scholarly journals Ionic Mechanisms Underlying Repetitive High-Frequency Burst Firing in Supragranular Cortical Neurons

2000 ◽  
Vol 20 (13) ◽  
pp. 4829-4843 ◽  
Author(s):  
Joshua C. Brumberg ◽  
Lionel G. Nowak ◽  
David A. McCormick
Keyword(s):  
High Frequency ◽  
Cortical Neurons ◽  
Burst Firing ◽  
Ionic Mechanisms ◽  
Frequency Burst

Ionic Mechanisms Underlying Burst Firing of Layer III Sensorimotor Cortical Neurons of the Cat: An In Vitro Slice Study

2001 ◽  
Vol 86 (2) ◽  
pp. 771-781 ◽  
Author(s):  
Yoshihiro Nishimura ◽  
Masaru Asahi ◽  
Koichi Saitoh ◽  
Hirofumi Kitagawa ◽  
Yuichi Kumazawa ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Burst Firing ◽  
Ammonium Bromide ◽  
Channel Blockers ◽  
Main Function ◽  
Channel Blockade ◽  
Initial Burst ◽  
Bursting Neurons ◽  
Ionic Mechanisms

We examined the ionic mechanisms underlying burst firing in layer III neurons from cat sensorimotor cortex by intracellular recording in a brain slice. Regular spiking was observed in 77.4% of 137 neurons in response to constant intracellular current pulses of 0.5- to 1-s duration. The rest of the neurons showed burst firing. An initial burst followed by regular-spike firing was seen in 71.0% of 31 bursting neurons. The rest of the bursting neurons ( n = 9) exhibited repetitive bursting. In the bursting neurons, spikes comprising the burst were triggered from the afterdepolarization (ADP) of the first spike of the burst. We examined the ionic mechanisms underlying the ADP by applying channel-blocking agents. The ADP was enhanced (rather than blocked) by Ca2+ channel blockade. This enhancement of the ADP by Ca2+channel blockade was apparent even after blockade of the afterhyperpolarization by apamin or intracellular Ca2+ chelation by EGTA. The firing rate of the regular-spiking cells was increased by apamin, intracellular EGTA or Ca2+ channel blockers. In 17.9% of the neurons examined ( n = 56), these agents switched the regular-spiking pattern into a bursting one. Burst firing could not be changed to regular spiking by these agents. Four neurons that responded with a single initial burst in control solution responded with repetitive bursting after application of these agents. We conclude that the main function of Ca2+ influx in layer III neurons is to activate Ca2+-dependent K+ conductance, which prevents or limits burst firing. At a time when spike amplitude was unchanged, the ADP was blocked and the burst firing changed to regular spiking by extracellularly applied tetrodotoxin (TTX) or intracellularly applied N-(2,6-dimethylphenylcarbamoylmethyl) triethyl ammonium bromide (QX314). We concluded that a TTX- and QX314-sensitive Na+ current underlies the ADP and therefore contributes to the burst firing of layer III neurons from the cat cortex.

scholarly journals Neural Burst Firing and Its Roles in Mental and Neurological Disorders

2021 ◽  
Vol 15 ◽  
Author(s):  
Jie Shao ◽  
Yunhui Liu ◽  
Dashuang Gao ◽  
Jie Tu ◽  
Fan Yang
Keyword(s):  
Neurological Disorders ◽  
High Frequency ◽  
Burst Firing ◽  
Specific Information ◽  
Neural Firing ◽  
Information Coding ◽  
Brain Areas ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Ionic Mechanisms

Neural firing patterns are critical for specific information coding and transmission, and abnormal firing is implicated in a series of neural pathologies. Recent studies have indicated that enhanced burst firing mediated by T-type voltage-gated calcium channels (T-VGCCs) in specific neuronal subtypes is involved in several mental or neurological disorders such as depression and epilepsy, while suppression of T-VGCCs relieve related symptoms. Burst firing consists of groups of relatively high-frequency spikes separated by quiescence. Neurons in a variety of brain areas, including the thalamus, hypothalamus, cortex, and hippocampus, display burst firing, but the ionic mechanisms that generating burst firing and the related physiological functions vary among regions. In this review, we summarize recent findings on the mechanisms underlying burst firing in various brain areas, as well as the roles of burst firing in several mental and neurological disorders. We also discuss the ion channels and receptors that may regulate burst firing directly or indirectly, with these molecules highlighted as potential intervention targets for the treatment of mental and neurological disorders.

