scholarly journals Selectivity for Grasp in Local Field Potential and Single Neuron Activity Recorded Simultaneously from M1 and F5 in the Awake Macaque Monkey

2008 ◽  
Vol 28 (43) ◽  
pp. 10961-10971 ◽  
Author(s):  
R. L. Spinks ◽  
A. Kraskov ◽  
T. Brochier ◽  
M. A. Umilta ◽  
R. N. Lemon
Keyword(s):  
Local Field ◽  
Local Field Potential ◽  
Single Neuron ◽  
Field Potential ◽  
Macaque Monkey ◽  
Neuron Activity ◽  
Single Neuron Activity

scholarly journals Amygdala input differentially influences prefrontal local field potential and single neuron encoding of reward-based decisions

2017 ◽  
Author(s):  
Frederic M. Stoll ◽  
Clayton P. Mosher ◽  
Sarita Tamang ◽  
Elisabeth A. Murray ◽  
Peter H. Rudebeck
Keyword(s):  
Local Field ◽  
Single Neuron ◽  
Field Potential ◽  
Neuron Activity ◽  
Single Neurons ◽  
Stimulus Choice ◽  
Reward Value ◽  
Before And After ◽  
Amygdala Lesions ◽  
Single Neuron Activity

ABSTRACTReward-guided behaviors require functional interaction between amygdala, orbital (OFC), and medial (MFC) divisions of prefrontal cortex, but the neural mechanisms underlying these interactions are unclear. Here, we used a decoding approach to analyze local field potentials (LFPs) recorded from OFC and MFC of monkeys engaged in a stimulus-choice task, before and after excitotoxic amygdala lesions. Whereas OFC LFP responses were strongly modulated by the amount of reward associated with each stimulus, MFC responses best represented which stimulus subjects decided to choose. This was counter to what we observed in the level of single neurons where their activity was closely associated with the value of the stimuli presented on each trial. After lesions of the amygdala, stimulus-reward value and choice encoding were reduced in OFC and MFC, respectively. However, while the lesion-induced decrease in OFC LFP encoding of stimulus-reward value mirrored changes in single neuron activity, reduced choice encoding in MFC LFPs was distinct from changes in single neuron activity. Thus, LFPs and single neurons represent different information required for decision-making in OFC and MFC. At the circuit-level, amygdala input to these two areas play a distinct role in stimulus-reward encoding in OFC and choice encoding in MFC.

Concomitant Single Neuron Activity, Local Field Potentials, and Cerebral Microdialysis in Neurosurgical Patients

Neurosurgery ◽  
1998 ◽  
Vol 43 (3) ◽  
pp. 706-706 ◽  
Author(s):  
Itzhak Fried ◽  
Eric Behnke ◽  
Nigel Maidment ◽  
Anatole Bragin ◽  
Katherine MacDonald ◽  
...  
Keyword(s):  
Local Field ◽  
Single Neuron ◽  
Local Field Potentials ◽  
Cerebral Microdialysis ◽  
Neuron Activity ◽  
Field Potentials ◽  
Neurosurgical Patients ◽  
Single Neuron Activity

scholarly journals Defective Excitatory/Inhibitory Synaptic Balance and Increased Neuron Apoptosis in a Zebrafish Model of Dravet Syndrome

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1199 ◽  
Author(s):  
Alexandre Brenet ◽  
Rahma Hassan-Abdi ◽  
Julie Somkhit ◽  
Constantin Yanicostas ◽  
Nadia Soussi-Yanicostas
Keyword(s):  
Local Field ◽  
Local Field Potential ◽  
Field Potential ◽  
Dravet Syndrome ◽  
Inhibitory Synapses ◽  
Neuron Activity ◽  
Loss Of Function ◽  
Zebrafish Model ◽  
Neuron Apoptosis

