High Frequency Bursts Research Articles

A computational study of the influence of synaptic cooperativity on synaptic plasticity in a hippocampal CA1 pyramidal cell

We use a computational model to investigate the possible cooperativity between coactive synapses, both within and between input pathways, in determining plasticity outcomes at individual synapses on a hippocampal CA1 pyramidal cell (PC). The detailed compartmental model of the PC, based on a reconstructed morphology, contains distributions of core ion channels that control voltage transients and calcium entry in the soma and dendrites. Of particular note are the increasing density of A-type potassium channels (KA) with distance in the apical dendrites that provide strong filtering of voltage transients, and high-voltage-gated calcium channels (VGCC) in the dendrites and spines that may contribute to calcium entry in spine heads. Groups of spatially diffuse or clustered excitatory synapses on spines in dendritic layers stratum lacunosum-moleculare (SLM), stratum radiatum (SR) and stratum oriens (SO) are stimulated with single spikes or high frequency bursts. Synaptic currents are mediated by AMPA and NMDA receptors. A proportion of the NMDAR-mediated current is carried by calcium ions. As an indicator of likely synaptic plasticity, the peak calcium level (pCa) obtained in each spine head is measured. Figure ​Figure11 shows results from typical simulations. Peak calcium initially is a somewhat linear function of the number of synchronously active synapses, until saturation. The gain is higher if the density of KA is reduced. With VGCCs, pCa becomes a nonlinear, sigmoidal function. Figure 1 Average spine head peak calcium due to single synchronous stimulation of different numbers of synapses in SLM, in four cell configurations (1) high (standard) KA, (2) high KA with VGCC, (3) low (one third) KA, (4) with VGCC. Error bars show standard deviation. ... Other results show that presynaptic burst stimulation is much more effective at raising spine head calcium levels than single stimuli. Similarly, small numbers of coactive synapses on a single oblique dendrite can achieve high pCa. Activity in one layer, such as SLM can affect pCa in another layer (SR) but only if KA is reduced. In summary, burst stimulation and colocalised activity are most likely to lead to high pCa and hence LTP. Cooperativity across dendritic pathways is possible, but needs specific cellular and stimulation conditions.

Developmental profiles of infant EEG: Overlap with transient cortical circuits

ObjectiveTo quantify spectral power in frequency specific bands and commonly observed types of bursting activities in the EEG during early human development. MethodsAn extensive archive of EEG data from human infants from 35 to 52weeks postmenstrual age obtained in a prior multi-center study was analyzed using power spectrum analyses and a high frequency burst detection algorithm. ResultsLow frequency power increased with age; however, high frequency power decreased from 35 to 45weeks. This unexpected decrease was largely attributable to a rapid decline in the number of high frequency bursts. ConclusionsThe decline in high frequency bursting activity overlaps with a developmental shift in GABA’s actions on neurons from depolarizing to hyperpolarizing and the dissolution of the gap junction circuitry of the cortical subplate. SignificanceWe postulate that quantitative characterization of features of the EEG unique to early development provide indices for tracking changes in specific neurophysiologic mechanisms that are critical for normal development of brain function.

Interictal high frequency oscillations in an animal model of infantile spasms

While infantile spasms is the most common catastrophic epilepsy of infancy and early-childhood, very little is known about the basic mechanisms responsible for this devastating disorder. In experiments reported here, spasms were induced in rats by the chronic infusion of TTX into the neocortex beginning on postnatal days 10–12. Studies of focal epilepsy suggest that high frequency EEG oscillations (HFOs) occur interictally at sites that are most likely responsible for seizure generation. Thus, our goal was to determine if HFOs occurred and where they occurred in cortex in the TTX model. We also undertook multiunit recordings to begin to analyze the basic mechanisms responsible for HFOs. Our results show that HFOs occur most frequently during hypsarrhythmia and NREM sleep and are most prominent contralateral to the TTX infusion site in the homotopic cortex and anterior to this region in frontal cortex. While HFOs were largest and most frequent in these contralateral regions, they were also commonly recorded synchronously across multiple and widely-spaced recordings sites. The amplitude and spatial distribution of interictal HFOs were found to be very similar to the high frequency bursts seen at seizure onset. However, the latter differed from the interictal events in that the high frequency activity was more intense at seizure onset. Microwire recordings showed that neuronal unit firing increased abruptly with the generation of HFOs. A similar increase in neuronal firing occurred at the onset of the ictal events. Taken together, results suggest that neocortical networks are abnormally excitable, particularly contralateral to TTX infusion, and that these abnormalities are not restricted to small areas of cortex. Multiunit firing coincident with HFOs is fully consistent with a neocortical hyperexcitability hypothesis particularly since they both occur at seizure onset.

