scholarly journals Four weeks lithium treatment alters neuronal dendrites in the rat hippocampus

2013 ◽  
Vol 16 (6) ◽  
pp. 1373-1382 ◽  
Author(s):  
Seong S. Shim ◽  
Michael D. Hammonds ◽  
Ronald F. Mervis
Keyword(s):  
Synaptic Plasticity ◽  
Lithium Treatment ◽  
Neuronal Morphology ◽  
Total Density ◽  
Dendritic Trees ◽  
Distal Half ◽  
Proximal Half ◽  
Area Ca1 ◽  
Dendritic Branching ◽  
Dendritic Branches

AbstractA large body of evidence from molecular, cellular and human studies suggests that lithium may enhance synaptic plasticity, which may be associated with its therapeutic efficacy. However, only a small number of studies have directly assessed this. To determine whether lithium treatment alters structural synaptic plasticity, this study examined the effect of 4 wk lithium treatment on the amount and distribution of dendrites in the dentate gyrus (DG) and hippocampal area CA1 of young adult rats. Following 4 wk lithium or control chow feeding, animals were decapitated, the hippocampi were prepared and stained using a rapid Golgi staining technique and the amount and distribution of the dendritic branching was evaluated using Sholl analyses (method of concentric circles). In the DG, lithium treatment increased the amount and distribution of dendritic branches in the proximal half of dendritic trees of the granule cells and reduced branching in the distal half. In area CA1, the same treatment also increased the number of dendritic branches in the proximal half of apical dendritic trees of CA1 pyramidal cells and reduced branching in the distal half of apical dendritic trees but had no effect on basilar dendritic trees. The lithium treatment altered the total density of dendritic trees in neither the DG nor area CA1. These findings suggest that, in the DG and apical CA1, chronic lithium treatment rearranges neuronal morphology to increase dendritic branching and distribution to where major afferent input is received.

SCALING BEHAVIOR OF THE DENDRITIC BRANCHES OF THALAMIC NEURONS

Fractals ◽  
1993 ◽  
Vol 01 (02) ◽  
pp. 171-178 ◽  
Author(s):  
KLAUS-D. KNIFFKI ◽  
MATTHIAS PAWLAK ◽  
CHRISTIANE VAHLE-HINZ
Keyword(s):  
Growth Process ◽  
Scaling Law ◽  
Branching Ratio ◽  
Scaling Behavior ◽  
Neuronal Growth ◽  
Thalamic Neurons ◽  
Dendritic Trees ◽  
Ventrobasal Complex ◽  
Dendritic Branches

The morphology of Golgi-impregnated thalamic neurons was investigated quantitatively. In particular, it was sought to test whether the dendritic bifurcations can be described by the scaling law (d0)n=(d1)n+(d2)nwith a single value of the diameter exponent n. Here d0 is the diameter of the parent branch, d1 and d2 are the diameters of the two daughter branches. Neurons from two functionally distinct regions were compared: the somatosensory ventrobasal complex (VB) and its nociceptive ventral periphery (VBvp). It is shown that for the neuronal trees studied in both regions, the scaling law was fulfilled. The diameter exponent n, however, was not a constant. It increased from n=1.76 for the 1st order branches to n=3.92 for the 7th order branches of neurons from both regions. These findings suggest that more than one simple intrinsic rule is involved in the neuronal growth process, and it is assumed that the branching ratio d0/d1 is not required to be encoded genetically. Furthermore, the results support the concept of the dendritic trees having a statistically identical topology in neurons of VB and VBvp and thus may be regarded as integrative modules.

Targeted disruption to NMDA receptor dependent synaptic plasticity in area CA1 of the hippocampus

2021 ◽  
pp. 113808
Author(s):  
Alejandra Arias-Cavieres ◽  
Ateh Fonteh ◽  
Carolina I. Castro-Rivera ◽  
Alfredo J. Garcia
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptor ◽  
Targeted Disruption ◽  
Area Ca1

Microtubules in the Heliozoan Axopodium

1971 ◽  
Vol 8 (1) ◽  
pp. 127-151
Author(s):  
Y. SHIGENAKA ◽  
L. E. ROTH ◽  
D. J. PIHLAJA
Keyword(s):  
Microscopic Study ◽  
Distal Portion ◽  
Distilled Water ◽  
Electron Microscopic ◽  
Reduced Order ◽  
Distal Half ◽  
Microtubule Array ◽  
Proximal Half ◽  
Microtubule Stability ◽  
High Lability

The precise microtubule array present in the heliozoan axopodium has been studied by experimental degradation by using the protein denaturing agent urea. Since concentrations used in typical applications were found to destroy the whole organism immediately, very dilute solutions, usually 0.15 M, were used to study axopodial retraction, which was shown to occur in 2 stages: the distal half reacts immediately and is lost in very few minutes, largely by release of segments, while retraction of the proximal half may extend over an hour. Recovery of axopodial length by removal of organisms to distilled water is possible if treatment is not carried to full axopodium loss, though organisms must be treated with solutions more dilute than 0.1 M to avoid lysis. Electron-microscopic study of retracting axopodia showed degradation of microtubules at innumerable points even in the proximal regions. Similar studies of untreated organisms showed that the typical microtubule array is found throughout the proximal portion but is progressively imprecise in the distal portion as the tip is approached. High lability to urea is therefore correlated with reduced order and reduced numbers of long linkage elements in the microtubule array. An intra-microtubule metastability is proposed and is discussed with regard to the formation of axonemes, the use of dilute urea to test microtubule stability differences, and the gradion hypothesis presented in previous work.

