scholarly journals Prolonged deficit of gamma oscillations in the peri-infarct cortex of mice after stroke

2020 ◽  
Author(s):  
M Hazime ◽  
M Alasoadura ◽  
R Lamtahri ◽  
P Quilichini ◽  
J Leprince ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Neuronal Excitability ◽  
Field Potential ◽  
Oscillatory System ◽  
Gamma Oscillations ◽  
Therapeutic Interventions ◽  
Oscillatory Activity ◽  
Infarct Zone ◽  
Neural Repair ◽  
Cortical Ischemia

AbstractDays and weeks after an ischemic stroke, the peri-infarct area adjacent to the necrotic tissue exhibits very intense synaptic reorganization aimed at regaining lost functions. In order to enhance functional recovery, it is important to understand the mechanisms supporting neural repair and neuroplasticity in the cortex surrounding the lesion. Brain oscillations of the local field potential (LFP) are rhythmic fluctuations of neuronal excitability aimed at synchronizing neuronal activity to organize information processing and plasticity. Although the oscillatory activity of the brain has been probed after stroke in both animals and humans using electroencephalography (EEG), the latter is ineffective to precisely map the oscillatory changes in the peri-infarct zone where synaptic plasticity potential is high. Here, we worked on the hypothesis that brain oscillatory system is altered in the surviving peri-infarct cortex, which may slow down functional repair and reduce the capacity to recovery. In order to document the relevance of this hypothesis, oscillatory power was measured at various distances from the necrotic core at 7 and 21 days after a permanent cortical ischemia induced in mice. Delta and theta oscillations remained at a normal power in the peri-infarct cortex, in contrast to gamma oscillations that displayed a rapid decrease, the closer we get to the lesion core. A broadband increase of power was also observed in the homotopic contralateral sites. Thus, the proximal peri-infarct cortex could become a target of therapeutic interventions aimed at correcting the oscillatory regimen. These results argue for the usefulness of therapeutic intervention aimed at boosting gamma oscillations in order to improve post-stroke functional recovery.

Increased Gamma Oscillatory Activity in the Subthalamic Nucleus During Tremor in Parkinson's Disease Patients

2009 ◽  
Vol 101 (2) ◽  
pp. 789-802 ◽  
Author(s):  
M. Weinberger ◽  
W. D. Hutchison ◽  
A. M. Lozano ◽  
M. Hodaie ◽  
J. O. Dostrovsky
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Subthalamic Nucleus ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Neuronal Firing ◽  
Oscillatory Activity ◽  
Frequency Range ◽  
Resting Tremor ◽  
Gamma Frequency

Rest tremor is one of the main symptoms in Parkinson's disease (PD), although in contrast to rigidity and akinesia, the severity of the tremor does not correlate well with the degree of dopamine deficiency or the progression of the disease. Studies suggest that akinesia in PD patients is related to abnormal increased beta (15–30 Hz) and decreased gamma (35–80 Hz) synchronous oscillatory activity in the basal ganglia. Here we investigated the dynamics of oscillatory activity in the subthalamic nucleus (STN) during tremor. We used two adjacent microelectrodes to simultaneously record neuronal firing and local field potential (LFP) activity in nine PD patients who exhibited resting tremor during functional neurosurgery. We found that neurons exhibiting oscillatory activity at tremor frequency are located in the dorsal region of STN, where neurons with beta oscillatory activity are observed, and that their activity is coherent with LFP oscillations in the beta frequency range. Interestingly, in 85% of the 58 sites examined, the LFP exhibited increased oscillatory activity in the low gamma frequency range (35–55 Hz) during periods with stronger tremor. Furthermore, in 17 of 26 cases where two LFPs were recorded simultaneously, their coherence in the gamma range increased with increased tremor. When averaged across subjects, the ratio of the beta to gamma coherence was significantly lower in periods with stronger tremor compared with periods of no or weak tremor. These results suggest that resting tremor in PD is associated with an altered balance between beta and gamma oscillations in the motor circuits of STN.

scholarly journals Perisynaptic GABA Receptors: The Overzealous Protector

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Andrew N. Clarkson
Keyword(s):  
Cell Death ◽  
Functional Recovery ◽  
Gaba Receptors ◽  
Neuronal Excitability ◽  
Neural Repair ◽  
Motor Maps ◽  
Motor Representations ◽  
The Brain ◽  
Limited Process ◽  
Repair Phase