Measurement of Leaked High-Frequency Burst Electric Field and EMI Evaluation for Cardiac Pacemaker in Fusion Facility

In this study, we measured the time variation of burst electric fields leaked from a heating device in the ion cyclotron range of high-frequency in an experimental fusion facility, and analyzed their statistical characteristics such as the amplitude probability distribution (APD) and crossing rate distribution (CRD). As a result, we found that the variation of the leaked electric field level is very irregular, far from the normal distribution. Moreover, the leaked electric field variation with time may reach 400 times in one second to cross its mode value. Although so, the maximum electric field intensity itself is much smaller than the ICNIRP safety guideline. In addition, we also evaluated the possibility of electromagnetic interference to an implanted cardiac pacemaker in the measured electromagnetic environment. We found that even in the worst case the interference voltage induced in the output of the pacemaker sensing circuit does still not exceed the threshold for a malfunction.

Dentate gyrus granule cell firing patterns can induce mossy fiber long‐term potentiation in vitro

Hippocampal granule cells transmit information about behaviorally-relevant stimuli to CA3 pyramidal cells via mossy fiber synapses. These synapses express a form of long-term potentiation (mfLTP) that is non-Hebbian and does not require NMDA receptors. mfLTP is thought to be induced and expressed presynaptically, hence, the major determinant of whether mfLTP occurs is activity in the granule cells. However, it remains unclear whether mfLTP can be induced by activity patterns that granule cells exhibit in vivo, and-if so-what context generates these patterns. To address these issues, we examined granule cell activity from in vivo recordings from rats during performance of a delayed nonmatch-to-sample (DNMS) task and found that granule cells exhibit a wide range of spike patterns. In vitro slice experiments in mice demonstrated that some, but not all, of these patterns of activity could induce mfLTP. By further defining the activity thresholds for mfLTP in hippocampal slices, we found that mfLTP can only be induced by spike patterns that fire in high frequency bursts with a low average firing frequency. Using this information, we then screened for suprathreshold bursts of activity during the DNMS task. In a subset of cells, suprathreshold bursts occurred preferentially during the sampling phase of the task. If suprathreshold bursting took place later, during the delay phase, task performance was disrupted. We conclude that mfLTP can be induced by granule cell spike patterns during a memory task, and that the timing of mfLTP induction can predict task performance.

Gaze shift duration, independent of amplitude, influences the number of spikes in the burst for medium-lead burst neurons in pontine reticular formation

Changes in the direction of the line of sight (gaze) allow successive sampling of the visual environment. Saccadic eye movements accomplish this goal when the head does not move. Medium-lead burst neurons (MLBs) in the paramedian pontine reticular formation (PPRF) discharge a high frequency burst of action potentials starting ~12ms before the saccade begins. A subgroup of MLBs rostral of abducens nucleus monosynaptically excites oculomotor neurons. The number of spikes in the presaccadic burst is correlated with the amplitude of the horizontal component of the saccade, and the peak discharge rate is correlated with peak eye velocity. During head-unrestrained gaze shifts, a linear relationship between the number of action potentials in MLB bursts and gaze (but not eye) amplitude has been reported. The anatomical connection of MLBs to motor neurons and the similarity between the phasic motor neuron burst and MLB discharge have raised questions about the usefulness of counting spikes in MLBs to determine their role in eye-head coordination. We investigated this issue using a behavioral technique that permits a dissociation of eye movement amplitude and duration during constant vector gaze shifts. Surprisingly, during gaze shifts of constant amplitude and direction, we observe a nearly linear, positive correlation between saccade duration and spike number associated with a negative correlation between spike number and saccade amplitude. These data constrain models of the oculomotor controller and may further define the time-dependence of hypothesized neural integration in this system.

