. 0
Traub; Cortical Oscillations 160 In the cerebellar cortex, the only excitatory cells -- the granule cells -- lie in the afferent stream of mossy fibers, and serve to distribute this stream along the parallel fibers. 0
Traub; Cortical Oscillations 160 All the cerebellar cortical neurons, other than granule cells, are inhibitory neurons, and all of the recurrent synaptic connections are GABAergic. 0
Traub; Cortical Oscillations 177 Basic Properties of Single Neurons and Gap Junctions 17
Traub; Cortical Oscillations 179 Cortical Neurons and Their Models 2
Traub; Cortical Oscillations 179 The study of the shapes and intrinsic properties of the vastly many types of neurons, and of the synaptic relations between neurons, is one of the most beautiful of scientific endeavors. 0
Traub; Cortical Oscillations 179 Gap junctions -- electrical synaptic connections whose activity appears to underlie a great many persistent network rhythms. 0
Traub; Cortical Oscillations 180 Physiological principles governing action potentials -- conventional fast action potentials and many other sorts of Ca2+-mediated action potentials. 1
Traub; Cortical Oscillations 180 Membrane conductances exist that are ion selective; that can produce transmembrane currents that are inward or outward; that have different time courses that can be characterized by state variables governed by differential equations involving time, membrane potential, and the state variables themselves; and which can involve multiple states having faster or slower kinetics (i.e. channels that have rapid activation/deactivation and slower inactivation/recovery). 0
Traub; Cortical Oscillations 180 Membrane conductances influence one another through the common medium of the local membrane potential: cooperativity exists even at the level of small membrane patches. 0
Traub; Cortical Oscillations 182 By being able to capture much of the intrinsic electrophysiology of neurons in relatively simple models, it becomes possible to simulate large networks of neurons on a parallel computer. 2
Traub; Cortical Oscillations 182 Simulation of a population of 15,000 cells, with multiple functional subclasses, is readily possible. 0
Traub; Cortical Oscillations 182 Simulation of networks of neurons is an essential tool in understanding oscillations. 0
Traub; Cortical Oscillations 182 Firing Patterns of Some Cortical Interneurons 0
Traub; Cortical Oscillations 182 Two firing patterns that are characteristic of interneurons are fast spiking (FS) and low-threshold spiking (LTS). 0
Traub; Cortical Oscillations 182 Interneurons may also exhibit regular spiking and bursting. 0
Traub; Cortical Oscillations 182 Fast spiking (FS) cells have narrow spikes, can fire rapidly, and have little or no accommodation (i.e. slowing of the frequency with repetitive firing). 0
Traub; Cortical Oscillations 182 Low threshold spiking (LTS) cells have somewhat broader spikes, fire an initial burst of spikes when depolarized from a hyperpolarized resting potential, and do not fire rapidly. 0
Traub; Cortical Oscillations 182 Classification of interneurons is a contentious and intricate subject. 0
Traub; Cortical Oscillations 183 Firing patterns associated with some interneurons: Fast Spiking (FS), Low Threshold Spiking (LTS). (diagram) 1
Traub; Cortical Oscillations 185 Cortical interneurons differ in the way they respond to oscillation-inducing neuromodulators. 2
Traub; Cortical Oscillations 185 One of the most effective tools for studying oscillation in vitro is to apply a neuromodulatory compound to the bath. The neuromodulator may then be capable of eliciting a network oscillation that last many hours. 0
Traub; Cortical Oscillations 186 Differential morphology, connectivity, firing patterns and sensitivity to neuromodulators in neocortical interneurons. (diagram) 1
Traub; Cortical Oscillations 187 Fast Rhythmic Bursting in Pyramidal Cells 1
Traub; Cortical Oscillations 187 Two types of firing pattern that have been seen in cortical principal neurons are fast rhythmic bursting (FRB), also called "chattering"; and regular spiking (RS). 0
