Alterations in τ Immunostaining in the Rat Hippocampus following Transient Cerebral Ischemia

1994 ◽  
Vol 14 (4) ◽  
pp. 554-564 ◽  
Author(s):  
James W. Geddes ◽  
Claudia Schwab ◽  
Susan Craddock ◽  
Janice L. Wilson ◽  
L. Creed Pettigrew
Keyword(s):  
Neuronal Damage ◽  
Hippocampal Formation ◽  
Molecular Layer ◽  
Neuronal Cell ◽  
Direct Result ◽  
Ischemic Insult ◽  
Vessel Occlusion ◽  
Neuronal Populations ◽  
Neuronal Cell Bodies ◽  
Hilar Neurons

Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. τ, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, τ, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. τ accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal τ immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased τ immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered τ immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of τ, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of τ is an early, sensitive, and selective marker of ischemic insult.

scholarly journals Lipid Peroxidation in Chronic Cerebral HypoperfusionInduced Neurodegeneration in Rats

2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Anil Kumar S ◽  
Saif SA ◽  
Oothuman P ◽  
Mustafa MIA
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipid Peroxidation ◽  
Neurodegenerative Disorders ◽  
Neuronal Damage ◽  
Neuronal Cell ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Vessel Occlusion

Introduction: Reduced cerebral blood fl ow is associated with neurodegenerative disorders and dementia, in particular. Experimental evidence has demonstrated the initiating role of chronic cerebral hypoperfusion in neuronal damage to the hippocampus, the cerebral cortex, the white matter areas and the visual system. Permanent, bilateral occlusion of the common carotid arteries of rats (two vessel occlusion - 2VO) has been introduced for the reproduction of chronic cerebral hypoperfusion as it occurs in Alzheimer’s disease and human aging. Increased generation of free radicals through lipid peroxidation can damage neuronal cell membrane. Markers of lipid peroxidation have been found to be elevated in brain tissues and body fl uids in neurodegenerative diseases, including Alzheimer’s disease, Parkinson disease and amyotrophic lateral sclerosis. Materials and Methods: Malondialdehyde (MDA), final product of lipid peroxidation, was estimated by thiobarbituric acid-reactive substances (TBARS) assay kit at eight weeks after induction of 2VO in the rats and control group. Results: Our study revealed a highly signifi cant (p<0.001) increase in the mean MDA concentration (12.296 ± 1.113 μM) in 2VO rats as compared to the control group (5.286 ± 0.363 μM) rats. Conclusion: Therapeutic strategies to modulate lipid peroxidation early throughout the course of the disease may be promising in slowing or possibly preventing neurodegenerative disorders.

Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model

2009 ◽  
Author(s):  
Gija Lee ◽  
Seokkeun Choi ◽  
Sungwook Kang ◽  
Samjin Choi ◽  
Jeonghoon Park ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Glutamate Release ◽  
Short Interval ◽  
Neuronal Cell ◽  
Release Time ◽  
Protective Mechanism ◽  
Time Interval ◽  
Extracellular Glutamate ◽  
Vessel Occlusion ◽  
Doppler Flowmetry

During the operation, surgeons in neurosurgical area usually performed the multiple temporary occlusions of parental artery which may induce the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this experiment, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model during repeated within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. During ischemia, the peak level of glutamate release was gradually decreased as 112.38±26.21 μM in first period, 82.63±18.50 μM in second period, and 48.58±11.89 μM in third period. The time interval between the ischemia induction and the beginning of glutamate release was increased as 106.7 ± 10.89 (sec) at first attack, 139.11 ± 3.87 (sec) in second attack, 169.00 ± 14.56 (sec) in third ischemic period. From the results of real-time monitoring about glutamate release in 11-VO model during repetitive ischemic episode, it was demonstrated that repetitive ischemia induced less glutamate release from neuronal cell than single ischemia due to endogeneous protective mechanism which delayed glutamate release time in later ischemic injury.

scholarly journals Immunocytochemical Study of an Early Microglial Activation in Ischemia

1992 ◽  
Vol 12 (2) ◽  
pp. 257-269 ◽  
Author(s):  
Jochen Gehrmann ◽  
Petra Bonnekoh ◽  
Takahito Miyazawa ◽  
Konstantin-Alexander Hossmann ◽  
Georg W. Kreutzberg
Keyword(s):  
Monoclonal Antibodies ◽  
Distribution Pattern ◽  
Rat Brain ◽  
Mhc Class Ii ◽  
Neuronal Damage ◽  
Dorsal Hippocampus ◽  
Neuronal Cell ◽  
Microglial Cells ◽  
Vessel Occlusion ◽  
Temporal And Spatial Distribution

