scholarly journals Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats

2021 ◽  
Vol 22 (11) ◽  
pp. 5883
Author(s):  
Ilia G. Komoltsev ◽  
Stepan O. Frankevich ◽  
Natalia I. Shirobokova ◽  
Aleksandra A. Volkova ◽  
Mikhail V. Onufriev ◽  
...  
Keyword(s):  
Neuronal Cell ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Hippocampal Damage ◽  
Sham Operation ◽  
Nissl Staining ◽  
Potential Association ◽  
Neuronal Cell Loss ◽  
Male Wistar Rats ◽  
Posttraumatic Seizures

Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), we assessed potential association of immediate posttraumatic seizures and changes in corticosterone (CS) levels with neuroinflammation and neuronal cell loss in the hippocampus. Indices of distant hippocampal damage (neurodegeneration and neuroinflammation) were assessed using histological analysis (Nissl staining, Iba-1 immunohistochemical staining) and ELISA (IL-1β and CS) 1, 3, 7 and 14 days after TBI or sham operation in male Wistar rats (n = 146). IL-1β was elevated only in the ipsilateral hippocampus on day 1 after trauma. CS peak was detected on day 3 in blood, the ipsilateral and contralateral hippocampus. Neuronal cell loss in the hippocampus was demonstrated bilaterally; in the ipsilateral hippocampus it started earlier than in the contralateral. Microglial activation was evident in the hippocampus bilaterally on day 7 after TBI. The duration of immediate seizures correlated with CS elevation, levels of IL-1β and neuronal loss in the hippocampus. The data suggest potential association of immediate post-traumatic seizures with CS-dependent neuroinflammation-mediated distant hippocampal damage.

scholarly journals The Neuroprotective Effect of Zingiber cassumunar Roxb. Extract on LPS-Induced Neuronal Cell Loss and Astroglial Activation within the Hippocampus

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ratchaniporn Kongsui ◽  
Napatr Sriraksa ◽  
Sitthisak Thongrong
Keyword(s):  
Proinflammatory Cytokine ◽  
Wistar Rats ◽  
Single Injection ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Cell Loss ◽  
Neuronal Cell Loss ◽  
Male Wistar Rats ◽  
Astroglial Activation ◽  
Zingiber Cassumunar

The systemic administration of lipopolysaccharide (LPS) has been recognized to induce neuroinflammation which plays a significant role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In this study, we aimed to determine the protective effect of Zingiber cassumunar (Z. cassumunar) or Phlai (in Thai) against LPS-induced neuronal cell loss and the upregulation of glial fibrillary acidic protein (GFAP) of astrocytes in the hippocampus. Adult male Wistar rats were orally administered with Z. cassumunar extract at various doses (50, 100, and 200 mg/kg body weight) for 14 days before a single injection of LPS (250 μg/kg/i.p.). The results indicated that LPS-treated animals exhibited neuronal cell loss and the activation of astrocytes and also increased proinflammatory cytokine interleukin- (IL-) 1β in the hippocampus. Pretreatment with Z. cassumunar markedly reduced neuronal cell loss in the hippocampus. In addition, Z. cassumunar extract at a dose of 200 mg/kg BW significantly suppressed the inflammatory response by reducing the expression of GFAP and IL-1ß in the hippocampus. Therefore, the results suggested that Z. cassumunar extract might be valuable as a neuroprotective agent in neuroinflammation-induced brain damage. However, further investigations are essential to validate the possible active ingredients and mechanisms of its neuroprotective effect.

scholarly journals Increased Densities of Binding Sites for the “Peripheral-Type” Benzodiazepine Receptor Ligand [3H]PK11195 in Vulnerable Regions of the Rat Brain in Thiamine Deficiency Encephalopathy

1994 ◽  
Vol 14 (1) ◽  
pp. 100-105 ◽  
Author(s):  
Dorothy K. Leong ◽  
Oanh Le ◽  
Luis Oliva ◽  
Roger F. Butterworth
Keyword(s):  
Binding Sites ◽  
Thiamine Deficiency ◽  
Neuronal Cell ◽  
Neuronal Loss ◽  
Benzodiazepine Receptor ◽  
Cell Loss ◽  
Brain Regions ◽  
Inferior Olivary Nucleus ◽  
Neuronal Cell Loss ◽  
Peripheral Type