Traub; Cortical Oscillations 187 Fast rhythmic bursting (FRB) behavior is unusual; it is found mostly in pyramidal neurons in superficial layers, but also in pyramidal and non-pyramidal neurons in other cortical layers, and also in the thalamus. 0
Traub; Cortical Oscillations 187 Regular spiking (RS) is the most common firing pattern seen in cortical pyramidal cells and spiny stellate cells; it is also found in some interneurons. 0
Traub; Cortical Oscillations 190 Pyramidal neurons, the most common class of cell morphology to be found in the cortex, concentrating on the large layer 5 pyramidal cells -- probably the most intensively studied cell type in the brain. 3
Traub; Cortical Oscillations 190 Intrinsic bursts are especially prominent during epileptiform events, where they are amplified by recurrent synaptic excitation, and can recur at frequencies as high as 20 Hz or more. 0
Traub; Cortical Oscillations 191 Regular spiking and intrinsic bursting in pyramidal neurons of rat visual cortex in vitro. (diagram) 1
Traub; Cortical Oscillations 195 Strikingly different patterns of Electrogenesis can occur in the Dendrites vis--vis the Soma. 4
Traub; Cortical Oscillations 196 The firing properties of Axons are not the same as for Somata. 1
Traub; Cortical Oscillations 196 Very fast brain oscillations depend for their generation on physical interactions between axons of principle (excitatory) neurons. Certain gamma and beta oscillations depend on such interactions as well. 0
Traub; Cortical Oscillations 196 Both the intrinsic properties of axons, and the means by which axons communicate with each other, are vital to the generation of oscillations. 0
Traub; Cortical Oscillations 196 The study of mammalian axons is technically difficult, partly because of their small size, and partly because of the myelin that ensheaths large portions of many of them. 0
Traub; Cortical Oscillations 197 In the late 1940s and early 1950s, Hodgkin and Huxley performed their classical experiments on, and analysis of, the generation and propagation of action potentials in the isolated squid giant axon. 1
Traub; Cortical Oscillations 197 Patch clamp recordings, starting in the early 1990s, became possible from the proximal axons of mammalian pyramidal cells and Purkinje cells. 0
Traub; Cortical Oscillations 197 Recordings (2003) from single axons of CA3 pyramidal cells showed that the refractory time of these axons range from about 2.5 to about 10 ms. 0
Traub; Cortical Oscillations 198 The somata of pyramidal cells can become so depolarized as to be unable to generate action potentials. This "depolarization block" is presumed to reflect voltage-dependent inactivation of Na+ channels. 1
Traub; Cortical Oscillations 199 Under most physiological conditions, action potentials are initiated in the proximal axon, in both pyramidal cells and Purkinje cell. 1
Traub; Cortical Oscillations 199 The axon initial segment of pyramidal cells is the site of inhibitory synapses, whose presynaptic elements belong to a specialized type of interneuron, the axo-axonic or chandelier cell. 0
Traub; Cortical Oscillations 203 Many brain oscillations -- particularly gamma oscillations -- are regulated by GABA-receptor-mediated synaptic inhibition. 4
Traub; Cortical Oscillations 207 There are differences between principal neurons and fast spiking interneurons, not only in synaptic currents and in cell shape, but also in the properties of the intrinsic membrane conductances, particularly the Na+ and K+ channels that are responsible for action potentials. 4
Traub; Cortical Oscillations 207 Bath application of kainate constitutes a particularly robust method for the induction of oscillations in cortical circuits, when used in concentrations of 1 M or less. 0
Traub; Cortical Oscillations 207 NMDA and AMPA glutamate receptors are constituted of different types of subunits, with receptor properties depending on which types of subunits have co-assembled. 0
Traub; Cortical Oscillations 212 Gap Junctions and the Notion of Electrical Coupling between Axons 5
Traub; Cortical Oscillations 212 Many brain oscillations depend on gap junctions, which can be visualized as a collection of small tunnels between cell interiors. 0