An attempt to find pharmacological therapies to treat stroke patients and minimize the extent of cell death has seen the failure of dozens of clinical trials. As a result, stroke/cerebral ischemia is the leading cause of lasting adult disability. Stroke-induced cell death occurs due to an excess release of glutamate. As a consequence to this, a compensatory increased release of GABA occurs that results in the subsequent internalization of synaptic GABAAreceptors and spillover onto perisynaptic GABAAreceptors, resulting in increased tonic inhibition. Recent studies show that the brain can engage in a limited process of neural repair after stroke. Changes in cortical sensory and motor maps and alterations in axonal structure are dependent on patterned neuronal activity. It has been assumed that changes in neuronal excitability underlie processes of neural repair and remapping of cortical sensory and motor representations. Indeed, recent evidence suggests that local inhibitory and excitatory currents are altered after stroke and modulation of these networks to enhance excitability during the repair phase can facilitate functional recovery after stroke. More specifically, dampening tonic GABA inhibition can afford an early and robust improvement in functional recovery after stroke.

Laminar profile of visual response properties in ferret superior colliculus

2013 ◽  
Vol 110 (6) ◽  
pp. 1333-1345 ◽  
Author(s):  
Iain Stitt ◽  
Edgar Galindo-Leon ◽  
Florian Pieper ◽  
Gerhard Engler ◽  
Andreas K. Engel
Keyword(s):  
Superior Colliculus ◽  
Receptive Fields ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Field Size ◽  
Oscillatory Activity ◽  
Visual Response ◽  
Afferent Pathways ◽  
Full Field ◽  
Response Properties

In the superior colliculus (SC), visual afferent inputs from various sources converge in a highly organized way such that all layers form topographically aligned representations of contralateral external space. Despite this anatomical organization, it remains unclear how the layer-specific termination of different visual input pathways is reflected in the nature of visual response properties and their distribution across layers. To uncover the physiological correlates underlying the laminar organization of the SC, we recorded multiunit and local field potential activity simultaneously from all layers with dual-shank multichannel linear probes. We found that the location of spatial receptive fields was strongly conserved across all visual responsive layers. There was a tendency for receptive field size to increase with depth in the SC, with superficial receptive fields significantly smaller than deep receptive fields. Additionally, superficial layers responded significantly faster than deeper layers to flash stimulation. In some recordings, flash-evoked responses were characterized by the presence of gamma oscillatory activity (40–60 Hz) in multiunit and field potential signals, which was strongest in retinorecipient layers. While SC neurons tended to respond only weakly to full-field drifting gratings, we observed very similar oscillatory responses to the offset of grating stimuli, suggesting gamma oscillations are produced following light offset. Oscillatory spiking activity was highly correlated between horizontally distributed neurons within these layers, with oscillations temporally locked to the stimulus. Together, visual response properties provide physiological evidence reflecting the laminar-specific termination of visual afferent pathways in the SC, most notably characterized by the oscillatory entrainment of superficial neurons.

scholarly journals Gamma oscillations in the somatosensory thalamus of a patient with a phantom limb: case report

2018 ◽  
Vol 129 (4) ◽  
pp. 1048-1055
Author(s):  
Diellor Basha ◽  
Jonathan O. Dostrovsky ◽  
Suneil K. Kalia ◽  
Mojgan Hodaie ◽  
Andres M. Lozano ◽  
...  
Keyword(s):  
High Frequency ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Phantom Limb ◽  
Oscillatory Activity ◽  
The Novel ◽  
Thalamic Neurons ◽  
Somatosensory Thalamus ◽  
Thalamocortical Dysrhythmia ◽  
Deep Brain

The amputation of an extremity is commonly followed by phantom sensations that are perceived to originate from the missing limb. The mechanism underlying the generation of these sensations is still not clear although the development of abnormal oscillatory bursting in thalamic neurons may be involved. The theory of thalamocortical dysrhythmia implicates gamma oscillations in phantom pathophysiology although this rhythm has not been previously observed in the phantom limb thalamus. In this study, the authors report the novel observation of widespread 38-Hz gamma oscillatory activity in spike and local field potential recordings obtained from the ventral caudal somatosensory nucleus of the thalamus (Vc) of a phantom limb patient undergoing deep brain stimulation (DBS) surgery. Interestingly, microstimulation near tonically firing cells in the Vc resulted in high-frequency, gamma oscillatory discharges coincident with phantom sensations reported by the patient. Recordings from the somatosensory thalamus of comparator groups (essential tremor and pain) did not reveal the presence of gamma oscillatory activity.

