scholarly journals Housing Complexity Alters GFAP-Immunoreactive Astrocyte Morphology in the Rat Dentate Gyrus

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Garrick Salois ◽  
Jeffrey S. Smith
Keyword(s):  
Dentate Gyrus ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Sensory Stimulation ◽  
Confocal Imaging ◽  
Branch Points ◽  
Substantial Evidence ◽  
Rodent Brain ◽  
Behavioral Abnormalities ◽  
Enriched Environments

Rats used in research are typically housed singly in cages with limited sensory stimulation. There is substantial evidence that housing rats in these conditions lead to numerous neuroanatomical and behavioral abnormalities. Alternatively, rats can be housed in an enriched environment in which rats are housed in groups and given room for exercise and exploration. Enriched environments result in considerable neuroplasticity in the rodent brain. In the dentate gyrus of the hippocampus, enriched environments evoke especially profound neural changes, including increases in the number of neurons and the number of dendritic spines. However, whether changes in astrocytes, a type of glia increasingly implicated in mediating neuroplasticity, are concurrent with these neural changes remains to be investigated. In order to assess morphological changes among astrocytes of the rat dentate gyrus, piSeeDB was used to optically clear 250 μm sections of tissue labeled using GFAP immunohistochemistry. Confocal imaging and image analysis were then used to measure astrocyte morphology. Astrocytes from animals housed in EE demonstrated a reduced distance between filament branch points. Furthermore, the most complex astrocytes were significantly more complex among animals housed in EE compared to standard environments.

scholarly journals Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation

2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Protein Kinase ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Protein Kinase D

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

scholarly journals Stress and Corticosteroids Aggravate Morphological Changes in the Dentate Gyrus after Early-Life Experimental Febrile Seizures in Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Jolien S. van Campen ◽  
Ellen V. S. Hessel ◽  
Kirsten Bohmbach ◽  
Giorgio Rizzi ◽  
Paul J. Lucassen ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Early Life ◽  
Morphological Changes ◽  
Febrile Seizures

Defective actin dynamics in dendritic spines: cause or consequence of age-induced cognitive decline?

2016 ◽  
Vol 397 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Till Georg Alexander Mack ◽  
Patricia Kreis ◽  
Britta Johanna Eickholt
Keyword(s):  
Dendritic Spines ◽  
Neuronal Excitability ◽  
Replicative Senescence ◽  
Morphological Changes ◽  
Actin Dynamics ◽  
Cellular Processes ◽  
Filament Dynamics ◽  
Neuronal Soma ◽  
Deteriorating Process ◽  
The Brain

Abstract Ageing is a complex deteriorating process that coincides with changes in metabolism, replicative senescence, increased resistance to apoptosis, as well as progressive mitochondria dysfunction that lead to an increase production and accumulation of reactive oxygen species (ROS). Although controversy on the paradigm of the oxidative damage theory of ageing exists, persuasive studies in Caenorhabditis elegans and yeast have demonstrated that manipulation of ROS can modify the process of ageing and influences the damage of proteins, lipids and DNA. In neurons, ageing impacts on the intrinsic neuronal excitability, it decreases the size of neuronal soma and induces the loss of dendrites and dendritic spines. The actin cytoskeleton is an abundant and broadly expressed system that plays critical functions in many cellular processes ranging from cell motility to controlling cell shape and polarity. It is thus hardly surprising that the expression and the function of actin in neurons is crucial for the morphological changes that occur in the brain throughout life. We propose that alterations in actin filament dynamics in dendritic spines may be one of the key events contributing to the initial phases of ageing in the brain.

Rapid morphological changes of dendritic spines induced by corticosteroids in rat hippocampus

2007 ◽  
Vol 58 ◽  
pp. S190
Author(s):  
Yoshimasa Komatsuzaki ◽  
Yasushi Hojo ◽  
Suguru Kawato
Keyword(s):  
Dendritic Spines ◽  
Morphological Changes ◽  
Rat Hippocampus

scholarly journals Design of an imaging probe to monitor real-time redistribution of L-type voltage gated calcium channels in astrocytic glutamate signalling

2020 ◽  
Author(s):  
Mitra Sadat Tabatabaee ◽  
Jeff Kerkovius ◽  
Frederic Menard
Keyword(s):  
Calcium Channels ◽  
Real Time ◽  
Morphological Changes ◽  
Fold Increase ◽  
Living Cells ◽  
Confocal Imaging ◽  
Excitatory Neurotransmitter ◽  
Imaging Probe ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