Traub; Cortical Oscillations 212 Gap junctions between principal neurons include pyramidal neurons, hippocampal dentate cells, and cerebellar Purkinje cells. 0
Traub; Cortical Oscillations 213 Chemical synapses do not make the the whole story of network connectivity, and a rather small number of strategically placed gap junctions can have striking and profound effects on network activities. 1
Traub; Cortical Oscillations 213 Junctions are confined to multicelled animals. They occur in extremely primitive animals, including coral animals, jellyfish, and sea anemones. They do not occur in plants, bacteria, or protozoa. 0
Traub; Cortical Oscillations 214 Gap junctions occur very early in development and are crucial for the embryo to develop properly. 1
Traub; Cortical Oscillations 214 Gap junctions in the heart are crucial to life; it is through them that cardiac action potential can conduct from myocyte to myocyte, so that an organized pattern of muscle contraction (and effective cardiac pumping) is possible. 0
Traub; Cortical Oscillations 214 Gap junctions are present between nerve cells, where they allow for a type of neuron-neuron signaling that compliments chemical synapses. 0
Traub; Cortical Oscillations 214 Gap junction channels have an aqueous interior through which ionic currents can flow -- the physical basis of electronic coupling between pairs of cells. 0
Traub; Cortical Oscillations 214 In addition to ionic currents, other molecular species (generally of molecular weight up to ~1000) can also pass through the gap junction channel. 0
Traub; Cortical Oscillations 215 The term "gap junction" refers to an assembly of contiguous, packed, gap junction channels, anywhere from just a few of them to many thousands. 1
Traub; Cortical Oscillations 215 Gap junction channels are likely to be packed tightly together, most often into a hexagonal array. 0
Traub; Cortical Oscillations 215 The gap junction assembly as a whole will have a characteristic shape, usually a disk or plaque, but possibly a ribbon or a network like (reticular) structure. 0
Traub; Cortical Oscillations 215 There may be yet another level of scaling, as pairs of cells may be connected by several gap junctions. 0
Traub; Cortical Oscillations 217 Structure of a Gap Junction Channel 2
Traub; Cortical Oscillations 217 High resolution x-ray crystallography would, in principle, provide structural data useful in understanding the biophysics of gap junction channels. However, most membrane proteins are unstable in solution, and do not lend themselves to crystallization. 0
Traub; Cortical Oscillations 217 Electron crystallographic structure of a recombinant cardiac gap junction. (diagram) 0
Traub; Cortical Oscillations 217 Adult mammalian brain regions and cell types for which gap junctions have been reported include the retina, basal ganglia, cerebral cortex, hippocampus, nucleus reticularis thalami, thalamocortical relay cells, inferior olive, and interneurons in the molecular layer of the cerebellum. 0
Traub; Cortical Oscillations 217 Cells of the inferior olive (a medullary structure) give rise to the cerebellar climbing fibers. 0
Traub; Cortical Oscillations 220 Gap Junctions and Interneuron Network Oscillations 3
Traub; Cortical Oscillations 220 There are a number of experimental oscillation models, at theta to gamma frequencies, in which pharmacologically isolated populations as GABAergic neurons generate network oscillations. 0
Traub; Cortical Oscillations 220 Hippocampal and neocortical interneuron network oscillation requires mutual GABAergic synaptic inhibition. 0
Traub; Cortical Oscillations 227 Dye coupling was described between principled cells in hippocampus and neocortex, beginning almost 30 years ago (1982). 7
Traub; Cortical Oscillations 227 The so-called percolation limit (in which one cell couples to one other, on average), the limit at which collective behavior becomes possible. 0
Traub; Cortical Oscillations 227 One cell coupled to 2.25 others, on average, well above the percolation limit -- but still well below the density of recurrent excitatory synaptic connections in CA1. 0
Traub; Cortical Oscillations 243 In Vitro Oscillations 16
