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.

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.

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 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 Thiamine Deficiency Induced Neurochemical, Neuroanatomical, and Neuropsychological Alterations: A Reappraisal

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Raffaele Nardone ◽  
Yvonne Höller ◽  
Monica Storti ◽  
Monica Christova ◽  
Frediano Tezzon ◽  
...  
Keyword(s):  
Thiamine Deficiency ◽  
Cortical Cell ◽  
Cell Loss ◽  
Brain Regions ◽  
Experimental Models ◽  
Neurological Sequela ◽  
Thalamic Nuclei ◽  
Chronic Alcoholic ◽  
Ethanol Abuse ◽  
And Function

Nutritional deficiency can cause, mainly in chronic alcoholic subjects, the Wernicke encephalopathy and its chronic neurological sequela, the Wernicke-Korsakoff syndrome (WKS). Long-term chronic ethanol abuse results in hippocampal and cortical cell loss. Thiamine deficiency also alters principally hippocampal- and frontal cortical-dependent neurochemistry; moreover in WKS patients, important pathological damage to the diencephalon can occur. In fact, the amnesic syndrome typical for WKS is mainly due to the damage in the diencephalic-hippocampal circuitry, including thalamic nuclei and mammillary bodies. The loss of cholinergic cells in the basal forebrain region results in decreased cholinergic input to the hippocampus and the cortex and reduced choline acetyltransferase and acetylcholinesterase activities and function, as well as in acetylcholine receptor downregulation within these brain regions. In this narrative review, we will focus on the neurochemical, neuroanatomical, and neuropsychological studies shedding light on the effects of thiamine deficiency in experimental models and in humans.

Sign in / Sign up

Export Citation Format

Share Document