Aluminum Suppresses Effect of Nicotine on Gamma Oscillations (20-40 Hz) in Mouse Hippocampal Slices

2018 ◽  
Vol 17 (6) ◽  
pp. 404-411 ◽  
Author(s):  
Syeda Mehpara Farhat ◽  
Touqeer Ahmed
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Cholinergic System ◽  
Acetylcholine Receptors ◽  
Peak Power ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Gamma Oscillation ◽  
Facilitatory Effect

Background: Aluminum (Al) causes neurodegeneration and its toxic effects on cholinergic system in the brain is well documented. However, it is unknown whether and how Al changes oscillation patterns, driven by the cholinergic system, in the hippocampus. Objective: We studied acute effects of Al on nicotinic acetylcholine receptors (nAChRs)-mediated modulation of persistent gamma oscillations in the hippocampus. Method: The field potential recording was done in CA3 area of acute hippocampal slices. Results: Carbachol-induced gamma oscillation peak power increased (1.32±0.09mV2/Hz, P<0.01) in control conditions (without Al) by application of 10µM nicotine as compared to baseline value normalized to 1. This nicotine-induced facilitation of gamma oscillation peak power was found to depend on non-α7 nAChRs. In slices with Al pre-incubation for three to four hours, gamma oscillation peak power was reduced (5.4±1.8mV2/Hz, P<0.05) and facilitatory effect of nicotine on gamma oscillation peak power was blocked as compared to the control (18.06±2.1mV2/Hz) or one hour Al pre-incubated slices (11.3±2.5mV2/Hz). Intriguingly wash-out, after three to four hours of Al incubation, failed to restore baseline oscillation power and its facilitation by nicotine as no difference was observed in gamma oscillation peak power between Al wash-out slices (3.4±1.1mV2/Hz) and slices without washout (3.6±0.9mV2/Hz). Conclusion: This study shows that at cellular level, exposure of hippocampal tissue to Al compromised nAChR-mediated facilitation of cholinergic hippocampal gamma oscillations. Longer in vitro Al exposure caused permanent changes in hippocampal oscillogenic circuitry and changed its sensitivity to nAChR-modulation. This study will help to understand the possible mechanism of cognitive decline induced by Al.

scholarly journals Superimposed gratings induce diverse response patterns of gamma oscillations in primary visual cortex

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Wang ◽  
Chuanliang Han ◽  
Tian Wang ◽  
Weifeng Dai ◽  
Yang Li ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Neural Mechanisms ◽  
Model Parameters ◽  
Response Patterns ◽  
Region Difference ◽  
High Gamma ◽  
Spiking Activity

AbstractStimulus-dependence of gamma oscillations (GAMMA, 30–90 Hz) has not been fully understood, but it is important for revealing neural mechanisms and functions of GAMMA. Here, we recorded spiking activity (MUA) and the local field potential (LFP), driven by a variety of plaids (generated by two superimposed gratings orthogonal to each other and with different contrast combinations), in the primary visual cortex of anesthetized cats. We found two distinct narrow-band GAMMAs in the LFPs and a variety of response patterns to plaids. Similar to MUA, most response patterns showed that the second grating suppressed GAMMAs driven by the first one. However, there is only a weak site-by-site correlation between cross-orientation interactions in GAMMAs and those in MUAs. We developed a normalization model that could unify the response patterns of both GAMMAs and MUAs. Interestingly, compared with MUAs, the GAMMAs demonstrated a wider range of model parameters and more diverse response patterns to plaids. Further analysis revealed that normalization parameters for high GAMMA, but not those for low GAMMA, were significantly correlated with the discrepancy of spatial frequency between stimulus and sites’ preferences. Consistent with these findings, normalization parameters and diversity of high GAMMA exhibited a clear transition trend and region difference between area 17 to 18. Our results show that GAMMAs are also regulated in the form of normalization, but that the neural mechanisms for these normalizations might differ from those of spiking activity. Normalizations in different brain signals could be due to interactions of excitation and inhibitions at multiple stages in the visual system.