Remote Electrical Stimulation by Means of Implanted Rectifiers

Miniaturization of active implantable medical devices is currently compromised by the available means for electrically powering them. Most common energy supply techniques for implants – batteries and inductive couplers – comprise bulky parts which, in most cases, are significantly larger than the circuitry they feed. Here, for overcoming such miniaturization bottleneck in the case of implants for electrical stimulation, it is proposed to make those implants act as rectifiers of high frequency bursts supplied by remote electrodes. In this way, low frequency currents will be generated locally around the implant and these low frequency currents will perform stimulation of excitable tissues whereas the high frequency currents will cause only innocuous heating. The present study numerically demonstrates that low frequency currents capable of stimulation can be produced by a miniature device behaving as a diode when high frequency currents, neither capable of thermal damage nor of stimulation, flow through the tissue where the device is implanted. Moreover, experimental evidence is provided by an in vivo proof of concept model consisting of an anesthetized earthworm in which a commercial diode was implanted. With currently available microelectronic techniques, very thin stimulation capsules (diameter <500 µm) deliverable by injection are easily conceivable.

P19.20 Does high frequency and theta burst transcranial magnetic stimulation affect the grip strength?

P19.20 Does high frequency and theta burst transcranial magnetic stimulation affect the grip strength?

Intrinsic membrane properties of spinal dorsal horn neurones modulate nociceptive information processingin vivo

The dorsal horn of the spinal cord is the first central relay where nociceptive inputs are processed. Based on the expression and modulation of intrinsic electrophysiological properties in in vitro slice preparations, dorsal horn neurones (DHNs) display different discharge patterns (tonic, plateau or rhythmic), which shape the neurone's response to sensory inputs. However, it is unclear whether intrinsic properties play any role in sensory processing in vivo. Using in vivo patch clamp recordings in the adult rat, we here examine whether these intrinsic properties are present, and to what extent they determine the DHN response to natural stimulation. We focused primarily on wide dynamic range neurones in deep laminae. These cells displayed a multicomponent peripheral receptive field, comprising an excitatory firing zone, a low-probability firing fringe, and adjacent inhibitory zones. Deep DHNs presented similar intrinsic properties to those observed in vitro, including plateau potentials. These plateaus, underlying high frequency accelerating discharges and after-discharges, were triggered by mechanical stimulation of the excitatory receptive field. Persistent activities induced by activation of plateau potentials were interrupted by stimulation of peripheral inhibitory zones. Moreover, we show that plateau activation is necessary for the expression of windup in response to repetitive, nociceptive stimulation. Finally, using the spinal nerve ligation model of neuropathy, we demonstrate a significant increase in the proportion of plateau neurones in deep dorsal laminae. Our data, therefore, establish that intrinsic amplification properties are expressed within intact spinal circuits and suggest their involvement in neuropathy-induced hyperexcitability of deep DHNs.

A window into the complexity of the dynamic rupture of the 2011 Mw 9 Tohoku-Oki earthquake

The 2011 Mw 9 Tohoku-Oki earthquake, recorded by over 1000 near-field stations and multiple large-aperture arrays, is by far the best recorded earthquake in the history of seismology and provides unique opportunities to address fundamental issues in earthquake source dynamics. Here we conduct a high resolution array analysis based on recordings from the USarray and the European network. The mutually consistent results from both arrays reveal rupture complexity with unprecedented resolution, involving phases of diverse rupture speed and intermittent high frequency bursts within slow speed phases, which suggests spatially heterogeneous material properties. The earthquake initially propagates down-dip, with a slow initiation phase followed by sustained propagation at speeds of 3 km/s. The rupture then slows down to 1.5 km/s for 60 seconds. A rich sequence of bursts is generated along the down-dip rim of this slow and roughly circular rupture front. Before the end of the slow phase an extremely fast rupture front detaches at about 5 km/s towards the North. Finally a rupture front propagates towards the south running at about 2.5 km/s for over 100 km. Key features of the rupture process are confirmed by the strong motion data recorded by K-net and KIK-net. The energetic high frequency radiation episodes within a slow rupture phase suggests a patchy image of the brittle-ductile transition zone, composed of discrete brittle asperities within a ductile matrix. The high frequency is generated mainly at the down-dip edge of the principal slip regions constrained by geodesy, suggesting a variation along dip of the mechanical properties of the mega thrust fault or their spatial heterogeneity that affects rise time.

