scholarly journals h-channels Contribute to Divergent Electrophysiological Properties of Supragranular Pyramidal Neurons in Human Versus Mouse Cerebral Cortex

2018 ◽  
Author(s):  
Brian E. Kalmbach ◽  
Anatoly Buchin ◽  
Jeremy A. Miller ◽  
Trygve E. Bakken ◽  
Rebecca D. Hodge ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Pyramidal Neurons ◽  
Electrophysiological Properties ◽  
Mouse Cerebral Cortex ◽  
H Channels

scholarly journals h-Channels Contribute to Divergent Intrinsic Membrane Properties of Supragranular Pyramidal Neurons in Human versus Mouse Cerebral Cortex

Neuron ◽  
2018 ◽  
Vol 100 (5) ◽  
pp. 1194-1208.e5 ◽  
Author(s):  
Brian E. Kalmbach ◽  
Anatoly Buchin ◽  
Brian Long ◽  
Jennie Close ◽  
Anirban Nandi ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Pyramidal Neurons ◽  
Membrane Properties ◽  
Mouse Cerebral Cortex ◽  
H Channels ◽  
Intrinsic Membrane Properties

scholarly journals h-channels contribute to divergent electrophysiological properties of supragranular pyramidal neurons in human versus mouse cerebral cortex

2018 ◽  
Author(s):  
Brian E Kalmbach ◽  
Anatoly Buchin ◽  
Jeremy A Miller ◽  
Trygve E Bakken ◽  
Rebecca D Hodge ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Temporal Cortex ◽  
Membrane Properties ◽  
Temporal Association ◽  
Biophysical Modeling ◽  
Electrophysiological Properties ◽  
Channel Expression ◽  
Subunit Expression ◽  
Gene Expression Studies ◽  
H Channels

SummaryGene expression studies suggest that differential ion channel expression contributes to differences in rodent versus human neuronal physiology. We tested whether h-channels more prominently contribute to the physiological properties of human compared to mouse supragranular pyramidal neurons. Single cell/nucleus RNA sequencing revealed ubiquitous HCN1-subunit expression in excitatory neurons in human, but not mouse supragranular layers. Using patch-clamp recordings, we found stronger h-channel-related membrane properties in supragranular pyramidal neurons in human temporal cortex, compared to mouse supragranular pyramidal neurons in temporal association area. The magnitude of these differences depended upon cortical depth and was largest in pyramidal neurons in deep L3. Additionally, pharmacologically blocking h-channels produced a larger change in membrane properties in human compared to mouse neurons. Finally, using biophysical modeling, we provided evidence that h-channels promote the transfer of theta frequencies from dendrite-to-soma in human L3 pyramidal neurons. Thus, h-channels contribute to between-species differences in a fundamental neuronal property.

scholarly journals BMP signaling alters aquaporin-4 expression in the mouse cerebral cortex

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kazuya Morita ◽  
Naoyuki Matsumoto ◽  
Kengo Saito ◽  
Toshihide Hamabe-Horiike ◽  
Keishi Mizuguchi ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Molecular Mechanisms ◽  
Water Movement ◽  
Water Channel ◽  
Bmp Signaling ◽  
Aquaporin 4 ◽  
Mammalian Brain ◽  
Physiological Conditions ◽  
Pathological Conditions ◽  
Mouse Cerebral Cortex

AbstractAquaporin-4 (AQP4) is a predominant water channel expressed in astrocytes in the mammalian brain. AQP4 is crucial for the regulation of homeostatic water movement across the blood–brain barrier (BBB). Although the molecular mechanisms regulating AQP4 levels in the cerebral cortex under pathological conditions have been intensively investigated, those under normal physiological conditions are not fully understood. Here we demonstrate that AQP4 is selectively expressed in astrocytes in the mouse cerebral cortex during development. BMP signaling was preferentially activated in AQP4-positive astrocytes. Furthermore, activation of BMP signaling by in utero electroporation markedly increased AQP4 levels in the cerebral cortex, and inhibition of BMP signaling strongly suppressed them. These results indicate that BMP signaling alters AQP4 levels in the mouse cerebral cortex during development.

scholarly journals Modeling human‐specific interlaminar astrocytes in the mouse cerebral cortex

2020 ◽  
Vol 529 (4) ◽  
pp. 802-810
Author(s):  
Ragunathan Padmashri ◽  
Baiyan Ren ◽  
Braden Oldham ◽  
Yoosun Jung ◽  
Ryan Gough ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Mouse Cerebral Cortex ◽  
Human Specific

scholarly journals Macromolecule biosynthesis: a key function of sleep

2007 ◽  
Vol 31 (3) ◽  
pp. 441-457 ◽  
Author(s):  
Miroslaw Mackiewicz ◽  
Keith R. Shockley ◽  
Micah A. Romer ◽  
Raymond J. Galante ◽  
John E. Zimmerman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Sleep Deprivation ◽  
Expression Patterns ◽  
State Level ◽  
Altered Expression ◽  
Mouse Cerebral Cortex ◽  
Genes Encoding ◽  
Function Of Sleep ◽  
Cellular Components

The function(s) of sleep remains a major unanswered question in biology. We assessed changes in gene expression in the mouse cerebral cortex and hypothalamus following different durations of sleep and periods of sleep deprivation. There were significant differences in gene expression between behavioral states; we identified 3,988 genes in the cerebral cortex and 823 genes in the hypothalamus with altered expression patterns between sleep and sleep deprivation. Changes in the steady-state level of transcripts for various genes are remarkably common during sleep, as 2,090 genes in the cerebral cortex and 409 genes in the hypothalamus were defined as sleep specific and changed (increased or decreased) their expression during sleep. The largest categories of overrepresented genes increasing expression with sleep were those involved in biosynthesis and transport. In both the cerebral cortex and hypothalamus, during sleep there was upregulation of multiple genes encoding various enzymes involved in cholesterol synthesis, as well as proteins for lipid transport. There was also upregulation during sleep of genes involved in synthesis of proteins, heme, and maintenance of vesicle pools, as well as antioxidant enzymes and genes encoding proteins of energy-regulating pathways. We postulate that during sleep there is a rebuilding of multiple key cellular components in preparation for subsequent wakefulness.

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