scholarly journals Selective Alterations in Postsynaptic Markers of Chandelier Cell Inputs to Cortical Pyramidal Neurons in Subjects with Schizophrenia

2009 ◽  
Vol 34 (9) ◽  
pp. 2112-2124 ◽  
Author(s):  
Dianne A Cruz ◽  
Cassandra L Weaver ◽  
Emily M Lovallo ◽  
Darlene S Melchitzky ◽  
David A Lewis
Keyword(s):  
Pyramidal Neurons ◽  
Chandelier Cell ◽  
Cortical Pyramidal Neurons

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

Calcium dysregulation and compensation in cortical pyramidal neurons of the R6/2 mouse model of Huntington’s disease

2021 ◽  
Vol 126 (4) ◽  
pp. 1159-1171
Author(s):  
Katerina D. Oikonomou ◽  
Elissa J. Donzis ◽  
Minh T. N. Bui ◽  
Carlos Cepeda ◽  
Michael S. Levine
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Calcium Transient ◽  
Two Photon Microscopy ◽  
Decay Times ◽  
Cortical Pyramidal Neurons ◽  
Receptor Blockers

We used two-photon microscopy to examine calcium influx induced by action potentials in cortical pyramidal neurons from a mouse model of Huntington’s disease (HD), the R6/2. The amplitude of somatic calcium transients was reduced in R6/2 mice compared with controls. This reduction was compensated by increased decay times, which could lead to reduced calcium buffering capacity. L-type calcium channel and ryanodine receptor blockers reduced calcium transient area in HD neurons, suggesting new therapeutic avenues.

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