Hypoxia inducible factor 1α links fast‐patterned muscle activity and fast muscle phenotype in rats

Exercise influences muscle phenotype by the specific pattern of action potentials delivered to the muscle, triggering intracellular signalling pathways. PO2 can be reduced by an order of magnitude in working muscle. In humans, carriers of a hyperactive polymorphism of the transcription factor hypoxia inducible factor 1α (HIF-1α) have 50% more fast fibres, and this polymorphism is prevalent among strength athletes. We have investigated the putative role of HIF-1α in mediating activity changes in muscle.When rat muscles were stimulated with short high frequency bursts of action potentials known to induce a fast muscle phenotype, HIF-1α increased by about 80%. In contrast, a pattern consisting of long low frequency trains known to make fast muscles slow reduced the HIF-1α level of the fast extensor digitorum longus (EDL) muscle by 44%. Nuclear protein extracts from normal EDL contained 2.3-fold more HIF-1α and 4-fold more HIF-1β than the slow soleus muscle, while von-Hippel-Lindau protein was 4.8-fold higher in slow muscles. mRNA displayed a reciprocal pattern; thus FIH-1 mRNA was almost 2-fold higher in fast muscle, while the HIF-1α level was half, and consequently protein/mRNA ratio for HIF-1α was more than 4-fold higher in the fast muscle, suggesting that HIF-1α is strongly suppressed post-transcriptionally in slow muscles.When HIF-1α was overexpressed for 14 days after somatic gene transfer in adult rats, a slow-to-fast transformation was observed, encompassing an increase in fibre cross sectional area, oxidative enzyme activity and myosin heavy chain. The latter was shown to be regulated at the mRNA level in C2C12 myotubes.

Frequency-dependent interaction of ultrashort E-fields with nociceptor membranes and proteins

We examined the influence of ultrashort pulses (USP) on sensory neurons. Single and high frequency bursts of 12 ns E-fields were presented to rat skin nociceptors that expressed distinct combinations of voltage-sensitive proteins. A single E-field pulse produced action potentials in all nociceptor subtypes at a critical threshold (E(c) ) of 403 V/cm. When configured into high frequency bursts, USP charge integrated to reduce the action potential threshold in a frequency and burst duration-dependent manner with E(c) as low as 16 V/cm (4000 Hz, 25 ms burst). There was no evidence of electroporation at field intensities near the E(c) for nociceptor activation. USP bursts activated a late, persistent Ca(++) flux that was identified as a dantrolene-sensitive Ca(++) -induced Ca(++) release (CICR). Influx of Ca(++) into the cell was required for the CICR and resulted in a reduction of the single pulse E(c) by about 50%.

Management of Localized Pneumothoraces After Pulmonary Resection With Intrapulmonary Percussive Ventilation

Intrapulmonary percussive ventilation (IPV) aims at clearing retained secretions through oscillary vibrations generated by high frequency bursts of gas delivered into the airways at rates between 200 and 300 breaths per minute and at a delivery pressure of 10 to 20 cm water. In addition, IPV can improve recruitment of alveolar units and deliver aerosolized medications. The use of IPV to resolve challenging postlobectomy localized pneumothoraces is hereafter described. Between January 2005 and March 2009, four patients with long-term complicated postresectional residual air spaces persisting 6 months (mean, 187 days) after primary surgery were treated by IPV. The type of operation was upper lobectomy and lower lobectomy-wedge resection in 1 and 3 patients, respectively. Mean preoperative and immediate postsurgical forced expiratory volume in the first second of expiration were 2.31 L and 1.49 L, respectively. Mean preoperative and immediate postsurgical forced vital capacity were 3.13 L and 2.1 L, respectively. Patients were subjected to 12-minute-long IPV sessions up to a total of 8 to 12 sessions administered every other day in an outpatient setting. Complete resolution of the spaces within a mean of 22 days of beginning of treatment was noted. The post-IPV forced expiratory volume in the first second of expiration and forced vital capacity were 1.72 and 2.4 liters, respectively. No treatment-related morbidity was observed. Intrapulmonary percussive ventilation can be expected to decisively contribute to resolving long-term localized pneumothoraces after subtotal pulmonary resections in an outpatient setting.