Transient arrest of the cerebral blood circulation results in neuronal cell death in selectively vulnerable regions of the rat brain. To elucidate further the involvement of glial cells in this pathology, we have studied the temporal and spatial distribution pattern of activated microglial cells in several regions of the ischemic rat brain. Transient global ischemia was produced in rats by 30 min of a four-vessel occlusion. Survival times were 1, 3, and 7 days after the ischemic injury. The microglial reaction was studied immunocytochemically using several monoclonal antibodies, e.g., against CR3 complement receptor and major histocompatibility complex (MHC) antigens. Two recently produced monoclonal antibodies against rat microglial cells, designated MUC 101 and 102, were also used to identify microglial cells. Following ischemia, the microglial reaction was correlated with the development of neuronal damage. The earliest presence of activated microglial cells was observed in the dorsolateral striatum, the CA1 area, and the dentate hilus of the dorsal hippocampus. However, the microglial reaction was not confined to areas showing selective neuronal damage, but also occurred in regions that are rather resistant to ischemia, such as the CA3 area. Particularly in the frontoparietal cortex, the appearance of MHC class II–positive microglial cells provided an early indication of the subsequent distribution pattern of neuronal damage. The microglial reaction would thus seem to be an early, sensitive, and reliable marker for the occurrence of neuronal damage in ischemia.

scholarly journals Direct Evidence for Acute and Massive Norepinephrine Release in the Hippocampus during Transient Ischemia

1989 ◽  
Vol 9 (6) ◽  
pp. 892-896 ◽  
Author(s):  
Mordecai Y.-T. Globus ◽  
Raul Busto ◽  
W. Dalton Dietrich ◽  
Elena Martinez ◽  
Isabel Valdés ◽  
...  
Keyword(s):  
Direct Evidence ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Fold Increase ◽  
Norepinephrine Release ◽  
Transient Ischemia ◽  
Vessel Occlusion ◽  
Extracellular Release ◽  
Induced Changes

Recent studies suggest the norepinephrine (NE) may play a regulatory role in neuronal cell death in the hippocampus after transient ischemia. However, ischemia-induced changes in extracellular NE release have not been demonstrated. In the present study, we utilized the microdialysis technique to measure extracellular NE levels in the hippocampus before, during, and after 20 min of global ischemia induced by two-vessel occlusion combined with systemic hypotension in the rat. Stable basal concentrations of extracellular NE were detected in three consecutive samples collected prior to ischemia (1.86 ± 1.21 pmol/ml of perfusate mean ± SEM). During ischemia, NE levels increased to 30.1 ± 5.5 pmol/ml, representing an 18-fold increase. The levels gradually returned to baseline by 40 min of reperfusion. These results are the first to demonstrate that acute and massive extracellular release of NE occurs in the hippocampus during ischemia and early recirculation. These results support the hypothesis that the activation of the noradrenergic system may play a significant role in modulating the development of ischemic neuronal damage.

scholarly journals CYTOCHEMICAL LOCALIZATION OF BRAIN NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE (OXIDIZED)-DEPENDENT DEHYDROGENASES QUALITATIVE AND QUANTITATIVE DISTRIBUTIONS

1974 ◽  
Vol 22 (1) ◽  
pp. 7-19 ◽  
Author(s):  
K. L. SIMS ◽  
F. C. KAUFFMAN ◽  
E. C. JOHNSON ◽  
V. M. PICKEL
Keyword(s):  
Nervous System ◽  
Nicotinamide Adenine Dinucleotide ◽  
Molecular Layer ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Neuronal Cell ◽  
Nicotinamide Adenine ◽  
Experimental Conditions ◽  
Cytochemical Localization ◽  
Neuronal Cell Bodies ◽  
Neuronal Processes