Traub; Cortical Oscillations 245 Very Fast Oscillations (VFO) 2
Traub; Cortical Oscillations 245 Consider mechanisms of very fast oscillations (VFO, faster than approximately 70 Hz) in telencephalic cortical structures (e.g. hippocampus, neocortex, and entorhinal cortex) and in cerebellar cortex. 0
Traub; Cortical Oscillations 245 VFO requires gap junctions, connecting the axons of principal neurons. 0
Traub; Cortical Oscillations 245 VFO can be generated without chemical synapses (in particular, without GABAA receptors), and even seem to be enhanced by the blockade of chemical synapses. 0
Traub; Cortical Oscillations 245 With chemical synapses imtact, both telencephalic and cerebellar cortex happily coexist with either lower frequency oscillations, or with transient synchronized discharges such a sharp waves. 0
Traub; Cortical Oscillations 245 VFO cannot be understood as arising from a system of coupled oscillators. 0
Traub; Cortical Oscillations 245 Telencephalic cortical VFO can be accounted for with a model in which electrical coupling is functionally strong, so that a spike in one axon may be able to evoke a spike in a coupled axon. 0
Traub; Cortical Oscillations 245 Cerebellar VFO can be accounted for with a model in which the coupling is relatively weak, so that only when multiple near-simultaneous spikes occur, in axons coupled to a selected axon, will the selected axon itself fire. 0
Traub; Cortical Oscillations 245 VFO In reasonably physiological conditions in vivo can occur spontaneously, superimposed on physiological sharp waves in the hippocampus and deep entorhinal cortex, and during the depolarizing phase of the slow oscillation; or it can be superimposed on cortical evoked responses that follow brief sensory inputs, in somatosensory and auditory modalities. 0
Traub; Cortical Oscillations 246 In all the cases of VFO oscillations, populations of cortical neurons become transiently depolarized. 1
Traub; Cortical Oscillations 246 VFO in nonepileptic conditions can occur superimposed on spontaneous (or also evoked) sharp waves. 0
Traub; Cortical Oscillations 246 It is possible to produce VFO without gamma or beta-2, but it is not clear if the reverse is true, at least for persistent rhythms. 0
Traub; Cortical Oscillations 246 VFO can occur a leading into an interictal burst or seizure, or superimposed upon burst complexes without a seizure. 0
Traub; Cortical Oscillations 246 VFO can also occur in isolation in epilepticogenic tissue, especially at frequencies above 250 or 300 Hz (so-called "fast ripples"). 0
Traub; Cortical Oscillations 246 Fast ripples can be generated in very small volumes of tissue, about 1 mm3. 0
Traub; Cortical Oscillations 246 Associated with epileptogenesis, VFO cannot occur leading in into an interictal burst or seizure; superimposed on synchronized bursts; or between bursts complexes. 0
Traub; Cortical Oscillations 246 Generation of VFO Does Not Require GABAergic Interneurons 0
Traub; Cortical Oscillations 247 When ripple oscillations were first discovered in the hippocampus (Buzski et al., 1992), it was immediately realized that interneurons could fire at the frequency of the ripple (~200 Hz), but that pyramidal cells -- at least the somata -- did not; and indeed, many pyramidal cell somata seemed not to fire at all. 1
Traub; Cortical Oscillations 247 Although it seemed natural to postulate that networks of fast-spiking interneurons generate the ripple oscillations, there are several reasons for rejecting this idea. 0
Traub; Cortical Oscillations 247 There are many examples of VFO occurring with chemical synaptic transmission completely blocked. 0
Traub; Cortical Oscillations 247 Somatic spiking is not the proper measure of pyramidal cell activity, as there is evidence for an antidromic (i.e. axonal) origin of spikes during VFO. 0
Traub; Cortical Oscillations 248 A network of pyramidal cells axons that are electrically coupled can generate population VFO. 1
Traub; Cortical Oscillations 248 Because AMPA receptor-mediated excitatory postsynaptic conductances (EPSCs) and fast spiking (FS) interneurons are so extremely rapid (decay time of order of 1 ms), the output of an oscillating pyramidal cell axon plexus can synaptically impose a coherent VFO in a population of FS cells -- and the FS cells, in turn, can impose coherent compound IPSPs on the pyramidal cells. 0