scholarly journals S-Ketamine Exerts Antidepressant Effects by Regulating Rac1 Gtpase Mediated Synaptic Plasticity in the Hippocampus of Stressed Rats

2021 ◽  
Author(s):  
Xianlin Zhu ◽  
Fan Zhang ◽  
Yufeng You ◽  
Hongbai Wang ◽  
Su Yuan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Molecular Mechanisms ◽  
Electrophysiological Study ◽  
Transmission Function ◽  
Long Term Potentiation ◽  
Neuronal Morphology ◽  
Antidepressant Effect ◽  
Mild Stress ◽  
Antidepressant Effects ◽  
Expression And Activity

Abstract Clinical studies have found that ketamine has a rapid and lasting antidepressant effect, especially in the case of patients with major depressive disorder (MDD). The molecular mechanisms, however, remain unclear. In this study, we observe the effects of S-Ketamine on the expression of Rac1, neuronal morphology, and synaptic transmission function in the hippocampus of stressed rats. Chronic unpredictable mild stress (CUMS) was used to construct stressed rats. The rats were given a different regimen of ketamine (20mg/kg, i.p.) and Rac1 inhibitor NSC23766 (50µg, ICV) treatment. The depression-like behavior of rats was evaluated by sucrose preference test and open-field test. The protein expression of Rac1, Glur1, synapsin1, and PSD95 in the hippocampus was detected by Western blot. Pull-down analysis was used to examine the activity of Rac1. Golgi staining and electrophysiological study were used to observe the neuronal morphology and long-term potentiation (LTP). Our results showed that ketamine can up-regulate the expression and activity of Rac1; increase the spine density and the expression of synaptic-related proteins such as Glur1, Synapsin1, and PSD95 in the hippocampus of stressed rats; reduce the CUMS-induced LTP impairments; and consequently improve depression-like behavior. However, Rac1 inhibitor NSC23766 could have effectively reversed ketamine-mediated changes in the hippocampus of rats and counteracted its antidepressant effects. The specific mechanism of S-ketamine's antidepressant effect may be related to the up-regulation of the expression and activity of Rac1 in the hippocampus of stressed rats, thus enhancing synaptic plasticity.

scholarly journals Genetic definition of two functional elements in a bacteriophage T4 host-range "cassette".

Genetics ◽  
1989 ◽  
Vol 122 (3) ◽  
pp. 471-479
Author(s):  
M Snyder ◽  
W B Wood
Keyword(s):  
Host Range ◽  
Bacteriophage T4 ◽  
Temperature Sensitive ◽  
Tail Fiber ◽  
Neighboring Gene ◽  
Distal Half ◽  
Bacterial Surface ◽  
Fiber Assembly ◽  
Proximal Half ◽  
Carboxy Terminal

Abstract Gene 37 of T4 encodes the major subunit of the distal half of the tail fiber. The distal tip of the fiber, comprised of the carboxy-terminal ends of two molecules of gene 37 product (gp37), carries the principal determinant of the phage host range. The gp37 carboxyl termini recognize the bacterial surface during infection, and, in addition, include a site required for interaction with the product of gp38 during distal half-fiber assembly. In the absence of interaction with gp38, gp37 polypeptides do not dimerize. Eleven temperature-sensitive mutants with defects located near the promoter-distal end of gene 37 were tested at nonpermissive temperatures for production of an antigen that is diagnostic of distal half-fiber assembly. Six of the mutations prevent distal half-fiber assembly. The other five allow assembly of distal half fibers, which combine with proximal half fibers and attach to phage particles, but the resulting phage do not adsorb to bacteria. These two classes of mutations define two adjacent but separate genetic regions, corresponding to two different functional domains in gp37. These two regions and the neighboring gene 38 comprise a functional unit that can be considered as a host-range "cassette," with features that are strikingly similar to corresponding functional units in other unrelated as well as related phages.

scholarly journals ANALYSIS ON THE EFFECT OF HALF ANGLE ON THE DISPLACEMENT OF PEDICLE SCREW DURING AXIAL PULL-OUT TEST IN CANCELLOUS BONE USING 2D AXISYMMETRIC FE MODEL

2021 ◽  
Vol 57 (2) ◽  
pp. 153-158
Author(s):  
Harikrishna Makaram ◽  
◽  
Ramakrishnan Swaminathan ◽  
Keyword(s):  
Pedicle Screw ◽  
High Stress ◽  
Pedicle Screws ◽  
Stress Transfer ◽  
Von Mises Stress ◽  
Fe Model ◽  
Distal Half ◽  
Proximal Half ◽  
Pull Out ◽  
Half Angle