scholarly journals Population dynamics of the modified theta model: macroscopic phase reduction and bifurcation analysis link microscopic neuronal interactions to macroscopic gamma oscillation

2014 ◽  
Vol 11 (95) ◽  
pp. 20140058 ◽  
Author(s):  
Kiyoshi Kotani ◽  
Ikuhiro Yamaguchi ◽  
Lui Yoshida ◽  
Yasuhiko Jimbo ◽  
G. Bard Ermentrout
Keyword(s):  
Bifurcation Analysis ◽  
Field Potential ◽  
Reversal Potential ◽  
Planck Equation ◽  
Gamma Oscillations ◽  
Gamma Oscillation ◽  
Synaptic Coupling ◽  
Time Constants ◽  
Shunting Inhibition ◽  
Synaptic Interactions

Gamma oscillations of the local field potential are organized by collective dynamics of numerous neurons and have many functional roles in cognition and/or attention. To mathematically and physiologically analyse relationships between individual inhibitory neurons and macroscopic oscillations, we derive a modification of the theta model, which possesses voltage-dependent dynamics with appropriate synaptic interactions. Bifurcation analysis of the corresponding Fokker–Planck equation (FPE) enables us to consider how synaptic interactions organize collective oscillations. We also develop the adjoint method (infinitesimal phase resetting curve) for simultaneous equations consisting of ordinary differential equations representing synaptic dynamics and a partial differential equation for determining the probability distribution of the membrane potential. This method provides a macroscopic phase response function (PRF), which gives insights into how it is modulated by external perturbation or internal changes of parameters. We investigate the effects of synaptic time constants and shunting inhibition on these gamma oscillations. The sensitivity of rising and decaying time constants is analysed in the oscillatory parameter regions; we find that these sensitivities are not largely dependent on rate of synaptic coupling but, rather, on current and noise intensity. Analyses of shunting inhibition reveal that it can affect both promotion and elimination of gamma oscillations. When the macroscopic oscillation is far from the bifurcation, shunting promotes the gamma oscillations and the PRF becomes flatter as the reversal potential of the synapse increases, indicating the insensitivity of gamma oscillations to perturbations. By contrast, when the macroscopic oscillation is near the bifurcation, shunting eliminates gamma oscillations and a stable firing state appears. More interestingly, under appropriate balance of parameters, two branches of bifurcation are found in our analysis of the FPE. In this case, shunting inhibition can effect both promotion and elimination of the gamma oscillation depending only on the reversal potential.

scholarly journals Frontal eye field microstimulation induces task-dependent gamma oscillations in the lateral intraparietal area

2012 ◽  
Vol 108 (5) ◽  
pp. 1392-1402 ◽  
Author(s):  
Elsie Premereur ◽  
Wim Vanduffel ◽  
Pieter R. Roelfsema ◽  
Peter Janssen
Keyword(s):  
Spatial Attention ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Oculomotor Control ◽  
Saccade Target ◽  
Frontal Eye Field ◽  
Alpha Power ◽  
Lateral Intraparietal Area ◽  
Electrical Microstimulation ◽  
Gamma Power

Macaque frontal eye fields (FEF) and the lateral intraparietal area (LIP) are high-level oculomotor control centers that have been implicated in the allocation of spatial attention. Electrical microstimulation of macaque FEF elicits functional magnetic resonance imaging (fMRI) activations in area LIP, but no study has yet investigated the effect of FEF microstimulation on LIP at the single-cell or local field potential (LFP) level. We recorded spiking and LFP activity in area LIP during weak, subthreshold microstimulation of the FEF in a delayed-saccade task. FEF microstimulation caused a highly time- and frequency-specific, task-dependent increase in gamma power in retinotopically corresponding sites in LIP: FEF microstimulation produced a significant increase in LIP gamma power when a saccade target appeared and remained present in the LIP receptive field (RF), whereas less specific increases in alpha power were evoked by FEF microstimulation for saccades directed away from the RF. Stimulating FEF with weak currents had no effect on LIP spike rates or on the gamma power during memory saccades or passive fixation. These results provide the first evidence for task-dependent modulations of LFPs in LIP caused by top-down stimulation of FEF. Since the allocation and disengagement of spatial attention in visual cortex have been associated with increases in gamma and alpha power, respectively, the effects of FEF microstimulation on LIP are consistent with the known effects of spatial attention.