This study compares the histochemical and microchemical localizations of nicotinamide adenine dinucleotide phosphate (reduced) and nicotinamide adenine dinucleotide (reduced) diaphorases and four nicotinamide adenine dinucleotide phosphate (oxidized)-dependent enzymes (glucose 6-phosphate, 6-phosphogluconate, malate and isocitrate dehydrogenases) in areas of rat metencephalon and spinal cord. For the four nicotinamide adenine dinucleotide phosphate (NADP) enzymes, the pattern of localization following use of a modified tetrazolium procedure was compared with quantitative data obtained by microdissection from the same areas in adjacent sections. Optimal experimental conditions for reaction pH, temperature, substrate, cofactor and divalent cation concentrations were used for both the quantitative analysis following microdissection and the histochemical tetrazolium procedure. Consecutive sections were also examined for isocitrate dehydrogenase (nicotinamide adenine dinucleotide (oxidized)) and nicotinamide adenine dinucleotide (reduced) diaphorase activities in addition to seriatim thionine reference sections. Our results indicate that, within the central nervous system, certain characteristic qualitative differences exist in the distribution of the nicotinamide adenine dinucleotide phosphate (oxidized)- and nicotinamide adenine dinucleotide (oxidized)-dependent dehydrogenase enzymes. Nicotinamide adenine, dinucleotide enzymes are visualized predominantly in neuronal cell bodies or neuropil consisting primarily of neuronal processes; in adjacent sections, NADP enzyme activities are visualized almost exclusively in glial elements with two important exceptions. The first is the cerebellar molecular layer where the results from both micro- and histochemical techniques indicate high levels of the NADP enzymes relative to other dehydrogenases and high activity relative to the levels of these NADP enzymes in other nervous system areas. The second exception occurs in those neuronal groups known to contain high levels of catecholamines; these data are the subject of a companion report.

scholarly journals Experimental Pneumococcal Meningitis: Impaired Clearance of Bacteria from the Blood Due to Increased Apoptosis in the Spleen in Bcl-2-Deficient Mice

2004 ◽  
Vol 72 (6) ◽  
pp. 3113-3119 ◽  
Author(s):  
Andreas Wellmer ◽  
Matthias von Mering ◽  
Annette Spreer ◽  
Ricarda Diem ◽  
Helmut Eiffert ◽  
...  
Keyword(s):  
Pneumococcal Meningitis ◽  
Neuronal Damage ◽  
Hippocampal Formation ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Clinical Score ◽  
Tight Rope ◽  
Induced Apoptosis ◽  
The Brain ◽  
Deficient Mice

ABSTRACT Necrotic and apoptotic neuronal cell death can be found in pneumococcal meningitis. We investigated the role of Bcl-2 as an antiapoptotic gene product in pneumococcal meningitis using Bcl-2 knockout (Bcl-2−/−) mice. By using a model of pneumococcal meningitis induced by intracerebral infection, Bcl-2-deficient mice and control littermates were assessed by clinical score and a tight rope test at 0, 12, 24, 32, and 36 h after infection. Then mice were sacrificed, the bacterial titers in blood, spleen, and cerebellar homogenates were determined, and the brain and spleen were evaluated histologically. The Bcl-2-deficient mice developed more severe clinical illness, and there were significant differences in the clinical score at 24, 32, and 36 h and in the tight rope test at 12 and 32 h. The bacterial titers in the blood were greater in Bcl-2-deficient mice than in the controls (7.46 ± 1.93 log CFU/ml versus 5.16 ± 0.96 log CFU/ml [mean ± standard deviation]; P < 0.01). Neuronal damage was most prominent in the hippocampal formation, but there were no significant differences between groups. In situ tailing revealed only a few apoptotic neurons in the brain. In the spleen, however, there were significantly more apoptotic leukocytes in Bcl-2-deficient mice than in controls (5,148 ± 3,406 leukocytes/mm2 versus 1,070 ± 395 leukocytes/mm2; P < 0.005). Bcl-2 appears to counteract sepsis-induced apoptosis of splenic lymphocytes, thereby enhancing clearance of bacteria from the blood.

scholarly journals In Vivo Calcium Imaging of Circuit Activity in Cerebellar Cortex

2005 ◽  
Vol 94 (2) ◽  
pp. 1636-1644 ◽  
Author(s):  
Megan R. Sullivan ◽  
Axel Nimmerjahn ◽  
Dmitry V. Sarkisov ◽  
Fritjof Helmchen ◽  
Samuel S.-H. Wang
Keyword(s):  
Cerebellar Cortex ◽  
Calcium Imaging ◽  
Time Course ◽  
Molecular Layer ◽  
Neuronal Cell ◽  
Calcium Transients ◽  
Two Photon ◽  
Neuronal Cell Bodies