Matching the oculomotor drive during head-restrained and head-unrestrained gaze shifts in monkey.

High-frequency burst neurons in the pons provide the eye velocity command (equivalently, the primary oculomotor drive) to the abducens nucleus for generation of the horizontal component of both head-restrained (HR) and head-unrestrained (HU) gaze shifts. We sought to characterize how gaze and its eye-in-head component differ when an "identical" oculomotor drive is used to produce HR and HU movements. To address this objective, the activities of pontine burst neurons were recorded during horizontal HR and HU gaze shifts. The burst profile recorded on each HU trial was compared with the burst waveform of every HR trial obtained for the same neuron. The oculomotor drive was assumed to be comparable for the pair yielding the lowest root-mean-squared error. For matched pairs of HR and HU trials, the peak eye-in-head velocity was substantially smaller in the HU condition, and the reduction was usually greater than the peak head velocity of the HU trial. A time-varying attenuation index, defined as the difference in HR and HU eye velocity waveforms divided by head velocity [alpha = (H(hr) - E(hu))/H] was computed. The index was variable at the onset of the gaze shift, but it settled at values several times greater than 1. The index then decreased gradually during the movement and stabilized at 1 around the end of gaze shift. These results imply that substantial attenuation in eye velocity occurs, at least partially, downstream of the burst neurons. We speculate on the potential roles of burst-tonic neurons in the neural integrator and various cell types in the vestibular nuclei in mediating the attenuation in eye velocity in the presence of head movements.

Ionic conditions modulate stimulus-induced capacitance changes in isolated neurohypophysial terminals of the rat

Peptidergic nerve terminals of the neurohypophysis (NH) secrete both oxytocin and vasopressin upon stimulation with peptide-specific bursts of action potentials from magnocellular neurons. These bursts vary in both frequency and action potential duration and also induce in situ ionic changes both inside and outside the terminals in the NH. These temporary effects include the increase of external potassium and decrease of external calcium, as well as the increase in internal sodium and chloride concentrations. In order to determine any mechanism of action that these ionic changes might have on secretion, stimulus-induced capacitance recordings were performed on isolated terminals of the NH using action potential burst patterns of varying frequency and action potential width. The results indicate that in NH terminals: (1) increased internal chloride concentration improves the efficiency of action potential-induced capacitance changes, (2) increasing external potassium increases stimulus-induced capacitance changes, (3) decreasing external calcium decreases the capacitance induced by low frequency broadened action potentials, while no capacitance change is observed with high frequency un-broadened action potentials, and (4) increasing internal sodium increases the capacitance change induced by low frequency bursts of broadened action potentials, more than for high frequency bursts of narrow action potentials. These results are consistent with previous models of stimulus-induced secretion, where optimal secretory efficacy is determined by particular characteristics of action potentials within a burst. Our results suggest that positive effects of increased internal sodium and external potassium during a burst may serve as a compensatory mechanism for secretion, counterbalancing the negative effects of reduced external calcium. In this view, high frequency un-broadened action potentials (initial burst phase) would condition the terminals by increasing internal sodium for optimal secretion by the physiological later phase of broadened action potentials. Thus, ionic changes occurring during a burst may help to make such stimulation more efficient at inducing secretion. Furthermore, these effects are thought to occur within the initial few seconds of incoming burst activity at both oxytocin and vasopressin types of NH nerve terminals.

Extending the bandwidth of long‐term plasticity at the cerebellar input stage

Extending the bandwidth of long‐term plasticity at the cerebellar input stage

High frequency excitation waveform for efficient operation of a xenon excimer dielectric barrier discharge lamp

The application of a high frequency (∼2.5 MHz) burst (amplitude-modulated sinusoidal) excitation voltage waveform is investigated for driving a fluorescent dielectric barrier discharge (DBD) light source. The excitation waveform presents a novel method for generating spatially stable homogeneous Xe DBD possessing a high conversion efficiency from electrical energy to VUV excimer radiation (∼172 nm), even at a significantly higher electrical energy deposition than realized by pulsed excitation. Simulation and experimental results predict discharge efficiencies around 60%. Lamp efficacy above 74 lm W−1 has been achieved. VUV emission and loss mechanisms are investigated extensively and the performance of burst and pulsed waveforms is compared both theoretically and experimentally.