scholarly journals Non-synaptic Cell-Autonomous Mechanisms Underlie Neuronal Hyperactivity in a Genetic Model of PIK3CA-Driven Intractable Epilepsy

2021 ◽  
Vol 14 ◽  
Author(s):  
Achira Roy ◽  
Victor Z. Han ◽  
Angela M. Bard ◽  
Devin T. Wehle ◽  
Stephen E. P. Smith ◽  
...  
Keyword(s):  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Genetic Model ◽  
Ex Vivo ◽  
Significant Proportion ◽  
Intractable Epilepsy ◽  
Therapeutic Interventions ◽  
Hippocampal Pyramidal Neurons ◽  
Phosphoinositide 3 Kinase

Patients harboring mutations in the PI3K-AKT-MTOR pathway-encoding genes often develop a spectrum of neurodevelopmental disorders including epilepsy. A significant proportion remains unresponsive to conventional anti-seizure medications. Understanding mutation-specific pathophysiology is thus critical for molecularly targeted therapies. We previously determined that mouse models expressing a patient-related activating mutation in PIK3CA, encoding the p110α catalytic subunit of phosphoinositide-3-kinase (PI3K), are epileptic and acutely treatable by PI3K inhibition, irrespective of dysmorphology. Here we report the physiological mechanisms underlying this dysregulated neuronal excitability. In vivo, we demonstrate epileptiform events in the Pik3ca mutant hippocampus. By ex vivo analyses, we show that Pik3ca-driven hyperactivation of hippocampal pyramidal neurons is mediated by changes in multiple non-synaptic, cell-intrinsic properties. Finally, we report that acute inhibition of PI3K or AKT, but not MTOR activity, suppresses the intrinsic hyperactivity of the mutant neurons. These acute mechanisms are distinct from those causing neuronal hyperactivity in other AKT-MTOR epileptic models and define parameters to facilitate the development of new molecularly rational therapeutic interventions for intractable epilepsy.

scholarly journals Coherent and intermittent ensemble oscillations emerge from networks of irregular spiking neurons

2016 ◽  
Vol 115 (1) ◽  
pp. 457-469 ◽  
Author(s):  
Mahmood S. Hoseini ◽  
Ralf Wessel
Keyword(s):  
Single Neuron ◽  
Experimental Studies ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Peak Frequency ◽  
Spiking Neurons ◽  
Network Activity ◽  
Cortical Circuits ◽  
Model Network ◽  
Low Rate

Local field potential (LFP) recordings from spatially distant cortical circuits reveal episodes of coherent gamma oscillations that are intermittent, and of variable peak frequency and duration. Concurrently, single neuron spiking remains largely irregular and of low rate. The underlying potential mechanisms of this emergent network activity have long been debated. Here we reproduce such intermittent ensemble oscillations in a model network, consisting of excitatory and inhibitory model neurons with the characteristics of regular-spiking (RS) pyramidal neurons, and fast-spiking (FS) and low-threshold spiking (LTS) interneurons. We find that fluctuations in the external inputs trigger reciprocally connected and irregularly spiking RS and FS neurons in episodes of ensemble oscillations, which are terminated by the recruitment of the LTS population with concurrent accumulation of inhibitory conductance in both RS and FS neurons. The model qualitatively reproduces experimentally observed phase drift, oscillation episode duration distributions, variation in the peak frequency, and the concurrent irregular single-neuron spiking at low rate. Furthermore, consistent with previous experimental studies using optogenetic manipulation, periodic activation of FS, but not RS, model neurons causes enhancement of gamma oscillations. In addition, increasing the coupling between two model networks from low to high reveals a transition from independent intermittent oscillations to coherent intermittent oscillations. In conclusion, the model network suggests biologically plausible mechanisms for the generation of episodes of coherent intermittent ensemble oscillations with irregular spiking neurons in cortical circuits.

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