In vivo two-photon calcium imaging provides the opportunity to monitor activity in multiple components of neural circuitry at once. Here we report the use of bulk-loading of fluorescent calcium indicators to record from axons, dendrites, and neuronal cell bodies in cerebellar cortex in vivo. In cerebellar folium crus IIa of anesthetized rats, we imaged the labeled molecular layer and identified all major cellular structures: Purkinje cells, interneurons, parallel fibers, and Bergmann glia. Using extracellular stimuli we evoked calcium transients corresponding to parallel fiber beam activity. This beam activity triggered prolonged calcium transients in interneurons, consistent with in vitro evidence for synaptic activation of N-methyl-d-aspartate receptors via glutamate spillover. We also observed spontaneous calcium transients in Purkinje cell dendrites that were identified as climbing-fiber-evoked calcium spikes by their size, time course, and sensitivity to AMPA receptor antagonist. Two-photon calcium imaging of bulk-loaded cerebellar cortex is thus well suited to optically monitor synaptic processing in the intact cerebellum.

The Red Neuronal Pigment in the Nervous System of the Mussel, Mytilus Edulis: Localization and Its Effect on Lateral Ciliary Activity with Spectral and Analytical Changes

1981 ◽  
Vol 39 ◽  
pp. 494-495
Author(s):  
Anthony A. Paparo ◽  
Judith A. Murphy
Keyword(s):  
Nervous System ◽  
Mytilus Edulis ◽  
Neuronal Cell ◽  
Ciliary Activity ◽  
Neuronal Cell Bodies ◽  
The Central Nervous System ◽  
Intracellular Organelles ◽  
The Common ◽  
The Individual ◽  
Cryostat Sections

The purpose of this study was to localize the red neuronal pigment in Mytilus edulis and examine its role in the control of lateral ciliary activity in the gill. The visceral ganglia (Vg) in the central nervous system show an over al red pigmentation. Most red pigments examined in squash preps and cryostat sec tions were localized in the neuronal cell bodies and proximal axon regions. Unstained cryostat sections showed highly localized patches of this pigment scattered throughout the cells in the form of dense granular masses about 5-7 um in diameter, with the individual granules ranging from 0.6-1.3 um in diame ter. Tissue stained with Gomori's method for Fe showed bright blue granular masses of about the same size and structure as previously seen in unstained cryostat sections.Thick section microanalysis (Fig.l) confirmed both the localization and presence of Fe in the nerve cell. These nerve cells of the Vg share with other pigmented photosensitive cells the common cytostructural feature of localization of absorbing molecules in intracellular organelles where they are tightly ordered in fine substructures.

Immunohistochemical Study of Intralaryngeal Ganglia in the Cat

1992 ◽  
Vol 106 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Kuniyoshi Tsuda ◽  
Takemoto Shin ◽  
Sadahiko Masuko
Keyword(s):  
Neuronal Cell ◽  
Superior Laryngeal Nerve ◽  
Exocrine Secretion ◽  
Nerve Fibers ◽  
Neuronal Cell Bodies ◽  
Calcitonin Gene ◽  
Dense Distribution ◽  
Recurrent Laryngeal Nerves ◽  
Immunohistochemical Techniques ◽  
Almost All

To study the mechanism of autonomic regulation in the larynx, intralaryngeal local ganglia of the cat were investigated using immunohistochemical techniques. Small intralaryngeal ganglia were found in the peripheral portions of internal branches of the superior laryngeal nerve. Ninety-one percent of the ganglionic neurons were immunoreactive (IR) to vasoactive intestinal polypeptide (VIP), and 10% of the VIP-IR cells were also immunoreactive to enkephalin (ENK) and/or substance P (SP). The immunoreactivity of neuronal cell bodies remained unchanged even after denervation of the bilateral superior and recurrent laryngeal nerves. A dense distribution of calcitonin gene-related peptide (CGRP)-IR nerve fibers was found around almost all neuronal cells in the intralaryngeal. ganglia. A few VIP-IR, ENK-IR, and SP-IR nerve fibers were also observed. Only the CGRP-IR fibers disappeared after the denervation experiments. in the laryngeal glands and mucosal arterioles, VIP-IR nerve terminals were found that were also immunoreactive to ENK and/or SP. However, these Immunoreactive nerve endings in the glands and arterioles remained after the denervation experiments. The results of our study indicate that laryngeal exocrine secretion and blood flow are regulated by postganglionic autonomic parasympathetic fibers from intralaryngeal ganglia that contain VIP alone or VIP with ENK and/or SP, and that these ganglionic neurons may be innervated by CGRP-IR extrinsic nerve fibers.

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