Pedicle screw fixations are commonly used in the treatment of spinal pathologies. For effective treatment, stable anchorage between the screw and bone is necessary. In this study, the influence of proximal and distal half angle of the screw, on the displacement of fixation and stress transfer are simulated using a 2D axisymmetric finite element model. A parametric study was performed by varying the proximal half-angle between 0° and 60° in steps of 10° and the distal half angles are considered as 30° and 40°. The material properties and boundary conditions are applied based on previous studies. Frictional contact is considered between the bone and screw. Results show that, displacement of fixation is observed to be minimum at a proximal half angle of 0° and maximum at an angle of 60°. High stress concentration is observed in first few threads with highest maximum von Mises stress at an angle of 60°. High stress transfer was obtained for proximal half-angles of 40° and 50°. It is observed that, this method might aid to develop better pedicle screws for treatment of Scoliosis.

scholarly journals N-Docosahexanoylethanolamine Reduces Microglial Activation and Improves Hippocampal Plasticity in a Murine Model of Neuroinflammation

2020 ◽  
Vol 21 (24) ◽  
pp. 9703
Author(s):  
Anna Tyrtyshnaia ◽  
Anatoly Bondar ◽  
Sophia Konovalova ◽  
Ruslan Sultanov ◽  
Igor Manzhulo
Keyword(s):  
Synaptic Plasticity ◽  
Microglial Activation ◽  
Hippocampal Slices ◽  
Morphological Characteristics ◽  
Long Term Potentiation ◽  
Structural Analog ◽  
Neuronal Morphology ◽  
Hippocampal Neurogenesis ◽  
Inflammatory Factors ◽  
Negative Effect

Chronic neuroinflammation is a common pathogenetic link in the development of various neurological and neurodegenerative diseases. Thus, a detailed study of neuroinflammation and the development of drugs that reduce or eliminate the negative effect of neuroinflammation on cognitive processes are among the top priorities of modern neurobiology. N-docosahexanoylethanolamine (DHEA, synaptamide) is an endogenous metabolite and structural analog of anandamide, an essential endocannabinoid produced from arachidonic acid. Our study aims to elucidate the pharmacological activity of synaptamide in lipopolysaccharide (LPS)-induced neuroinflammation. Memory deficits in animals were determined using behavioral tests. To study the effects of LPS (750 µg/kg/day, 7 days) and synaptamide (10 mg/kg/day, 7 days) on synaptic plasticity, long-term potentiation was examined in the CA1 area of acute hippocampal slices. The Golgi–Cox method allowed us to assess neuronal morphology. The production of inflammatory factors and receptors was assessed using ELISA and immunohistochemistry. During the study, functional, structural, and plastic changes within the hippocampus were identified. We found a beneficial effect of synaptamide on hippocampal synaptic plasticity and morphological characteristics of neurons. Synaptamide treatment recovered hippocampal neurogenesis, suppressed microglial activation, and significantly improved hippocampus-dependent memory. The basis of the phenomena described above is probably the powerful anti-inflammatory activity of synaptamide, as shown in our study and several previous works.

Neonatal Anesthesia and dysregulation of the Epigenome

2021 ◽  
Author(s):  
Omar Hoseá Cabrera ◽  
Nemanja Useinovic ◽  
Vesna Jevtovic-Todorovic
Keyword(s):  
Synaptic Plasticity ◽  
Apoptotic Cell ◽  
Neuronal Morphology ◽  
Developmental Neurotoxicity ◽  
Affective Behavior ◽  
Neuronal Function ◽  
Public Health Importance ◽  
Behavioral Deficits ◽  
And Behavior ◽  
Critical Public Health

Abstract Each year, millions of infants and children are anesthetized for medical and surgical procedures. Yet, a substantial body of preclinical evidence suggests that anesthetics are neurotoxins that cause rapid and widespread apoptotic cell death in the brains of infant rodents and non-human primates. These animals have persistent impairments in cognition and behavior many weeks or months after anesthesia exposure, leading us to hypothesize that anesthetics do more than simply kill brain cells. Indeed, anesthetics cause chronic neuropathology in neurons that survive the insult, which then interferes with major aspects of brain development, synaptic plasticity, and neuronal function. Understanding the phenomenon of anesthesia-induced developmental neurotoxicity is of critical public health importance because clinical studies now report that anesthesia in human infancy is associated with cognitive and behavioral deficits. In our search for mechanistic explanations for why a young and pliable brain cannot fully recover from a relatively brief period of anesthesia, we have accumulated evidence that neonatal anesthesia can dysregulate epigenetic tags that influence gene transcription such as histone acetylation and DNA methylation. In this review, we briefly summarize the phenomenon of anesthesia-induced developmental neurotoxicity. We then discuss chronic neuropathology caused by neonatal anesthesia, including disturbances in cognition, socio-affective behavior, neuronal morphology, and synaptic plasticity. Finally, we present evidence of anesthesia-induced genetic and epigenetic dysregulation within the developing brain that may be transmitted intergenerationally to anesthesia-naïve offspring.

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