Traub; Cortical Oscillations 249 A pyramidal cell axonal plexus can generate population VFO provided: (1) electrical coupling is present, (2) the axons are sufficiently excitable, and (3) there is at least some degree of spontaneous activity. 1
Traub; Cortical Oscillations 249 Nonsynaptic VFO occurs in other brain regions besides hippocampal pyramidal cell regions. 0
Traub; Cortical Oscillations 249 The somatic firing rate can be much lower than the population oscillation frequency, but each population wave is accompanied either by a full spike, or by a spikelet in a given neuron. 0
Traub; Cortical Oscillations 250 VFO occurs without chemical synapses, but requires gap junctions. 1
Traub; Cortical Oscillations 250 Full somatic action potentials, in any given neuron, do not follow that population frequency. 0
Traub; Cortical Oscillations 251 The gap junctional coupling between pyramidal cells is extremely sparse, with each cell (at least in hippocampal CA1) coupled to approximately 2 others. 1
Traub; Cortical Oscillations 251 VFO can be coherent over distances greater than 300 in CA1, i.e. it is coherent across population of hundreds, or thousands, of neurons, despite the extremely low gap junctional connectivity. 0
Traub; Cortical Oscillations 251 The most economical hypothesis for the experimental observations is to suppose that coupled axons generate VFO. 0
Traub; Cortical Oscillations 252 We would not expect electrically coupled axons to behave as phase coupled oscillators, because of the extreme nonlinearity of the axonal membrane (due to the presence of either a high density, or low for threshold, or both for Na+ channels). 1
Traub; Cortical Oscillations 252 Simulated a large network of axonally coupled neurons at low coupling densities. 0
Traub; Cortical Oscillations 252 Axonally coupled networks can produce VFO with sparse coupling under quite general conditions: 0
Traub; Cortical Oscillations 252 Condition (1), Axonally coupled networks can produce VFO when the density of connections (i.e. gap junctions) was higher than one gap junction per axon, on average, the so-called percolation limit; but the density was not so high that all the axons started to fire at maximal frequency. 0
Traub; Cortical Oscillations 252 In an earlier study, the average density was kept below three or four gap junctions per axon. 0
Traub; Cortical Oscillations 252 Condition (2), Axonally coupled networks can produce VFO when the conductance of a gap junction (or junctions) between a coupled pair of axons was large enough that an action potential in one axon could induce an action potential in the other (provided the other is not absolutely refractory). 0
Traub; Cortical Oscillations 252 The minimum value of the gap junction conductance will depend on the intrinsic membrane properties, and on how far the gap junction is from the soma. 0
Traub; Cortical Oscillations 252 Condition (3), Axonally coupled networks can produce VFO when there is a source of background spontaneous action potentials, so-called atopic spikes. The frequency of ectopic spikes could be very low (e.g. 0.05 Hz per axon), but not zero. 0
Traub; Cortical Oscillations 253 Graph theory has developed into a rich branch of mathematics; a collection of vertices, or nodes, along with the collection of edges, each edge connects a pair of vertices. 1
Traub; Cortical Oscillations 254 How long are the paths between different vertices? Waves of activity will begin with spontaneous spikes that spread along the edges, or gap junctions, and the period will be determined by how many edges must be crossed (on average) to reach a majority of the population. 1
Traub; Cortical Oscillations 254 Percolation limit -- If parameter c is less than 0.5, then each vertex connects to less than one other vertex on average. 0
Traub; Cortical Oscillations 256 Structural Properties of Large Random Graphs (diagram) 2
Traub; Cortical Oscillations 256 Parameter c is the ratio of the number of edges to the number of nodes (or vertices). 0
