scholarly journals The Identification Of Cortical Pyramidal Neurons Using A Rpp Based Algorithm

2018 ◽  
Author(s):  
Yelena Kolezeva
Keyword(s):  
Biomedical Research ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Rapid Development ◽  
Cortical Pyramidal Neuron ◽  
Cortical Pyramidal Neurons ◽  
Linear And Nonlinear ◽  
Effective Integration

AbstractAppropriately classifying neuronal subgroups is critical to numerous downstream procedures in several disciplines of biomedical research. The cortical pyramidal neuron characterization technology has achieved rapid development in recent years. However, capturing true neuronal features for accurate pyramidal neuron characterization and segmentation has remained elusive. In the current study, a novel global preserving estimate algorithm is used to capture the non-linearity in the features of cortical pyramidal neuron after Factor Algorithm. Our results provide evidence for the effective integration of the original linear and nonlinear neuronal features and achieves better characterization performance on multiple cortical pyramidal neuron databases through array matching.

scholarly journals Local glutamate-mediated dendritic plateau potentials change the state of the cortical pyramidal neuron

2021 ◽  
Vol 125 (1) ◽  
pp. 23-42
Author(s):  
Peng P. Gao ◽  
Joseph W. Graham ◽  
Wen-Liang Zhou ◽  
Jinyoung Jang ◽  
Sergio Angulo ◽  
...  
Keyword(s):  
Time Constant ◽  
Computer Model ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Basal Dendrite ◽  
Plateau Potentials ◽  
Voltage Imaging ◽  
Plateau Potential ◽  
Cortical Pyramidal Neurons ◽  
Afferent Inputs

In cortical pyramidal neurons, we recorded glutamate-mediated dendritic plateau potentials with voltage imaging and created a computer model that recreated experimental measures from dendrite and cell body. Our model made new predictions, which were then tested in experiments. Plateau potentials profoundly change neuronal state: a plateau potential triggered in one basal dendrite depolarizes the soma and shortens membrane time constant, making the cell more susceptible to firing triggered by other afferent inputs.

Increased Excitability and Inward Rectification in Layer V Cortical Pyramidal Neurons in the Epileptic Mutant Mouse Stargazer

1997 ◽  
Vol 77 (2) ◽  
pp. 621-631 ◽  
Author(s):  
Eric Di Pasquale ◽  
Karl D. Keegan ◽  
Jeffrey L. Noebels
Keyword(s):  
Action Potential ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Mutant Mouse ◽  
Inward Rectification ◽  
Single Action ◽  
Cortical Pyramidal Neurons ◽  
Layer V ◽  
Whole Cell Recordings ◽  
Spike Wave

Di Pasquale, Eric, Karl D. Keegan, and Jeffrey L. Noebels. Increased excitability and inward rectification in layer V cortical pyramidal neurons in the epileptic mutant mouse stargazer. J. Neurophysiol. 77: 621–631, 1997. The excitability of layer V cortical pyramidal neurons was studied in vitro in the single-locus mutant mouse stargazer ( stg), a genetic model of spike wave epilepsy. Field recordings in neocortical slices from mutant mice bathed in artificial cerebrospinal fluid revealed spontaneous synchronous network discharges that were never present in wild-type slices. Intracellular and whole cell recordings from stg/ stg neurons in deep layers showed spontaneous giant depolarizing excitatory postsynaptic potentials generating bursts of action potentials, and a 78% reduction in the afterburst hyperpolarization. Whole cell recordings revealed gene-linked differences in active membrane properties in two types of regular spiking neurons. Single action potential rise and decay times were reduced, and the rheobase current was decreased by 68% in mutant cells. Plots of spike frequency-current relationships revealed that the gain of this relation was augmented by 29% in the mutant. Comparisons of visually identified pyramidal neuron firing properties in both genotypes revealed no difference in single action potential afterhyperpolarization. Voltage-clamp recordings showed an approximately threefold amplitude increase in a cesium-sensitive inward rectifier. No cell density or soma size differences were observed in the layer V pyramidal neuron population between the two genotypes. These results demonstrate an autonomous increase in cortical network excitability in a genetic epilepsy model. This defect could lower the threshold for aberrant thalamocortical spike wave oscillations in vivo, and may contribute to the mechanism of one form of inherited absence epilepsy.

Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice

2020 ◽  
Vol 12 (570) ◽  
pp. eabc1492
Author(s):  
Lawrence S. Hsieh ◽  
John H. Wen ◽  
Lena H. Nguyen ◽  
Longbo Zhang ◽  
Stephanie A. Getz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Pyramidal Neurons ◽  
Focal Cortical Dysplasia ◽  
Repetitive Firing ◽  
Intracellular Camp ◽  
Main Role ◽  
Channel Activity ◽  
Mechanistic Target Of Rapamycin ◽  
Cortical Pyramidal Neurons ◽  
Causative Link

The causative link between focal cortical malformations (FCMs) and epilepsy is well accepted, especially among patients with focal cortical dysplasia type II (FCDII) and tuberous sclerosis complex (TSC). However, the mechanisms underlying seizures remain unclear. Using a mouse model of TSC- and FCDII-associated FCM, we showed that FCM neurons were responsible for seizure activity via their unexpected abnormal expression of the hyperpolarization-activated cyclic nucleotide–gated potassium channel isoform 4 (HCN4), which is normally not present in cortical pyramidal neurons after birth. Increasing intracellular cAMP concentrations, which preferentially affects HCN4 gating relative to the other isoforms, drove repetitive firing of FCM neurons but not control pyramidal neurons. Ectopic HCN4 expression was dependent on the mechanistic target of rapamycin (mTOR), preceded the onset of seizures, and was also found in diseased neurons in tissue resected from patients with TSC and FCDII. Last, blocking HCN4 channel activity in FCM neurons prevented epilepsy in the mouse model. These findings suggest that HCN4 play a main role in seizure and identify a cAMP-dependent seizure mechanism in TSC and FCDII. Furthermore, the unique expression of HCN4 exclusively in FCM neurons suggests that gene therapy targeting HCN4 might be effective in reducing seizures in FCDII or TSC.

scholarly journals Gonadal Hormones Modulate the Dendritic Spine Densities of Primary Cortical Pyramidal Neurons in Adult Female Rat

2009 ◽  
Vol 19 (11) ◽  
pp. 2719-2727 ◽  
Author(s):  
J.-R. Chen ◽  
Y.-T. Yan ◽  
T.-J. Wang ◽  
L.-J. Chen ◽  
Y.-J. Wang ◽  
...  
Keyword(s):  
Adult Female ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Gonadal Hormones ◽  
Female Rat ◽  
Cortical Pyramidal Neurons

scholarly journals The Transcription Factor Cux1 Regulates Dendritic Morphology of Cortical Pyramidal Neurons

PLoS ONE ◽  
2010 ◽  
Vol 5 (5) ◽  
pp. e10596 ◽  
Author(s):  
Ning Li ◽  
Chun-Tao Zhao ◽  
Ying Wang ◽  
Xiao-Bing Yuan
Keyword(s):  
Transcription Factor ◽  
Pyramidal Neurons ◽  
Dendritic Morphology ◽  
Cortical Pyramidal Neurons

Testosterone modulation of dendritic spines of somatosensory cortical pyramidal neurons

2013 ◽  
Vol 218 (6) ◽  
pp. 1407-1417 ◽  
Author(s):  
Jeng-Rung Chen ◽  
Tsyr-Jiuan Wang ◽  
Seh-Hong Lim ◽  
Yueh-Jan Wang ◽  
Guo-Fang Tseng
Keyword(s):  
Dendritic Spines ◽  
Pyramidal Neurons ◽  
Cortical Pyramidal Neurons
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