Quantitative receptor autoradiography was used to evaluate the density of high-affinity binding sites for the “peripheral-type” benzodiazepine receptor (PTBR) ligand [3H]PK11195 in brain regions of the rat at different stages of pyrithiamine-induced thiamine deficiency encephalopathy, an experimental model of the Wernicke-Korsakoff syndrome (WKS). Assessment of the density of [3H]PK11195 binding sites in thiamine-deficient animals showing no neurologic signs of thiamine deficiency encephalopathy, and revealed no significant alterations compared with pair-fed control animals in any brain region studied. Densities of [3H]PK11195 binding sites were, however, significantly increased in brain regions of the rat at the symptomatic stage, where increased densities were seen in the inferior colliculus (233% increase, p < 0.001), inferior olivary nucleus (154% increase, p < 0.001) and thalamus (up to 107% increase, p < 0.001). Histologic studies of these same brain regions revealed evidence of neuronal cell loss and concomitant gliosis. Densities of [3H]PK11195 binding sites in nonvulnerable brain regions that showed no histologic evidence of neuronal loss, such as the cerebral cortex, hippocampus, and caudate-putamen, were not significantly different from those in control animals. Increased densities of binding sites for the PTBR ligand probably reflect glial proliferation and are consistent with an excitotoxic mechanism in the pathogenesis of neuronal cell loss in thiamine deficiency encephalopathy. Positron emission tomography (PET) using [11C]PK11195 could offer a potentially useful diagnostic tool in WKS in humans.

Neuronal Cell Loss in the CA3 Subfield of the Hippocampus Following Cortical Contusion Utilizing the Optical Disector Method for Cell Counting

1997 ◽  
Vol 14 (6) ◽  
pp. 385-398 ◽  
Author(s):  
STANLEY A. BALDWIN ◽  
TONYA GIBSON ◽  
C. TODD CALLIHAN ◽  
PATRICK G. SULLIVAN ◽  
ERICK PALMER ◽  
...  
Keyword(s):  
Neuronal Cell ◽  
Cell Loss ◽  
Cell Counting ◽  
Optical Disector ◽  
Neuronal Cell Loss ◽  
Cortical Contusion

scholarly journals Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

2020 ◽  
Vol 21 (17) ◽  
pp. 6246
Author(s):  
Tatiana Anan’ina ◽  
Alena Kisel ◽  
Marina Kudabaeva ◽  
Galina Chernysheva ◽  
Vera Smolyakova ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Brain Slices ◽  
Global Cerebral Ischemia ◽  
Hippocampal Damage ◽  
Sham Operation ◽  
Ischemic Brain ◽  
Stratum Pyramidale ◽  
Male Wistar Rats ◽  
First Time ◽  
The Brain

(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus.

scholarly journals Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results

2005 ◽  
Vol 63 (4) ◽  
pp. 972-976 ◽  
Author(s):  
Pauline Rangel ◽  
Roberta Monterazzo Cysneiros ◽  
Ricardo Mario Arida ◽  
Marly de Albuquerque ◽  
Diego Basile Colugnati ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Seizure Activity ◽  
Hippocampal Formation ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Cell Number ◽  
Control Group ◽  
Cell Counts

OBJECTIVE: To further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced status epilepticus (SE) METHOD: Adult male Wistar rats were divided into four groups: (A) control rats, received neither pilocarpine nor lovastatin (n=5); (B) control rats, received just lovastatin (n=5); (C) rats that received just pilocarpine (n=5); (D) rats that received pilocarpine and lovastatin (n=5). After pilocarpine injection (350mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20mg/kg via an oesophagic probe immediately and 24 hours after SE induction. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl method. RESULTS: The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1= 26.8 ± 13.67; CA3= 38.1 ± 7.2; hilus= 43.8 ± 3.95) when compared with control group animals (Group A: CA1= 53.2 ± 9.63; CA3= 63.5 ± 13.35; hilus= 59.08 ± 10.24; Group B: CA1= 74.3 ± 8.16; CA3= 70.1 ± 3.83; hilus= 70.6 ± 5.10). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 ± 17.88) was statically significant increased when compared with animals that just presented SE. CONCLUSION: Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE.

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