scholarly journals Abnormal High-Frequency Burst Firing of Cerebellar Neurons in Rapid-Onset Dystonia-Parkinsonism

2014 ◽  
Vol 34 (35) ◽  
pp. 11723-11732 ◽  
Author(s):  
R. Fremont ◽  
D. P. Calderon ◽  
S. Maleki ◽  
K. Khodakhah
Keyword(s):  
High Frequency ◽  
Rapid Onset ◽  
Burst Firing ◽  
Cerebellar Neurons ◽  
Frequency Burst

scholarly journals High-fidelity transmission of high-frequency burst stimuli from peripheral nerve to thalamic nuclei in children with dystonia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Estefanía Hernandez-Martin ◽  
Enrique Arguelles ◽  
Yifei Zheng ◽  
Ruta Deshpande ◽  
Terence D. Sanger
Keyword(s):  
Deep Brain Stimulation ◽  
Peripheral Nerve ◽  
Brain Stimulation ◽  
High Frequency ◽  
Sensory Information ◽  
Brain Structures ◽  
High Fidelity ◽  
Thalamic Nuclei ◽  
Frequency Burst ◽  
Deep Brain

AbstractHigh-frequency peripheral nerve stimulation has emerged as a noninvasive alternative to thalamic deep brain stimulation for some patients with essential tremor. It is not known whether such techniques might be effective for movement disorders in children, nor is the mechanism and transmission of the peripheral stimuli to central brain structures understood. This study was designed to investigate the fidelity of transmission from peripheral nerves to thalamic nuclei in children with dystonia undergoing deep brain stimulation surgery. The ventralis intermediate (VIM) thalamus nuclei showed a robust evoked response to peripheral high-frequency burst stimulation, with a greatest response magnitude to intra-burst frequencies between 50 and 100 Hz, and reliable but smaller responses up to 170 Hz. The earliest response occurred at 12–15 ms following stimulation onset, suggesting rapid high-fidelity transmission between peripheral nerve and thalamic nuclei. A high-bandwidth, low-latency transmission path from peripheral nerve to VIM thalamus is consistent with the importance of rapid and accurate sensory information for the control of coordination and movement via the cerebello-thalamo-cortical pathway. Our results suggest the possibility of non-invasive modulation of thalamic activity in children with dystonia, and therefore the possibility that a subset of children could have beneficial clinical response without the need for invasive deep brain stimulation.

scholarly journals High-frequency burst spiking in layer 5 thick-tufted pyramids of rat primary somatosensory cortex encodes exploratory touch

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Christiaan P. J. de Kock ◽  
Jean Pie ◽  
Anton W. Pieneman ◽  
Rebecca A. Mease ◽  
Arco Bast ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Information Content ◽  
High Frequency ◽  
Temporal Structure ◽  
Cell Types ◽  
Primary Somatosensory Cortex ◽  
Excitatory Cell ◽  
Cortical Microcircuit ◽  
Subcortical Regions ◽  
Frequency Burst

AbstractDiversity of cell-types that collectively shape the cortical microcircuit ensures the necessary computational richness to orchestrate a wide variety of behaviors. The information content embedded in spiking activity of identified cell-types remain unclear to a large extent. Here, we recorded spike responses upon whisker touch of anatomically identified excitatory cell-types in primary somatosensory cortex in naive, untrained rats. We find major differences across layers and cell-types. The temporal structure of spontaneous spiking contains high-frequency bursts (≥100 Hz) in all morphological cell-types but a significant increase upon whisker touch is restricted to layer L5 thick-tufted pyramids (L5tts) and thus provides a distinct neurophysiological signature. We find that whisker touch can also be decoded from L5tt bursting, but not from other cell-types. We observed high-frequency bursts in L5tts projecting to different subcortical regions, including thalamus, midbrain and brainstem. We conclude that bursts in L5tts allow accurate coding and decoding of exploratory whisker touch.

