Presynaptic K+ channels play a clucial role in ischemia-induced neuronal damage in rat hippocampal CA1 regions

2000 ◽  
Vol 38 ◽  
pp. S39
Author(s):  
K Kodama
Keyword(s):  
Neuronal Damage ◽  
K Channels ◽  
Hippocampal Ca1

scholarly journals Gynura procumbens Root Extract Ameliorates Ischemia-Induced Neuronal Damage in the Hippocampal CA1 Region by Reducing Neuroinflammation

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 181
Author(s):  
Woosuk Kim ◽  
Hyo Young Jung ◽  
Dae Young Yoo ◽  
Hyun Jung Kwon ◽  
Kyu Ri Hahn ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Biological Properties ◽  
Root Extract ◽  
Ischemic Damage ◽  
Neuroprotective Effects ◽  
Hippocampal Ca1 ◽  
Vehicle Treated Group

Gynura procumbens has been used in Southeast Asia for the treatment of hypertension, hyperglycemia, and skin problems induced by ultraviolet irradiation. Although considerable studies have reported the biological properties of Gynura procumbens root extract (GPE-R), there are no studies on the effects of GPE-R in brain damages, for example following brain ischemia. In the present study, we screened the neuroprotective effects of GPE-R against ischemic damage and neuroinflammation in the hippocampus based on behavioral, morphological, and biological approaches. Gerbils received oral administration of GPE-R (30 and 300 mg/kg) every day for three weeks and 2 h after the last administration, ischemic surgery was done by occlusion of both common carotid arteries for 5 min. Administration of 300 mg/kg GPE-R significantly reduced ischemia-induced locomotor hyperactivity 1 day after ischemia. Significantly more NeuN-positive neurons were observed in the hippocampal CA1 regions of 300 mg/kg GPE-R-treated animals compared to those in the vehicle-treated group 4 days after ischemia. Administration of GPE-R significantly reduced levels of pro-inflammatory cytokines such as interleukin-1β, -6, and tumor necrosis factor-α 6 h after ischemia/reperfusion. In addition, activated microglia were significantly decreased in the 300 mg/kg GPE-R-treated group four days after ischemia/reperfusion compared to the vehicle-treated group. These results suggest that GPE-R may be one of the possible agents to protect neurons from ischemic damage by reducing inflammatory responses.

scholarly journals N-Acetylaspartate to Total Creatine Ratio in the Hippocampal CA1 Sector after Transient Cerebral Ischemia in Gerbils: Influence of Neuronal Elements, Reactive Gliosis, and Tissue Atrophy

2003 ◽  
Vol 23 (6) ◽  
pp. 700-708 ◽  
Author(s):  
Kuni Konaka ◽  
Hirokazu Ueda ◽  
Ji-Yao Li ◽  
Masayasu Matsumoto ◽  
Saburo Sakoda ◽  
...  
Keyword(s):  
High Performance ◽  
Neuronal Damage ◽  
Immunohistochemical Analysis ◽  
Reactive Astrogliosis ◽  
Hippocampal Ca1 ◽  
Total Creatine ◽  
Temporal Profiles ◽  
Hippocampal Ca1 Sector ◽  
Good Linear Correlation ◽  
Observation Period

The authors compared temporal profiles of Nacetylaspartate (NAA) and the NAA/total creatine ratio with neuronal and astrocytic densities and with tissue atrophy in the hippocampal CA1 sector of gerbils after 5-minute bilateral forebrain ischemia and subsequent reperfusion for up to 6 months. The CA1 sector was dissected from 20-μm lyophilized sections (n = 5) for NAA, phosphocreatine, and creatine assays using high-performance liquid chromatography. Adjacent 10-μm sections were used for immunohistochemical analysis to follow neuronal and astrocytic responses. The NAA concentration was significantly ( P<0.01) decreased after 7 days but leveled off thereafter. The NAA/total creatine (phosphocreatine + creatine) ratio was significantly decreased after 7 days and further decreased ( P<0.05) after 6 months. Extensive neuronal damage developed beyond 7 days, while reactive astrogliosis progressed throughout the observation period. There was a good linear correlation ( P<0.01) between astroglial density and the NAA/total creatine ratio beyond 7 days. The thickness of the CA1 sector was significantly reduced after 1 month and further reduced after 6 months. Although both NAA level and the NAA/total creatine ratio seemed to be indicators of neuronal damage, the latter could be influenced by reactive astrogliosis with progression of tissue atrophy.

scholarly journals Hypoxia with inflammation and reperfusion alters membrane resistance by dynamically regulating voltage-gated potassium channels in hippocampal CA1 neurons

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yoon-Sil Yang ◽  
Joon Ho Choi ◽  
Jong-Cheol Rah
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Input Resistance ◽  
Delayed Rectifier ◽  
Hcn Channels ◽  
Neural Function ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

AbstractHypoxia typically accompanies acute inflammatory responses in patients and animal models. However, a limited number of studies have examined the effect of hypoxia in combination with inflammation (Hypo-Inf) on neural function. We previously reported that neuronal excitability in hippocampal CA1 neurons decreased during hypoxia and greatly rebounded upon reoxygenation. We attributed this altered excitability mainly to the dynamic regulation of hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels and input resistance. However, the molecular mechanisms underlying input resistance changes by Hypo-Inf and reperfusion remained unclear. In the present study, we found that a change in the density of the delayed rectifier potassium current (IDR) can explain the input resistance variability. Furthermore, voltage-dependent inactivation of A-type potassium (IA) channels shifted in the depolarizing direction during Hypo-Inf and reverted to normal upon reperfusion without a significant alteration in the maximum current density. Our results indicate that changes in the input resistance, and consequently excitability, caused by Hypo-Inf and reperfusion are at least partially regulated by the availability and voltage dependence of KV channels. Moreover, these results suggest that selective KV channel modulators can be used as potential neuroprotective drugs to minimize hypoxia- and reperfusion-induced neuronal damage.

NCX3 knockout mice exhibit increased hippocampal CA1 and CA2 neuronal damage compared to wild-type mice following global cerebral ischemia

2008 ◽  
Vol 210 (1) ◽  
pp. 268-273 ◽  
Author(s):  
Graham J. Jeffs ◽  
Bruno P. Meloni ◽  
Sophie Sokolow ◽  
Andre Herchuelz ◽  
Stéphane Schurmans ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Knockout Mice ◽  
Neuronal Damage ◽  
Global Cerebral Ischemia ◽  
Wild Type ◽  
Hippocampal Ca1

scholarly journals Dexamethasone Aggravates Ischemia-Induced Neuronal Damage by Facilitating the Onset of Anoxic Depolarization and the Increase in the Intracellular Ca2+ Concentration in Gerbil Hippocampus

1998 ◽  
Vol 18 (3) ◽  
pp. 274-280 ◽  
Author(s):  
Naoto Adachi ◽  
Junfeng Chen ◽  
Keyue Liu ◽  
Shinzo Tsubota ◽  
Tatsuru Arai
Keyword(s):  
Direct Current ◽  
Neuronal Damage ◽  
Induced Membrane ◽  
Potential Shift ◽  
Hippocampal Ca1 ◽  
Intracellular Ca ◽  
Current Potential ◽  
Ischemic Neuronal Injury

The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 μg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 μg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

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