Traub; Cortical Oscillations 256 Parameter c is equal to one half the mean index, the average number of edges emanating from each node. 0
Traub; Cortical Oscillations 260 Shunting by gap junctions. In a random graph, the statistical distribution of the number of edges on a vertex is Poisson. In a large random graphs, there will always be a few vertices with a large number of edges. 4
Traub; Cortical Oscillations 260 An axonal plexus with random topology will lead to the existence of a few axons that are gap-junctionally connected to many other axons. 0
Traub; Cortical Oscillations 260 A large number of gap junctions will act as a shunt, so that if one axon fires, its spike may not be communicated. 0
Traub; Cortical Oscillations 260 Random graphs that are sufficiently large contain reentry cycles of any given order (length). 0
Traub; Cortical Oscillations 260 Very fast oscillations (VFO) can occur nested with a slower oscillation, beta-2 (20-30 Hz). 0
Traub; Cortical Oscillations 260 Slower membrane currents and synaptic currents break VFO up into packets. 0
Traub; Cortical Oscillations 260 Beta-2 oscillation exists with intact chemical synaptic transmission, but does not depend on it. 0
Traub; Cortical Oscillations 260 Beta-2 oscillation does depend on gap junctions. 0
Traub; Cortical Oscillations 261 VFO and beta-2 oscillation can coexist, one nested on the other. 1
Traub; Cortical Oscillations 261 The data suggest that an axonal, and perisomatic, phasic hyperpolarizing current can serve to break VFO into short epochs, separated by a longer epochs. The duration of the longer epochs is determined by the kinetics of the hyperpolarizing process. 0
Traub; Cortical Oscillations 262 VFO also occurs nested with persistent hippocampal and medial entorhinal gamma oscillations. 1
Traub; Cortical Oscillations 262 Persistent gamma oscillations require both gap junctions and chemical synapses, specifically, AMPA receptors and GABAA receptors. 0
Traub; Cortical Oscillations 262 The data suggest that synaptic inhibition in perisomatic regions is acting to break VFO into short segments -- an effect that will be possible if axonal gap junctions are not located too distant from the soma and initial segment. 0
Traub; Cortical Oscillations 262 VFO is coherent over distances of at least 300 , so that hundreds of cells (at least) must be participating. 0
Traub; Cortical Oscillations 262 VFO in the hippocampus, neocortex, and other telencephalic structures arises because of relatively rare spontaneous action potentials, percolating from axon to axon across gap junctions, with period determined by the global topological network structure, rather than by intrinsic membrane or synaptic conductances. 0
Traub; Cortical Oscillations 269 Beta-2 Oscillations 7
Traub; Cortical Oscillations 269 Beta oscillations (10-30 Hz) can occur during the slow oscillation of sleep, during the memory phase of a cognitive task (typically associated with behavioral immobility), and in the course of auditory evoked potentials. 0
Traub; Cortical Oscillations 269 Beta oscillations can occur during status epilepticus. 0
Traub; Cortical Oscillations 269 Enhanced beta activity occurs in Parkinsonian syndromes. 0
Traub; Cortical Oscillations 269 Decreased beta frequency phase synchrony, of cortical oscillations, has been demonstrated in schizophrenia. 0
Traub; Cortical Oscillations 269 There are many other observations of beta oscillations occurring in the cortex during sensory stimulation and cognitive tasks. 0
Traub; Cortical Oscillations 269 Beta-2 oscillations (20-30 Hz) can be nested with very fast oscillations (VFO). 0
Traub; Cortical Oscillations 270 In secondary somatosensory cortex, gamma oscillations are generated in superficial layers, and beta-2 in deep layers. 1
Traub; Cortical Oscillations 270 Intracellular recordings have shown that it is intrinsically bursting pyramidal cells that robustly participate in the beta-2 oscillation. 0
Traub; Cortical Oscillations 270 Cell may have voltage fluctuations at a time lock to a population oscillation, and yet the somata fire at much lower rates than the population frequency. 0