ABSTRACTPurposeIn the brain, astrocytes are non-excitable cells that undergo rapid morphological changes when stimulated by the excitatory neurotransmitter glutamate. We developed a chemical probe to monitor how glutamate affects the density and distribution of astrocytic L-type voltage-gated calcium channels (LTCC).ProceduresThe imaging probe FluoBar1 was created from a barbiturate ligand modified with a fluorescent coumarin moiety. The probe selectivity was examined with colocalization analyses of confocal fluorescence imaging in U118-MG and transfected COS-7 cells. Living cells treated with 50 nM FluoBar1 were imaged in real time to reveal changes in density and distribution of astrocytic LTCCs upon exposure to glutamate.ResultsFluoBar1 was synthesized in ten steps. The selectivity of the probe was demonstrated with immunoblotting and confocal imaging of immunostained cells expressing the CaV1.2 isoform of LTCCs proteins. Applying FluoBar1 to astrocyte model cells U118-MG allowed us to measure a 5-fold increase in fluorescence density of LTCCs upon glutamate exposure.ConclusionsImaging probe FluoBar1 allows the real-time monitoring of LTCCs in living cells, revealing for first time that glutamate causes a rapid increase of LTCC membranar density in astrocyte model cells. FluoBar1 may help tackle previously intractable questions about LTCC dynamics in cellular events.

Abstract P502: Abnormal Myocyte Calcium Dynamics And The Resultant Contraction Band Formation Of The Rat Heart Under Irreversible Injury By Membrane Permeabilization

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Yuma Morishita ◽  
Shoko Tamura ◽  
Kentaro Mochizuki ◽  
Yoshinori Harada ◽  
Hideo Tanaka
Keyword(s):  
Fluorescence Intensity ◽  
High Frequency ◽  
Time Course ◽  
Morphological Changes ◽  
Confocal Imaging ◽  
Band Formation ◽  
Contraction Band Necrosis ◽  
Scanning Confocal Microscopy ◽  
The Individual ◽  
Contraction Band

Ca 2+ overload is a cardinal feature of cardiomyocyte injury, and its progression to irreversible state leads to cell death. However, unknowns are the precise spatiotemporal changes in the myocyte Ca 2+ dynamics and the relevant cell morphology of irreversibly injured hearts. On the hypothesis that myocytes exhibit high-frequency Ca 2+ waves and contraction band necrosis in saponin-permeabilized injured heart, we observed changes in the Ca 2+ dynamics and the relevant morphological changes in the subepicardial myocardium of the Fluo4-loaded rat hearts (n = 14) by rapid-scanning confocal microscopy (100 frames/s) under Langendorff perfusion with 0.3 mM Ca 2+ -Tyrode solution including 0.4 % saponin at 30°C. Also performed was confocal imaging of tetramethylrhodamine methyl ester (TMRM) fluorescence of the myocardium. Under quasi-quiescence of the heart after dissection of the SA node, individual myocytes barely exhibited spontaneous Ca 2+ waves, whereas after commencement of saponin perfusion high-frequency (118 ± 9.7 /min/cell, mean ± SEM) Ca 2+ waves (hereafter, “agonal waves”) emerged within 1 min, showing asynchronous, oscillatory contractions in the individual myocytes with a V prop of 124 ± 2.5 μm/s (n = 60). Subsequently, the waves gradually decreased in frequency with concomitant slowing of its decay time course, and eventually, disappeared in 6 min; myocytes exhibited high, static Fluo4-fluorescence intensity. Along with the progression of Ca 2+ overload by saponin, the TMRM fluorescence intensity was discretely lost in individual myocytes. The myocytes showing the agonal waves exhibited contraction bands, i.e., band-like aggregations of the actin fibers. Under mechanical arrest of the heart by 2,3-butanedione monoxime (20 mM), saponin still induced the agonal waves with a frequency of 253 ± 10.6 /cell/min and V prop of 118 ± 2.1 μm/s (n = 60); however, contraction bands were barely seen.In conclusion, irreversible myocyte injury by saponin provoked agonal Ca 2+ waves and oscillatory contractions indicating progressive Ca 2+ overload and the following mitochondrial damage, which may provide deeper insights into understanding the mechanism of contraction band necrosis.