Encoding properties of the wing hinge stretch receptor in the hawkmothManduca sexta

2001 ◽  
Vol 204 (21) ◽  
pp. 3693-3702 ◽  
Author(s):  
Mark A. Frye
Keyword(s):  
Manduca Sexta ◽  
Instantaneous Frequency ◽  
High Frequency ◽  
Dynamic Deformation ◽  
Stretch Receptor ◽  
Tonic Firing ◽  
Frequency Burst ◽  
Natural Dynamic ◽  
Oscillation Rate

SUMMARYTo characterize the in vivo responses of the wing hinge stretch receptor of Manduca sexta, I recorded its activity and simultaneously tracked the up-and-down motion of the wing while the hawkmoth flew tethered in a wind tunnel. The stretch receptor fires a high-frequency burst of spikes near each dorsal stroke reversal. The onset of the burst is tightly tuned to a set-point in wing elevation, and the number of spikes contained within the burst encodes the maximal degree of wing elevation during the stroke. In an effort to characterize its mechanical encoding properties, I constructed an actuator that delivered deformations to the wing hinge and simultaneously recorded the resultant stretch and tension and the activity of the stretch receptor. Stimuli included stepwise changes in length as well as more natural dynamic deformation that was measured in vivo. Step changes in length reveal that the stretch receptor encodes the static amplitude of stretch with both phasic and tonic firing dynamics. In vivo sinusoidal deformation revealed (i) that the timing of stretch receptor activity is tightly phase-locked within the oscillation cycle, (ii) that the number of spikes per burst is inversely related to oscillation frequency and (iii) that the instantaneous frequency of the burst increases with oscillation rate. At all oscillation rates tested, the instantaneous frequency of the burst increases with amplitude.

scholarly journals High-frequency burst vagal nerve simulation therapy in a natural primate model of genetic generalized epilepsy

2017 ◽  
Vol 138 ◽  
pp. 46-52 ◽  
Author(s):  
C.Á. Szabó ◽  
F.S. Salinas ◽  
A.M. Papanastassiou ◽  
J. Begnaud ◽  
M. Ravan ◽  
...  
Keyword(s):  
High Frequency ◽  
Vagal Nerve ◽  
Primate Model ◽  
Generalized Epilepsy ◽  
Frequency Burst

scholarly journals Blink-Perturbed Saccades in Monkey. II. Superior Colliculus Activity

2000 ◽  
Vol 83 (6) ◽  
pp. 3430-3452 ◽  
Author(s):  
H.H.L.M. Goossens ◽  
A. J. Van Opstal
Keyword(s):  
Superior Colliculus ◽  
Firing Rate ◽  
High Frequency ◽  
Displacement Vector ◽  
Neural Mechanism ◽  
Fixed Number ◽  
Deep Layers ◽  
The Mean ◽  
Reflex Blinks ◽  
Frequency Burst

Trigeminal reflex blinks evoked near the onset of a saccade cause profound spatial-temporal perturbations of the saccade that are typically compensated in mid-flight. This paper investigates the influence of reflex blinks on the discharge properties of saccade-related burst neurons (SRBNs) in intermediate and deep layers of the monkey superior colliculus (SC). Twenty-nine SRBNs, recorded in three monkeys, were tested in the blink-perturbation paradigm. We report that the air puff stimuli, used to elicit blinks, resulted in a short-latency (∼10 ms) transient suppression of saccade-related SRBN activity. Shortly after this suppression (within 10–30 ms), all neurons resumed their activity, and their burst discharge then continued until the perturbed saccade ended near the extinguished target. This was found regardless whether the compensatory movement was into the cell's movement field or not. In the limited number of trials where no compensation occurred, the neurons typically stopped firing well before the end of the eye movement. Several aspects of the saccade-related activity could be further quantified for 25 SRBNs. It appeared that 1) the increase in duration of the high-frequency burst was well correlated with the (two- to threefold) increase in duration of the perturbed movement. 2) The number of spikes in the burst for control and perturbed saccades was quite similar. On average, the number of spikes increased only 14%, whereas the mean firing rate in the burst decreased by 52%. 3) An identical number of spikes were obtained between control and perturbed responses when burst and postsaccadic activity were both included in the spike count. 4) The decrease of the mean firing rate in the burst was well correlated with the decrease in the velocity of perturbed saccades. 5) Monotonic relations between instantaneous firing rate and dynamic motor error were obtained for control responses but not for perturbed responses. And 6) the high-frequency burst of SRBNs with short-lead and long-lead presaccadic activity (also referred to as burst and buildup neurons, respectively) showed very similar features. Our findings show that blinking interacts with the saccade premotor system already at the level of the SC. The data also indicate that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensation for blink-related perturbations. We propose that these interactions occur downstream from the motor SC and that the latter may encode the desired displacement vector of the eyes by sending an approximately fixed number of spikes to the brainstem saccadic burst generator.

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