Traub; Cortical Oscillations 270 Somata firing at much lower rates than the population frequency occurs in the inferior olive. 0
Traub; Cortical Oscillations 271 Somatosensory cortex beta-2 oscillation requires gap junctions. 1
Traub; Cortical Oscillations 271 The beta-2 oscillation, as a population phenomenon, cannot be understood as a system of coupled cellular oscillators. 0
Traub; Cortical Oscillations 274 Not only are gap junctions required for beta-2, but chemical synapses appear not to be required, at least not beyond providing tonic excitation to the network. 3
Traub; Cortical Oscillations 276 Somatosensory cortex beta-2 appears to be an exclusively gap junction mediated type of oscillation. 2
Traub; Cortical Oscillations 276 Beta-2 isolation can occur in nested with VFO. 0
Traub; Cortical Oscillations 276 Beta-2 oscillations have been observed in primary motor cortex, M1. These oscillations have several properties in common with somatosensory cortex beta-2. 0
Traub; Cortical Oscillations 276 Analysis of phase delays indicates that M1 beta-2 oscillation originates in deep layers. 0
Traub; Cortical Oscillations 276 Unlike somatosensory cortex, M1 cortex does not exhibit gamma oscillation in the superficial layers. 0
Traub; Cortical Oscillations 280 There are multiple forms of beta rhythm in the cortex, and most have close associations with prior or ongoing gamma rhythms. 4
Traub; Cortical Oscillations 280 More and more frequency bands within the EEG range are discovered to have a clearly defined and distinct mechanisms. 0
Traub; Cortical Oscillations 280 Robust existence of gamma and beta-2 rhythms provides an ideal starting point to address the issue of multiple coexistent frequency bands. 0
Traub; Cortical Oscillations 280 The pattern of temporal interactions between deep and superficial layers of the cortex generate beta-2 and temporal gamma frequency oscillations. 0
Traub; Cortical Oscillations 280 With strong excitation of somatosensory cortex, the beta-2 and gamma rhythms have no stable phase relationship, suggesting that the beta-2 rhythm is operating to disconnect the main input areas in a cortical column (layer 4 and above) from the primary descending output layer (layer 5). 0
Traub; Cortical Oscillations 281 Once the excitation of cortex is reduced, both the beta-2 and gamma periods are present in individual neurons, but they are organized such that one gamma period is followed by one beta-2 period, repeatedly. 1
Traub; Cortical Oscillations 281 The population rhythm is manifest as if sum of these two original periods -- resulting in a slower beta-1 frequency rhythm. 0
Traub; Cortical Oscillations 281 Theoretically, interactions between co-express frequencies may occur throughout the dynamic range of the EEG, placing gap junction-mediated network phenomena at the very heart of cortical dynamics. 0
Traub; Cortical Oscillations 282 Persistent Gamma Oscillations 1
Traub; Cortical Oscillations 289 Persistent Gamma Oscillation Requires Gap Junctions 7
Traub; Cortical Oscillations 289 The gap junctions required for persistent gamma oscillations are those between primary cells. 0
Traub; Cortical Oscillations 289 Electrical coupling has been found to be a extremely rare between interneurons. 0
Traub; Cortical Oscillations 291 During persistent gamma oscillation, pyramidal cell firing is sparse, but (on average) leads the firing of fast-spiking interneurons by a few milliseconds. 2
Traub; Cortical Oscillations 293 Interneuron gap junctions modulate the power of persistent gamma oscillations. 2
Traub; Cortical Oscillations 295 GABAA receptors can excite the pyramidal cell axonal plexus to generate VFO. 2
Traub; Cortical Oscillations 295 IPSPs repeatedly interrupt VFO, to generate persistent gamma oscillations. 0
Traub; Cortical Oscillations 298 Fast rhythmic bursting (FRB) cells (chattering cells) are necessary for persistent gamma oscillation in superficial layers of auditory cortex. 3
Traub; Cortical Oscillations 301 Action potentials during persistent gamma oscillations are predicted to be antidromic. 3
Traub; Cortical Oscillations 302 Epileptiform Discharges In Vitro 1
Traub; Cortical Oscillations