Dravet syndrome is a type of severe childhood epilepsy that responds poorly to current anti-epileptic drugs. In recent years, zebrafish disease models with Scn1Lab sodium channel deficiency have been generated to seek novel anti-epileptic drug candidates, some of which are currently undergoing clinical trials. However, the spectrum of neuronal deficits observed following Scn1Lab depletion in zebrafish larvae has not yet been fully explored. To fill this gap and gain a better understanding of the mechanisms underlying neuron hyperexcitation in Scn1Lab-depleted larvae, we analyzed neuron activity in vivo using combined local field potential recording and transient calcium uptake imaging, studied the distribution of excitatory and inhibitory synapses and neurons as well as investigated neuron apoptosis. We found that Scn1Lab-depleted larvae displayed recurrent epileptiform seizure events, associating massive synchronous calcium uptakes and ictal-like local field potential bursts. Scn1Lab-depletion also caused a dramatic shift in the neuronal and synaptic balance toward excitation and increased neuronal death. Our results thus provide in vivo evidence suggesting that Scn1Lab loss of function causes neuron hyperexcitation as the result of disturbed synaptic balance and increased neuronal apoptosis.

scholarly journals Defective excitatory/inhibitory synaptic balance and increased neuron apoptosis in a zebrafish model of Dravet syndrome

2019 ◽  
Author(s):  
Alexandre Brenet ◽  
Rahma Hassan-Abdi ◽  
Julie Somkhit ◽  
Constantin Yanicostas ◽  
Nadia Soussi-Yanicostas
Keyword(s):  
Local Field ◽  
Local Field Potential ◽  
Field Potential ◽  
Dravet Syndrome ◽  
Inhibitory Synapses ◽  
Neuron Activity ◽  
Loss Of Function ◽  
Zebrafish Model ◽  
Neuron Apoptosis

AbstractDravet syndrome is a type of severe childhood epilepsy that responds poorly to current anti-epileptic drugs. In recent years, zebrafish disease models with Scn1Lab sodium channel deficiency have been generated to seek novel anti-epileptic drug candidates, some of which are currently undergoing clinical trials. However, the spectrum of neuronal deficits observed following Scn1Lab depletion in zebrafish larvae has not yet been fully explored. To fill this gap and gain a better understanding of the mechanisms underlying neuron hyperexcitation in Scn1Lab-depleted larvae, we analyzed neuron activity in vivo using combined local field potential recording and transient calcium uptake imaging, studied the distribution of excitatory and inhibitory synapses and neurons as well as investigated neuron apoptosis. We found that Scn1Lab-depleted larvae displayed recurrent epileptiform seizure events, associating massive synchronous calcium uptakes and ictal-like local field potential bursts. Scn1Lab-depletion also caused a dramatic shift in the neuronal and synaptic balance toward excitation and increased neuronal death. Our results thus provide in vivo evidence suggesting that Scn1Lab loss of function causes neuron hyperexcitation as the result of disturbed synaptic balance and increased neuronal apoptosis.

scholarly journals Decoupling Action Potential Bias from Cortical Local Field Potentials

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Stephen V. David ◽  
Nicolas Malaval ◽  
Shihab A. Shamma
Keyword(s):  
Local Field ◽  
Field Potential ◽  
Primary Auditory Cortex ◽  
Neuronal Population ◽  
Neuron Activity ◽  
Small Subset ◽  
Population Activity ◽  
Local Field Potential Lfp ◽  
Single Neuron Activity ◽  
Filtering Procedure

Neurophysiologists have recently become interested in studying neuronal population activity through local field potential (LFP) recordings during experiments that also record the activity of single neurons. This experimental approach differs from early LFP studies because it uses high impendence electrodes that can also isolate single neuron activity. A possible complication for such studies is that the synaptic potentials and action potentials of the small subset of isolated neurons may contribute disproportionately to the LFP signal, biasing activity in the larger nearby neuronal population to appear synchronous and cotuned with these neurons. To address this problem, we used linear filtering techniques to remove features correlated with spike events from LFP recordings. This filtering procedure can be applied for well-isolated single units or multiunit activity. We illustrate the effects of this correction in simulation and on spike data recorded from primary auditory cortex. We find that local spiking activity can explain a significant portion of LFP power at most recording sites and demonstrate that removing the spike-correlated component can affect measurements of auditory tuning of the LFP.

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