Postischemic Morphological Changes of the Dentate Gyrus in the Gerbil During Reperfusion

2001 ◽  
Vol 7 (S2) ◽  
pp. 658-659
Author(s):  
S.M. Yu ◽  
J.C. Wang
Keyword(s):  
Carotid Artery ◽  
Dentate Gyrus ◽  
Common Carotid Artery ◽  
Morphological Changes ◽  
Membrane Damage ◽  
Immunocytochemical Staining ◽  
Silk Suture ◽  
Pathophysiological Mechanism ◽  
Ischemic Lesion ◽  
Ischemic Period

Postischemic lesion following reperfusion have been investigated in the gerbil by temporary occlusion of a common carotid artery. Two phenomena have been reported in injured ischemic cells: the inability to restore mitochondrial function and evidence of plasma membrane damage. For Further understanding the pathophysiological mechanism of ischemic lesion, we have evaluated the various ischemic period and early postischemic reperfusion. in addition to the morphological changes of the dentate gyrus by light microscopy, we employed the immunocytochemical staining for iNOS and eNOS.The mongolian gerbil, Meriones unguiculatus, were anesthetized with α-chloralose (350mg/kg), bilateral common carotid artery occlusion was induced for 90 minutes. The right common carotid artery was ligated with 5-0 silk suture, and the left was clamped by a micro vascular/miniature aneurysmal clip. After an ischemic period of 90 minutes, restoration of the blood flow of the left common carotid artery was accomplished by withdrawing the microvascular clip.

scholarly journals Essential Tremor

2015 ◽  
Vol 22 (2) ◽  
pp. 108-118 ◽  
Author(s):  
Elan D. Louis
Keyword(s):  
Essential Tremor ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Neurological Diseases ◽  
The United States ◽  
The Past ◽  
Degenerative Disorders ◽  
Postmortem Studies ◽  
New Formulation ◽  
Cell Interface

Essential tremor (ET) is one of the most common neurological diseases, with an estimated 7 million affected individuals in the United States. Postmortem studies in the past few years have resulted in new knowledge as well as a new formulation of disease pathophysiology. This new formulation centers on the notion that ET might be a disease of the cerebellum and, more specifically, the Purkinje cell (PC) population. Indeed, several investigators have proposed that ET may be a “Purkinjopathy.” Supporting this formulation are data from controlled postmortem studies demonstrating (1) a range of morphological changes in the PC axon, (2) abnormalities in the position and orientation of PC bodies, (3) reduction in the number of PCs in some studies, (4) morphological changes in and pruning of the PC dendritic arbor with loss of dendritic spines, and (5) alterations in both the PC-basket cell interface and the PC-climbing fiber interface in ET cases. This new formulation has engendered some controversy and raised additional questions. Whether the constellation of changes observed in ET differs from that seen in other degenerative disorders of the cerebellum remains to be determined, although initial studies suggest the likely presence of a distinct profile of changes in ET.

scholarly journals Immature Dentate Gyrus: An Endophenotype of Neuropsychiatric Disorders

2013 ◽  
Vol 2013 ◽  
pp. 1-24 ◽  
Author(s):  
Hideo Hagihara ◽  
Keizo Takao ◽  
Noah M. Walton ◽  
Mitsuyuki Matsumoto ◽  
Tsuyoshi Miyakawa
Keyword(s):  
Dentate Gyrus ◽  
Neuropsychiatric Disorders ◽  
Emotional Behavior ◽  
Knockout Mutant ◽  
Potential Implication ◽  
Behavioral Abnormalities ◽  
Normal Cognitive Function ◽  
Chronic Fluoxetine ◽  
Almost All ◽  
Abnormal Behaviors

Adequate maturation of neurons and their integration into the hippocampal circuit is crucial for normal cognitive function and emotional behavior, and disruption of this process could cause disturbances in mental health. Previous reports have shown that mice heterozygous for a null mutation inα-CaMKII, which encodes a key synaptic plasticity molecule, display abnormal behaviors related to schizophrenia and other psychiatric disorders. In these mutants, almost all neurons in the dentate gyrus are arrested at a pseudoimmature state at the molecular and electrophysiological levels, a phenomenon defined as “immature dentate gyrus (iDG).” To date, the iDG phenotype and shared behavioral abnormalities (including working memory deficit and hyperlocomotor activity) have been discovered in Schnurri-2 knockout, mutant SNAP-25 knock-in, and forebrain-specific calcineurin knockout mice. In addition, both chronic fluoxetine treatment and pilocarpine-induced seizures reverse the neuronal maturation, resulting in the iDG phenotype in wild-type mice. Importantly, an iDG-like phenomenon was observed in post-mortem analysis of brains from patients with schizophrenia/bipolar disorder. Based on these observations, we proposed that the iDG is a potential endophenotype shared by certain types of neuropsychiatric disorders. This review summarizes recent data describing this phenotype and discusses the data’s potential implication in elucidating the pathophysiology of neuropsychiatric disorders.

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