Enhancement of intrinsic neuronal excitability‐mediated by a reduction in hyperpolarization‐activated cation current (I h ) in hippocampal CA1 neurons in a rat model of traumatic brain injury

Hippocampus ◽  
2020 ◽  
Author(s):  
Seyed Asaad Karimi ◽  
Narges Hosseinmardi ◽  
Mohammad Sayyah ◽  
Razieh Hajisoltani ◽  
Mahyar Janahmadi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Neuronal Excitability ◽  
Ca1 Neurons ◽  
Cation Current ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

scholarly journals Mild Traumatic Brain Injury Decreases Spatial Information Content and Reduces Place Field Stability of Hippocampal CA1 Neurons

2020 ◽  
Vol 37 (2) ◽  
pp. 227-235 ◽  
Author(s):  
John I. Broussard ◽  
John B. Redell ◽  
Jing Zhao ◽  
Mark E. Maynard ◽  
Nobuhide Kobori ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Information Content ◽  
Mild Traumatic Brain Injury ◽  
Spatial Information ◽  
Place Field ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

Sodium Hydrosulfide Post-conditioning Protects Hippocampal CA1 Neurons from Neuronal Cell Injury in the Rat Model of Transient Global Cerebral Ischemia Through Activation of Extracellular-regulated Kinases Signaling

2019 ◽  
Vol 16 (2) ◽  
pp. 156-165
Author(s):  
ChengPing Bai ◽  
ChenLiang Zhao
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Neuronal Cell ◽  
Global Cerebral Ischemia ◽  
Sodium Hydrosulfide ◽  
Ca1 Neurons ◽  
Transient Global Cerebral Ischemia ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Pre Treatment

Introduction: The effect of hydrogen sulfide (H2S) on global cerebral ischemia remains partially understood. This study aimed to investigate the neuroprotective effect of sodium hydrosulfide (NaHS, a donor of H2S) post-conditioning and its underlying mechanism in a transient global cerebral ischemia (tGCI) model. Materials & Methods: The tGCI rat model was established by the four-vessel occlusion method. Wistar rats were randomly assigned into 6 groups: sham, tGCI, tGCI +NaHS, tGCI+vehicle, tGCI+U0126 and tGCI+U0126+NaHS groups. Neurons survival was assessed by Nissl staining and NeuN immunostaining. Levels of extracellular extracellular-regulated kinases (ERK)1/2 and p-ERK1/2 were determined by western blot and immunohistochemistry (IHC). Intraperitoneal injection of NaHS (24 μmol/kg) at 24 h post-tGCI attenuated tGCI-induced decrease of the survival and NeuN-positive neurons in the hippocampal CA1 subregion. Results: Compared to the sham group, tGCI significantly up-regulated p-ERK1/2 protein at 26 and 48 h post-tGCI. NaHS post-conditioning further enhanced the phosphorylation of ERK1/2 at 26, 48 and 168 h post-tGCI. Nevertheless, U0126 (an inhibitor of MEK1/2) pre-treatment reduced the p-ERK1/2 level in both the tGCI+ U0126 group and the tGCI+ U0126+ NaHS group. IHC staining revealed that p-ERK1/2-positive cell could be observed in several hippocampal subregions of the rats receiving NaHS post-conditioning. Immunofluorescence staining showed that some neurons were double-stained with p-ERK1/2 and NeuN. Furthermore, U0126 pre-treatment significantly attenuated the protective effect of NaHS post-conditioning on the neurons survival and NeuNpositive neurons in CA1 subregion. Conclusion: These results suggested that NaHS post-conditioning can protect hippocampal CA1 neurons from tGCI-induced injury, at least partially, through activation of ERK1/2 signaling.

scholarly journals TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 459 ◽  
Author(s):  
Frauke Kepura ◽  
Eva Braun ◽  
Alexander Dietrich ◽  
Tim D. Plant
Keyword(s):  
Metabotropic Glutamate Receptor ◽  
Dendritic Morphology ◽  
Current Increase ◽  
Ca1 Neurons ◽  
Cation Current ◽  
Hippocampal Ca1 Neurons ◽  
Group I ◽  
Hippocampal Ca1 ◽  
Voltage Dependent ◽  
Nonselective Cation Current

The cation channel subunit TRPC1 is strongly expressed in central neurons including neurons in the CA1 region of the hippocampus where it forms complexes with TRPC4 and TRPC5. To investigate the functional role of TRPC1 in these neurons and in channel function, we compared current responses to group I metabotropic glutamate receptor (mGluR I) activation and looked for major differences in dendritic morphology in neurons from TRPC1+/+ and TRPC1−/− mice. mGluR I stimulation resulted in the activation of a voltage-dependent nonselective cation current in both genotypes. Deletion of TRPC1 resulted in a modification of the shape of the current-voltage relationship, leading to an inward current increase. In current clamp recordings, the percentage of neurons that responded to depolarization in the presence of an mGluR I agonist with a plateau potential was increased in TRPC1−/− mice. There was also a small increase in the minor population of CA1 neurons that have more than one apical dendrite in TRPC1−/− mice. We conclude that TRPC1 has an inhibitory effect on receptor-operated nonselective cation channels in hippocampal CA1 neurons probably as a result of heterotetramer formation with other TRPC isoforms, and that TRPC1 deletion has only minor effects on dendritic morphology.

Ischemic preconditioning protects the hippocampal CA1 neurons by inhibiting synaptic activity in rat

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S300-S300
Author(s):  
Thomas J Sick ◽  
Ami P Raval ◽  
Isabel Saul ◽  
Kunjan R Dave ◽  
Raul Busto ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Synaptic Activity ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

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