Modeling action potential initiation using voltage-gated ion-channels kinetics from L5 pyramidal neurons of the rat cortex

Discussion • Sodium currents were measured from L5 pyramidal neurons using six stimulation protocols in the nucleated and outside-out configurations of the patch-clamp technique and fit to several kinetic models of voltage-gated sodium channels. • Out of a dozen voltage-gated sodium channel (VGSC) models (only relevant configurations shown) it appears that the most simplified, a four-state-16-parameter, Hidden-Markov-Model (HMM) provides the best fit for the data. • The ability of the chosen HMM model to simulate generation and propagation of action potentials (APs) in L5 pyramidal neurons was tested relative to the most prevalent and complete model of morphological influence on firing pattern. • The combination of the simplified HMM and a Hodgkin-Huxley-like voltage-gated potassium channel model provides the best simile of high frequency bursts of APs in L5 pyramidal neurons. • Further development and investigation of an adequate voltage-gated potassium channel HMM is needed to replace the HH paradigm. • The chosen HMM should be further tested on other types of VGSCs from various neurons and compared to the performance of other HMM. Figure 1: Fitting Newly Devised Models to Experimentally Recorded Voltage-Gated Na+ Channels Currents from neocortical pyramidal neurons –results of fitting a data set containing five pulse protocols to the kinetic model formalisms shown in the insets. A, A 16 kinetic parameters model consisting of two closed states, an open state and an inactivated state, with the maximal conductance of each protocol providing an extra parameter. The transition rate functions were defined as kij=aij.ezij .Vm and kji=aji.e-zji .Vm for i<j. B, An example of the fit achieved by the model shown in A to activation traces consisting of inward currents recorded in the nucleated configuration of the patch-clamp technique that were produced by a 100 ms pre-pulse to -130 mV followed by a 20 ms pulse to voltages between -130 to -25 mV at 5 mV increments. C, A 32 kinetic parameters model consisting of three closed states, an open state and two inactivated states, the maximal conductances and transition rate functions were included as in A. D, The same data as in B fit with the model shown in C. 1 ms 100 pA B

Links between complex spikes and multiple synaptic plasticity mechanisms in the cerebellar cortex

Introduction In the classic cerebellar learning theory the climbing fiber (CF) is activated when the movement is inaccurate and this activation leads changes in the synaptic strength and in the Purkinje cell (PC) output [1,2]. Stimulation of a single CF activates hundreds of synaptic contacts across PC dendrites and triggers a high frequency burst of spikes called complex spike (CS) [3]. However, it is still unclear how changes in the complex spike probability and the time interval between the parallel fiber (PF) and CF inputs will affect the PC single spike response and learning, considering multiple plasticity mechanisms present at PF and CF synapses [4]. In this work, we used a computational model for synaptic transmission to simulate both longterm and short-term plasticity [5,6] and a single compartmental model of the PC [7] to investigate the links between CS probability, multiple plasticity mechanisms and changes in the PC output. The computational model includes the post-synaptic expression of long-term depression between CF and PC [8], long-term potentiation and depression between PF and PC [5] and short-term facilitation between PF and PC [6]. The models were based in previous models for synaptic transmission and were validated according to the available experimental data (Figure 1).

Pulse and Meter as Neural Resonance

The experience of musical rhythm is a remarkable psychophysical phenomenon, in part because the perception of periodicities, namely pulse and meter, arise from stimuli that are not periodic. One possible function of such a transformation is to enable synchronization between individuals through perception of a common abstract temporal structure (e.g., during music performance). Thus, understanding the brain processes that underlie rhythm perception is fundamental to explaining musical behavior. Here, we propose that neural resonance provides an excellent account of many aspects of human rhythm perception. Our framework is consistent with recent brain-imaging studies showing neural correlates of rhythm perception in high-frequency oscillatory activity, and leads to the hypothesis that perception of pulse and meter result from rhythmic bursts of high-frequency neural activity in response to musical rhythms. High-frequency bursts of activity may enable communication between neural areas, such as auditory and motor cortices, during rhythm perception and production.